PEMICU 1 BLOK PENGINDERAAN

Vivian Saputra
405140126
 LI
• Anatomi Mata (Ruang Orbita, palpebra, otot persarafan, bulbus
oculi,vaskularisasi mata, apparatus lacrimalis)
• Histologi Mata
• Fisiologi penglihatan (struktur refraktif, media refraksi, akomodasi,
fototransduksi, jaras penglihatan, mekanisme pergerakan bola
mata, alira aqueous humour)
• Keluhan mata tenang & penglihatan menurun (macam-macam &
definisi)
• Etiologi & patfis
• Anamnesis, PF, PP, pemeriksaan visus, oftalmoskopi, tonometri
• Tatalaksana farmakologi & non-farmakologi (kacamata – resep
kacamata)
• Prognosis & komplikasi
• Kegawatdaruratan pada kelainan mata.
ANATOMI MATA
Rongga Orbita

Rongga orbita berbentuk

piramid segi empat terletak di
skeleton fasialis.

Orbit: Bones

1. Frontal bone
2. Optic canal
3. Ethmoidal foramina
4. Ethmoid bone
5. Lacrimal groove
6. Lacrimal bone
7. Palatine bone
8. Maxilla
9. Inferior orbital fissure
10. Zygomatic bone
11. Greater wing of sphenoid
12. Superior orbital fissure
13. Lesser wing of sphenoid
 Rongga Orbita

http://keywordteam.net/gallery/419002.html
 Palpebra & Conjunctiva

D B
A
4
2
1
6

5
3
C
 Apparatus Lacrimalis
6. Tendon of levator palpebrae superioris muscle

5. Lacrimal gland

1. Lacrimal canaliculi

2. Lacrimal sac

4. Puncta
3. Nasolacrimal duct
 2. Medial
rectus ORBIT: EXTRA-
OCULAR MUSCLES
3. Superior
rectus
5. Levator
4. Lateral palpebrae
rectus superioris

1. Superior
oblique

7. Inferior 6. Inferior
oblique rectus
 18. Long
Bulbus Oculi
posterior 1. Postremal
cliliary artery (vitreous) chamber
17. Short 2. Ora serrata
posterior
ciliary 3. Posterior
arteries chamber
16. Optic 4. Anterior
nerve [II] chamber
15. Optic 5. Cornea
disc
14. Fovea 6. Lens
centralis
7. Iris
8. Scleral venous
sinus
13. Sclera 9. Ciliary body
12. Choroid 11.
Retina
10. Anterior ciliary artery
HISTOLOGI
Tunics of the eye
• Terdiri dari 3 lapisan:
– Tunica fibrosa  membentuk lapisan luar yg kuat pada
mata
– Tunica vasculosa  lapisan tengah yg berpigmen dan
mempunyai pmebuluh darah
– Neutral tunic (Retina)  lapisan paling dalam.
 Tunica fibrosa
• Terdiri dari sklera dan kornea
– Sklera  menutupi 5/6 bgn posterior mata
– Kornea  menutupi 1/6 bgn anterior mata
• Sklera
– Hampir tdk ada pembuluh darah
– Terdiri dari kolagen tipe 1 dan elastic fibers
• Kornea
– Bgn anterior dari tunica fibrosa yg transparan, avaskular, dan
highly innervated yg menonjol ke anterior
– Terbagi menjadi 5 lapisan:
• Corneal epithelium
• Bowman’s membrane
• Stroma
• Descemet’s membrane
• Corneal endothelium
 Lapisan2 kornea
• Corneal epithelium
– Lanjutan dari konjungtiva
– A stratified, squamous, nonkeratinized epithelium
– Banyak dipersarafI oleh free nerve endings
– The basal cells have a high proliferative capacity
important for renewal and repair of the corneal
surface and emerge from stem cells in the
corneoscleral limbus that encircles the cornea.
– The corneal epithelium also functions in transferring
water and ions from the stroma into the conjunctival
sac.
 Lapisan2 kornea
• Bowman’s membrane
– Terletak di bawah corneal epithelium
– Terdiri dr type 1 collagen fibers
– Bowman’s membrane disintesis oleh corneal epithelium dan stroma
– Sensory nerve fibers pass through this structure to enter and terminate in the
epithelium.
• Stroma
– Bgn paling tebal dari kornea (90% dr ketebalan kornea)
– Terbentuk dari collagenous connective tissue (sebagian besar terdiri dr
kolagen tipe 1)
• Descemet’s membrane
– Basement membrane yg tebal dan terletak di antara stroma dan endothelium
• Corneal endothelium
– Melapisi permukaan internal kornnea
– Simple squamous epithelium
– Untuk sintesis protein yg penting untuk menjaga descement membrane
– Membrannya punya sodium pump yg transport sodium ions (Na+) ke anterior
chamber, dan ion tersebut secara pasif diikuti oleh chloride ions (Cl-) dan air.
– Excess fluid di stroma direabsorbsi oleh endotelium dan menjaga stroma
tetap terdehidrasi (faktro yg mempengaruhi kualitas refraktif kornea)
 Tunica vasculosa
• Terdiri dari:
– Choroid
– Cilliary body
– iris
 Choroid
• Lapisan berpigmen pada dinding posterior bola
mata yg menempel secara longgar pada tunica
fibrosa
• Warna hitam pada koroid krn terdapat banyak
melanosit
• Krn kaya akan pembuluh darah kecil  disebut
choriocapillary layer  berfungsi untuk memberi
nutriens ke retina
• Koroid dipisahkan dari retina oleh bruch’s
membrane
Cilliary body
 Lensa
• Tersusun oleh 3 bagian: kapsul lensa, epitel subkapsul,
dan serat2 lensa
• Kapsul lensa:
– Kebanyakan mengandung kolagen tipe IV dan glikoprotein yg
menutupi sel epitel dan membungkus keseluruhan lensa
• Epitel subkapsul:
– Hanya terdapat pada bgn anterior dan permukaan lateral
lensa, terletak persis di bawah kapsul lensa
– Disusun oleh selapis sel kuboid yg saling berhubungan
melalui gap junction
• Serat2 lensa
– Terletak di bawah epitel subkapsul dan kapsul lensa
– Sel2 ini akan diisi oleh kristalin yg merupakan protein lensa
yg akan meningkatkan indeks refraksi serat2 lensa
 Retina / Neutral tunic
• Retina merupakan lapisan ketiga / lapisan
terdalam bola mata yg mengandung sel2
fotoreseptor, yaitu sel batang dan sel kerucut
• Optic disk  terletak di dinding posterior 
tempat keluar saraf optik  tdk mengandung
fotoreseptor  dikenal sbg bintik buta
• 2,5 mm lateral dr optic disk  terdapat
makula lutea (yellow spot), ditengahnya
terdapat cekungan yg disebut fovea sentralis
 10 lapisan
retina
1. Epitel pigmen
2. Lapisan batang dan
kerucut
3. Membran limitan luar
4. Lapisan inti luar
5. Lapisan pleksiform luar
6. Lapisan inti dalam
7. Lapisan pleksiform
dalam
8. Lapisan sel2 ganglion
9. Lapisan serat nervus
opticus
10. Membran limitan
dalam
FISIOLOGI
Phsyiology Laurelee sherwood
Proses Refraksi
 Phototransduction by retinal cells (
convert light stimuli  neural signals)
1. An outer segment, which lies closest to the eye’s exterior,
facing the choroid. It detects the light stimulus.

2. An inner segment, which lies in the middle of the

photoreceptor’s length. It contains the metabolic
machinery of the cell.

3. A synaptic terminal, which lies closest to the eye’s interior,

facing the bipolar cells. It transmits the signal generated in the
photoreceptor on light stimulation to these next cells in the
Visual pathway.
Visual Pathway
Ganong
Review of Medical Phsyiology
COLOR VISION
Mata Tenang dengan Penurunan
Penglihatan Perlahan
 Penurunan visus perlahan : 9. Buta senja
1. Retinopati diabetikum 10. Degenerasi makula
2. Katarak 11. Hipertensi retinopati
3. Miopia 12. Anisometropi
4. Hipermetropi 13. Diplopia
5. Presbiopi 14. Keratokonus
LI 4
6. Glaukoma 15. Strabismus
7. Astigmatisme 16. Retinitis pigmentosa
8. Ambliopia
 Kelainan Refraksi
• Berkas cahaya paralel yang masuk ke mata
tidak jatuh tepat di retina ( ametropia)
• Miopia
• Hipermetropia
• Astigmatisma
• Presbiopia
 Miopia
• Keadaan dimana bayangan dari obyek yang jauh
difokuskan di depan retina oleh mata yang tidak
berakomodasi
• Disebabkan oleh kekuatan optik yang terlalu tinggi
karena cenderung cembung atau panjang aksial bola
mata yang terlalu besar
• Klasifikasi
• Manifestasi klinis :
– Sangat ringan : <1D
a. Penglihatan jarak
– Ringan : 1 – 3D
jauh yang buram
– Sedang : 3 – 6 D
b. Nyeri kepala
– Tinggi : 6 – 10 D
c. Kecenderungan
– Sangat tinggi : > 10 D
juling saat
melihat jauh
 Pemeriksaan
• Apabila menggunakan +0,5 D menjadi kabur,
gunakan lensa negatif terkecil
• Tambahkan lensa negatif sampai pasien dapat
membaca huruf pada baris 6/6
• Derajat yang dicatat adalah lensa sferis negatif
terkecil yang dapat memperbaiki tajam
penglihatan pasien
• Lakukan tes Duke Elder untuk melihat apakah
adanya koreksi yang berlebihan dengan
menambahkan + 0,25 D. target harus negatif
 Tatalaksana
• Menggunakan lensa sferis negatif dengan
kekuatan terkecil
• Ed = pasien dianjurkan untuk melakukan
aktivitas yang memanfaatkan penglihatan jauh
 Hipermtropia
• Bayangan obyek difokuskan di belakang retina
oleh mata yang tidak berakomodasi
• Disebabkan oleh power optic yang tidak kuat
• Manifestasi klinis :
• Klasifikasi : 1. Ps tua / >3 D biasanya
penglihatan jauh kabur
– Hipermetropia manifes 2. Penglihatan dekat cepat
• Absolut dan fakultatif buram
3. Nyeri kepala yang dipicu
– Hipermetropia laten saat melihat dekat
– Hipermetropia total 4. Sensitif terhadap cahaya
5. Spasme akomodasi
 Pemeriksaan
• Tambahkan kekuatan lensa sferis + hingga ps dapat
membaca pada baris 6/6
• Apabila baris 6/6 sudah terbaca maka tambahkan
0,25 D, tanya apakah masih dapat membaca pada
baris 6/6
• Apabila masih dapat terlihat jelas, maka tambahkan
sampai pandangan jadi kabur.
• Catat kekuatan lensa terbesar yang memberikan
penglihatan terbaik
 Tatalaksana
• Menggunakan lensa sferis positif dengan kekuatan
terbesar
• Ed  sebaiknya kacamata digunakan untuk
membantu relaksasi otot mata saatu melihat jauh
dan melihat dekat
 Astigmatisma
• Klasifikasi berdasarkan letak
• Mata menghasilkan titik fokus
bayangan dengan 1. Astigmatisma miopia
titik fokus multipel simpleks
2. Astigmatisma miopia
• Etiologi : kompositus
– Kelainan kornea 3. Astigmatisma campuran
– Kelainan lensa 4. Astigmatisma hiperopia
simpleks
• Klasifikasi 5. Astigmatisma hiperopia
– Reguler komopsitus
• with rule, against • Manifestasi klinis
rule
1. Penglihatan buram
– Ireguler 2. Head tilting
3. Menyipitkan mata untuk melihat jelas
4. Bahan bacaaan dilihat dekat aar jelas
 Tatalaksana
• Pada pasien astigmat anak, berikan koreksi
astigmat penuh
• Pada pasien astigmat dewasa, dicoba untuk
diberikan koreksi astigmat penuh. Pasien
diedukasi bahwa terdapat kemungkinan
pusing selama pemakaian kacamata
• Untuk menurunkan distorsi, gunakan lensa
silinder negatif
 https://www.aoa.org/documents/optometrists/QRG-17.pdf

Presbiopia
• Presbiopia adalah kondisi fisiologis normal
ireversibel yang mengganggu kemampuan untuk
melihat dengan jelas di dekat. Ini adalah hasil dari
penurunan bertahap pada amplitudo akomodatif
(yaitu, dari sekitar 15 dioptri pada anak usia dini
sampai 1 dioptri sebelum usia 60 tahun) karena
perubahan elastisitas kapsul dan lensa dan
terhadap perubahan ukuran keseluruhan dan
Bentuk lensa.
• Klasifikasi : - insipien presbiopia
- functional presbiopia
- absolut presbiopia
- premature presbiopia
- nocturnal presbiopia
• Faktor resiko : - Age (e.g., usually occurring at or
after age 40 ), uncorrected visual, pekerjaan yang
melibatkan tuntunan visual, gender ( paling sering
perempuan), Ocular disease or trauma (e.g.,
kerusakan lensa, zonula, dan prosesus siliaris),
Systemic disease (e.g., diabetes mellitus, multiple
sclerosis, cardiovascular accidents, vascular
insufficiency, myasthenia gravis, anemia, influenza,
measles),
 Tanda dan gejala
Tanda dan gejala :
• Beberapa tanda dan gejala miopia meliputi:
• kesulitan membaca cetakan kecil
• Harus menahan bahan bacaan lebih jauh dari jarak lengan
• Masalah melihat benda yang dekat dengan Anda
• Sakit kepala
• Ketegangan mata
Pemeriksaan Preesbiopia
- Ps diberi kartu baca  jarak baca 30-40 cm
- Membaca huruf terkecil
- Beri lensa sferis + 1,00 D dinaikkan perlahan hingga tulisan terkecil pada kartu
baca terbaca
- Dilakukan pd satu mata terlebih dahulu baru dilanjutkan mata yang lainnya.
 Tatalaksana
• Tidak ada obat untuk presbiopia.
• Beberapa perawatan yang bisa dilakukan untuk memperbaiki
penglihatan dengan menggunakan kaca mata korektif, lensa
kontak, atau operasi.
• Pemberian lensa atau kaca mata plus (+).
• Kaca mata bentuknya lebih tebal pada bagian bawahnya
(konveks) untuk penglihatan jarak dekat dan datar atau biasa
pada bagian atasnya untuk penglihatan jarak jauh.
 Source : American Academy Of Ophthalmology

Tatalaksana
• Keratoplasty konduktif (CK) menggunakan energi
radiofrekuensi untuk mengubah kelengkungan kornea.
• Operasi LASIK (laser-assisted in situ keratomielusis) .
• Penggantian lensa mata alami dengan dengan lensa
sintetis, yang disebut implan lensa intraokuler.
 Katarak
• Stiap keadaan kekeruhan lensa
yg dpt terjadi akibat hidrasi (
pe+ cairan) lensa,denaturasi
protein lensa atau ke2 nya
• Kekeruhan mengenai ke2 mata
& berjalan progresif /dpt tdk
mengalami prubahan dlm wktu
yg lama
• Pnyakit pd usia lanjut (
umumnya)
• E:
– Bahan toksik (kimia /fisik)
– Kracunan bbrp jenis obat :
kortikosteroid ,ergot
eserin,antikolinesterase topikal
– Kelainan sistemikyg dpt
mnimbulkan katarak :
DM,galaktosemi,distrofi
miotonik
– Ktarak jg dpt ditemukan dlm
keadaan tnpa adanya kelainan
mata /sistemik
• Fisik
• Kimia
• Pnyakit predisposisi
• Genetik & gg perkembangan
• Infeksi virus saat janin
• Usia
FKUI
ILMU PENYAKIT MATA
• Gejala: bila mungkin,tonometri
– Psien dgn katarak mngluh
pnglihatan berasap &
tajam pnglihatan mnurun
• Klasifikasi katarak:
progresif – Berdasarkan usia katarak
dpt diklasifikasikan dlm:
– Lensa keruhlensa tdk
• Katarak
transparan pupil bsa kongenitalkatarak yg
berwarna putih /abu terjdi pd usia dibwh 1 thn
• Katarak juvenilkatarak yg
terjdi > 1 thn
• Px yang dilakukan pd
• Katarak sensil katarak
psien katarak : px slit lamp stlh usia 50 thn
,funduskopi pd ke2 mata
 Katarak Senil
• Kekeruhan lensa yg terdapat
pd usia lanjut ( diatas 50
thn)
• Prubahan lensa pd usia
lanjut :
– Kapsul
• Menebal & krg elastis ( ¼
dibanding anak2)
• Mulai presbiopia
• Bentuk lamel kapsul
berkurang
• Trlihat bahan granular
– Epitel makin tipis
• Sel epitel pd ekuator
bertambah besar dan berat
• Bengkak dan vakuolisasi
mitokondria yg nyata
– Serat lensa:
• Lbh ireguler
• Pd kortek jelas kerusakan
serat sel
• Brown sclerotic nucleus
,sinar uv lama kelamaan
mrubah protein nukleus (
histidin dll) lensa
• Korteks tdk berwrna karena:
kadar a.askorbat tinggi &
mnghalangi fotooksidasi
– Sinar tdk bnyak mngubah
protein pd serat muda
 Acquired cataract
• Age Related Cataract – due to the deposition of urochrome pigment,
(best assessed with an oblique slit lamp beam)
a) Subcapsular Cataract
• Anterior subcapsular cataract lies directly
under the lens capsule c) Cortical Cataract :
• associated with fibrous metaplasia of the lens • Cortical cataract may involve the anterior
epithelium. /posterior lens cortex.
• Posterior subcapsular opacity lies just in front • The opacities start as clefts and vacuoles
of the posterior capsule and has a granular or between lens fibres due to cortical hydration
plaque-like appearance typically appears black • Opacification result inwedge shaped /radial
and vacuolated (retroilumination) spoke like opacities ( inferonasal quadrant
• Common symptom : glare & reduced vision
under bright lighting condition symptoms are
increased by:
– miosis, such as occurs during near visual activity
and in bright sunlight.
b) Nuclear sclerotic cataract :
• Nuclear cataract is an exaggeration of normal
ageing change
• associated with myopia due to an increase in
the refractive index of the nucleus.
• Nuclear sclerotic cataract is characterized by a
yellowish hue

Kanski Clinical Opthalmology

Vaughan & Ashbury
Fig. 9.2 Age-related cataract. (A) Cortical;
 Cataract Maturity
Cataract maturity
• Immature cataract is one in which the
lens is partially opaque.

• Mature cataract is one in which the

lens is completely opaque

• Hypermature cataract has a shrunken

and wrinkled anterior capsule ( due
to leakage of water out of the lens.
• Morgagnian cataract is a hypermature
cataract in which liquefaction of the
cortex has allowed the nucleus to
sink inferiorly
 Cataract in Systemic Disease
a) Diabetes Mellitus b) Atopic dermatitis
• Hyperglycaemia is reflected in a high level • About 10% of patients with severe atopic
of glucose in the aqueous humour  dermatitis develop cataracts
diffuses into the lens. • these are often bilateral and may mature
– glucose is metabolized into sorbitol, which quickly.
accumulates within the lens, resulting in
secondary osmotic overhydration.
– may affect the refractive index of the lens • Shield-like dense anterior subcapsular
with consequent fluctuation of refraction plaque that wrinkles the anterior capsule
– Cortical fluid vacuoles develop and later is characteristic.
evolve into frank opacities.
– Classic diabetic cataract, which is actually
rare, consists of snowflake cortical opacities.
 Secondary Cataract
A secondary (complicated) cataract develops as
a result of other primary ocular disease.
• Chronic anterior uveitis is the most common
cause of secondary cataract, the incidence
being related to the duration and intensity of
inflammation.
• High myopia
• Acute congestive angle closure
 Management
• Operasi katarak ekstrakapsular
– Dilakukan pngeluaran isi lensa dgn memcah /mrobek
kapsul lensa anterior shingga masa lensa dan korteks lensa
dpt keluar
– Trmsk: ekstraksi linear,aspirasi &irigasi
– Pnyulit yg dpt timbul: katarak sekunder
• Operasi katarak intrakapsular:
– P’mbedahan dgn mngeluarkan sluruh lensa bersama
kapsul
– KI  tdk boleh dilakukan pd ps krg dari 40 thn
– Pnyulit: astigma,glaukoma,uveitis,endoftalmitis dan
perdarahan
 Glaukoma
• Glaukoma berarti hijau hambatan pupil)
kebiruan yg mmberikan kesan • Pd glaukoma akan ada
wrna pd pupil ps glaukoma lemahnya fungsi mata dgn cacat
• Kelainan mata glaukoma lapang pandang & krusakan
ditandai dgn mningkatnya anatomi ( brupa ekskavasi serta
tekanan bola mata,atrofi papil degenerasi papil saraf optik
saraf optik & mnciutnya lapang )kebutaan
pandang – Luas /dlmnya ekskavasi (
• Pnyakit yg ditandai dgn pnggaungan) pd glaukoma
pninggian tekanan intraokular kongenital dipakai sbg indikator
ini disebabkan o/ progresifitas glaukoma
– Ber+ produksi cairan mata oleh
bdn siliar
– br – nya pngeluaran cairan
mata didaerah sudut bilik
mata/dicelah pupil ( glaukoma
FKUI
ILMU KESEHATAN MATA
 Klasifikasi Glaukoma
• Klasifikasi Vaughen:
– Glaukoma primer
• Glaukoma sudut terbuka
• Glaukoma sudut smpit
– Glaukoma kongenital
• Primer /infantil
• Mnyertai kelainan kongenital lain
– Glaukoma sekunder:
• Prubahan lensa
Fig. 10.51 Moderate to marked glaucoma.
• Kelainan uvea
• Trauma
• Bedah
• Steroid
 Pathophysiology of Glaucoma
• Major mechanism of visual loss in
glaucoma retinal ganglion cell
apoptosis thinning of the inner
nuclear & nerve fiber layers of retina
& axonal loss in optic nerves
• In primary open angle glaucoma 
• Optic disc becomes atrophic ,with
enlargment of optic cup
• The effect of raised TIO are
influenced by the time course &
magnitude of the rise TIO
• In acute angle closure glaucoma
TIO reache 60-80 mmhg (
resulting in acute ischemic damage
to the iris with corneal edema &
optic nerve damage)
The TIO does not usually rise above
30 mmHg & retinal ganglion cells
may susceptible to damage ( from
TIO pressure in the normal range)
/major mechanism of damage 
optic nerve head ischemia .
Vaughan & Ashbury
Clinical opthalmology
 Primary open angel glaucoma
• Primary open-angle glaucoma
(POAG) is a commonly bilateral
disease of adult onset.
It is characterized by:
– IOP >21 mmHg at some stage.
– Glaucomatous optic nerve
damage.
– An open anterior chamber
angle.
– Characteristic visual field loss
as damage progresses.
– Absence of signs of secondary
glaucoma or a
nonglaucomatous cause for the
optic neuropathy.
• RISK FACTOR:
– IOP higher the IOP ,the
greater glaucoma ( IOP of 4
mmhg or more)
– Race :4x more common
develop at earlier age
– Family history of POAG
– DM
– Myopia ( speculated that this
may be due to mechanical
factors ( optic disk)
– Contraceptive pill  long term
oral contraceptive pill
– Vascular disease (ex
,hypertension,poor ocular
perfusion )
– Translaminar pressure gradiant
– Optic disc area
– Ocular perfusion presure
 Pathogenesis of glaucomatous
optic neuropathy
• Retinal ganglion cell death may be involved:
in glaucoma occurs – Direct mechanical
predominantly through damage to retinal nerve
apoptosis (programmed fibres at the optic nerve
cell death) head.
• After injury cascade of – Ischaemic damage,
proliferation in astrocyte possibly due to
compression of blood
& glial cell ,matrix vessels supplying the
extracellular & optic nerve head.
remodelling • Common pathways of
• One or both of the damage.
following mechanisms
 DIAGNOSIS
• History – Colour vision
– Visual symptoms – Slit lamp
– Previous opthalmic history – Tonometry
– Family history – Gonioscopy
– Past medical history – Optic disc examination
– Current medication
– Social history including
smoking & alcohol intake
– Allergies
• Examination:
– Visual acuity
– Pupils
 Treatment Goals
Treatment goals
• Proportional reduction. An alternative
strategy is to aim for a reduction in IOP by •
a certain percentage – often 30% – and
then monitor, aiming for a further
reduction if progression occurs.
• Response to progression
Medical Therapy
Commencing medical therapy
○ Any drug chosen should be prescribed in
the lowest concentration consistent with
the desired therapeutic effect, and
administered as infrequently as possible.
• Ideally the drug with the fewest potential
side effects should be used.
• Initial treatment is usually with one type
of medication, typically a prostaglandin
analogue or beta-blocker.
N/review after starting medication 4-8
weeks
– Response to the drug against the target IOP
– If the response satisfactory asses set
further 3-6 months
• Surgery trabeculectomy
• PROGNOSIS
– Ps will not become blind in their lifetime
– POAG the lifetime chance of blindness in
both eyes has historically been 5–10%;
 Primary Angle Closure Glaucoma
• angle closure’ refers to occlusion of the
trabecular meshwork by the peripheral iris
(iridotrabecular contact – ITC) obstructing
aqueous outflow.
• Classification
– Primary angle closure suspect (PACS)
• Gonioscopy (shows posterior meshwork ITC in 3/
more quadrant)
• Normal IOP,optic disc & visual field
• Pigment smudging /narrow angle approach (20
degree/less)

– Primary angle closure ( PAC)

• Gonioscopy shows 3 /more quadrant of ITC with
raised IOP /excessive pigment smudging
• Normal optic disc & field
– Primary angle closure glaucoma
• ITC in 3/more quadrant
• Optic nerve damage from an episode of severe
IOP elevation
 Mechanism
• Mechanism involved can be categorized according anatomical level :
– Relative pupilary block
• Failure of aquos flow throw pupil lead to a pressure differential between
anterior & posterior chamber resulting anterior bowing of the iris
• Relieved by iridotomy ( equalize anterior & posterior chamber pressure)
– non pupillary block
• Associated with deeper anterior chamber
• Ptient with non pupillary block (particulary those with plateau iris)
• Plateau irisuncommon condition which CAO depth is normal but anterior
chamber angle is very narrow becausee of anterior position of ciliary
procesuss
– Reduced aqueous outflow
• Appositional obstruction of iris
• Risk Factors
– Age (relative pupillary
block about 60 years )
– Gender ( Female>>)
– Race (far eastern )
– Family history
– Refraction eyes with “
pure” pupillary block are
typically hypermetropic – Sign:
– Axial length ( short eyes
tend to have shallow
AC)
• Diagnosis
– Symptoms
• Asymtomatic (include
intermittenly/chronic
elevated IOP)
• Intermittent mild
symptoms of blurring
(“smoke filled room) &
haloes ( rainbow around
light) ( due corneal
epithelial edema)
• Acutely with decrease
vision,redness,headache
• Precipitating factor:
– Watch tv in dark room
– Pharmacological
mydriasis
– topiramate
• Acute primary angle
closure
– VA 6/60
– IOP usually high ( 50-
100 mmhg)
– Conjunctival hyperami
with circumcorneal
injection
– Corneal epithelial
edema
– Anterior chamber
shallow
– Unreactive mid-dilated
vertically oval pupil
 Investigation
• Anterior Segment OCT :
ultrasound biomicroscopy
• Anterior chamber depth
measurement
• Biometry
• Posterior segment USG
• Provocative test
• THERAPY
– PACS laser iridotomy
– APAC
• Acetazolamid 500 mg is
given IV if IOP > 50 mmhg &
orally if IOP <50 mmhg
• If treatment IV an additional
oral dose of acetazolamid (
may be given ps is not low
body weight)
– KI: sulfonamid allergy &
angle closure secondary to
topiramat
• Apraclonidine 0,5%-1%
,timolol 0,5 % & prednisone
1% /dexamethasone 0,1%
affected eye ( leaving 5
minutes each)
• Pilocarpine 2-4 % ( one drop
to affected eye ,repeated
after half an hour)
 Normal Tension Glaucoma
is characterized by:
• IOP consistently equal to or less
than 21 mmHg.
• Signs of optic nerve damage in
a characteristic glaucomatous
pattern.
• An open anterior chamber
angle.
• Visual field loss as damage
progresses
• No features of secondary
glaucoma or a non-
glaucomatous cause for the
neuropathy.
• RISK Factors:
– Age
– Gender
– Race
– Family history
– CCT (lower in ps with NTG)
– Abnormal vasoregulation
– Systemic hypotension
– Obstructive sleep apnea
– Autoantibody level
– Ocular perfusion pressure (
may be lower in POAG)
– Myopia
 Retinopati Diabetikum
• Kelainan retina ( retinopati) yg
ditemukan pd penderita DM
• Retinopati akibat DM brupa
aneurismata,melebarnya vena
,perdarahan & eksudat lemak
• Retinopati mrupakan gejala DM
utama pd mata:
– Mikroaneurisma
– Perdarahan dlm bntuk
titik,garis,bercak yg biasanya
trletak dkat mikroaneurisma di
polus posterior
– Dilatasi p.d balik dgn lumenny
ireguler dan berkelok2
– Hard exudate infiltrasi lipid
ke dlm retina (ireguler
)(kekuningan)
– Soft exudate cotton wool
patches (iskemia retina)
– Pmbuluh darah baru pd retina
biasanya trletak dipermukaa
jaringan
• Neovaskularisasi ( proliferasi sel
endotel pmbuluh darah)
– Edema retina dgn tanda
hilangnya gmabaran retina
trutama daerah makula
(shingga gg tajam pnglihatan)
– Hiperlipidemia
• Biasany dit bilateral,simetris &
progresif 3 bntk:
– Mikroaneurisma,prdarahan bercak
,edema
– Makulopati: edema retina & gg fungsi
makula
– Proliferasi: vaskularisasi retina & bdn kaca
– Klasifikasi retinopati diabetes :
• Derajat 1 : mikroanerisma dgn /tnpa
eksudat lemak pd fundus okuli
• Derajat 2 : mikroaneurisma ,perdarahan
bintik dan bercak dgn /tnpa eksudat
lemak pd fundus okuli
• Derajat 3 mikroaneurisma ,perdarahan
bintik danb ercak trdpt neovaskularisasi &
proliferasi pd fundus okuli

dot and blot haemorrhages;

(D) deep dark haemorrhages
 Keratoconus
• is a progressive disorder in which central or paracentral
corneal stromal thinning occurs, accompanied by apical
protrusion and irregular astigmatism.
• Approximately 50% of normal fellow eyes will progress to KC
within 16 years.
• It can be graded by the highest axis of corneal power on
keratometry as
– mild (<48 D)
– moderate (48–54 D)
– severe (>54 D)
 Keratoconus
• Diagnosis
– Symptoms. Unilateral impairment of vision due to progressive
myopia and astigmatism; occasionally, initial presentation is
with acute hydrops.
– Signs :
• Direct ophthalmoscopy shows a fairly well delineated ‘oil
droplet’ reflex
• Retinoscopy shows an irregular ‘scissoring’ reflex.
• Slit lamp biomicroscopy shows very fine, vertical, deep
stromal stress lines, which disappear with pressure on the
globe.
• Epithelial iron deposits, best seen with a cobalt blue filter,
may surround the base of the cone (Fleischer ring)
• Progressive corneal protrusion in a cone configuration, with
thinning maximal at the apex.
 Treatment
• LASIK is contraindicated
• patients should be screened for KC prior to corneal refractive surgery.
– Eye rubbing should be avoided.
– Spectacles or soft contact lenses are generally sufficient in early
cases.
– Rigid contact lenses, sometimes scleral, are required for higher
degrees of astigmatism.
– Corneal collagen cross-linking (CXL), using riboflavin drops to
photosensitize the eye followed by exposure to ultraviolet-A light,
may stabilize or even reverse ectasia.
– Intracorneal ring segment implantation using laser or mechanical
channel creation
– Keratoplasty, either penetrating or deep anterior lamellar
(DALK), may be necessary in patients with severe disease.
 Anisometropia
• Anisometropia is a difference in refractive error between the
two eyes
• major cause of amblyopia because the eyes cannot
accommodate independently and the more hyperopic eye is
chronically blurred
• Refractive correction of anisometropia is complicated by
differences in size of the retinal images (aniseikonia)
• Correction
– Spectacle  difference in retinal image size of
approximately 25%, which is rarely tolerable
– Contact lens  difference in image size to approximately
6%, which can be tolerated
– Intraocular lens  difference of less than 1%
 Retinopati Hipertensi
• Kelainan retina & PD retina akibat tekanan darah tinggi.
• Kelainan PD dapat berupa penyempitan umum atau
setempat, percabangan PD yg tajam, fenomena crossing atau
sklerose PD.
A. Penyempitan (spasme) PD tampak sebagai :
• PD (terutama arteriol retina) berwarna lebih pucat.
• Kaliber pembuluh yg jadi lebih kecil atau iregular
(karena spasme lokal)
 Retinopati Hipertensi
B. Bila kelainan berupa sklerosis dapat tampak sebagai :
• Refleks copper wire
• Refleks silver wire
• Sheating
• Lumen PD yg iregular
• Terdapat fenomena crossing:
– Elevasi : pengangkatan vena o/ arteri di bawahnya.
– Deviasi : penggeseran posisi vena o/ arteri yg bersilangan dgn
vena tsb dgn sudut persilangan lebih kecil.
– Kompresi : penekanan kuat o/ arteri yg menyebabkan
bendungan vena.
 Retinopati Hipertensi
• Kelainan PD dapat mengakibatkan retinopati hipertensi,
dapat berupa perdarahan atau eksudat retina (yg pada
daerah makula memberikan gambaran seperti bintang)
• Eksudat retina dapat berbentuk:
– Cotton wool patches (merupakan edema serat saraf retina
akibat mikroinfark sesudah penyumbatan arteriole.
– Eksudat pungtata yg tersebar
– Eksudat putih pada daerah yg tak tentu dan luas.
 Klasifikasi Retinopati Hipertensi
• Berdasarkan bagian I.P. Mata, RSCM :
– Tipe 1 :
• Fundus hipertensi dgn atau tanpa retinopati, tidak ada sklerose, &
ada pada org muda.
• Pada funduskopi : arteri menyempit & pucat, arteri meregang &
percabangan tajam, perdarahan ada atau tidak ada, eksudat ada
atau tidak ada.

– Tipe 2 :
• Fundus hipertensi dgn atau tanpa retinopati sklerose senil,
terdapat pada orang tua.
• Funduskopi : PD tampak mengalami penyempitan, pelebaran &
sheating setempat.
Perdarahan retina ada atau tidak ada. Tidak ada edema papil.
 Klasifikasi Retinopati Hipertensi
• Berdasarkan bagian I.P. Mata, RSCM :
– Tipe 3 :
• Fundus dgn retinopati hipertensi dgn arteriosklerosis,
terdapat pada orang muda.
• Funduskopi : penyempitan arteri, kelokan bertambah
fenomena crossing perdarahan multipel, cotton wool
patches, makula star figure.

– Tipe 4 :
Hipertensi yang progresif
• Funduskopi : edema papil, cotton wool patches, hard
eksudat, dan star figure exudate yg nyata.
AGE-RELATED MACULAR
DEGENERATION
 AGE-RELATED MACULAR DEGENERATION
• is a degenerative disorder • Risk factors :
affecting the macula. – Age
• It is characterized by the – Race
presence of specific clinical – Heredity
findings, including drusen and
RPE changes, in the absence of – Smoking
another disorder. – Dietary factors.
• Later stages of the disease are – Aspirin
associated with impairment of
vision.
• The prevalence increases with
age and symptoms are rare in
patients under 50 years of age.
 Classification
• Conventionally, AMD has been divided into two main types:
– Dry (non-exudative, non-neovascular) AMD is the most
common form, comprising around 90% of diagnosed
disease.
• Geographic atrophy (GA) is the advanced stage of dry
AMD.
– Wet (exudative, neovascular) AMD is much less common
than dry, but is associated with more rapid progression to
advanced sight loss.
Early Age-Related Macular Degeneration
Late Age-Related Macular Degeneration
 Prophylactic Therapy
• Recommended daily supplementation based on AREDS2:
– Vitamin E (400 IU).
– Vitamin C (500 mg).
– Lutein (10 mg).
– Zeaxanthin (2 mg).
– Zinc (25–80 mg)
– Copper (2 mg).
• A liberal green leafy vegetable intake confers a lower risk of
AMD.
• Cessation of smoking should be advised.
• Protective measures against exposure to excessive sunlight
should be considered.
 Treatment of Neovascular Age-Related Macular
Degeneration
• Conventional retinal laser• Bevacizumab
photocoagulation • Surgery (part of clinical trial)
• photodynamic therapy – surgical removal of the
• anti-VEGF therapy choroidal neovascular
• Pegaptanib (intravitreal membrane, macular
injection every 6 weeks) translocation, and retinal
– binds the major pigment epithelial
pathogenic isoform of transplantation
vascular endothelial
growth factor, VEGF165
• Ranibizumab
– able to bind all isoforms
of VEGF
STRABISMUS
 Strabismus
• Suatu keadaan dimana kedudukan kedua bola mata tidak ke
satu arah.
• Pada strabismus, sumbu bola tidak berpotongan pada satu
titik benda yang dilihat.
• Pasien dgn strabismus akan mengeluh mata lelah atau
astenopia, penglihatan kurang pada satu mata, lihat ganda
(diplopia), & sering menutup sebelah mata.
• Faktor resiko : Riwayat keluarga , kelainan refraksi & kondisi
medis.
• Penyulit supresi dini : terjadinya ambliopia & fiksasi eksternal.
 Klasifikasi Strabismus
1. Apparent squint atau pseudostrabismus
2. Latent squint (Heterophoria)
3. Manifest squint (Heterotropia)
 Pseudostrabismus
• Pasien kadang-kadang terlihat
seperti juling tetapi dengan
pemeriksaan tidak terdapat
tanda” juling.
• Mungkin disebabkan adanya
epikantus  mengakibatkan
bagian nasal sklera tidak
terlihat jelas.
• Pasien terlihat seperti ada
juling ke dalam.
• Kelainan ini merupakan
gambaran karakteristik pada
pas. dgn ras Mongol.
 Heteroforia
• Keadaan kedudukan bola mata yg normal namun akan timbul
penyimpangan (deviasi) apabila refleks fusi terganggu.
• Macam-macam heteroforia berdasarkan bidang
penyimpangannya :
– Bidang horizontal : esoforia & eksoforia
– Bidang vertikal : hipo atau hiperforia
– Bidang frontal : insiklofori & eksiklofori
• Penyebab : akibat tidak seimbangnya atau insufisiensinya otot
penggerak mata.
• 75-90% penduduk yg menderita heteroforia, biasanya tanpa
keluhan.
 Esoforia
• Suatu penyimpangan sumbu • Sudut penyimpangan sama besar
penglihatan ke arah nasal yg saat melihat jauh & dekat = basic
tersembunyi oleh karena masih type.
adanya refleks fusi. • Terapi :
• Esoforia yg punya sudut – Memberikan koreksi
penyimpangan lebih besar pada saat hipermetropia u/ ↓ rangsang
melihat jauh dibandingkan melihat akomodasi berlebihan.
dekat disebabkan o/ suatu – Memberikan miotika u/
insufisiensi divergen. menghilangkan akomodasinya.
• Esoforia yg punya sudut – Memberikan prisma base out yg
penyimpangan lebih kecil pada dibagi sama besar mata kanan &
waktu melihat dekat disebabkan kiri.
oleh suatu ekses konvergen.
– Tindakan operasi
 Eksoforia / Strabismus Divergen Laten
• Suatu tendensi penyimpangan•
sumbu penglihatan ke arah
temporal.
• Pada eksoforia akan terjadi
deviasi ke luar pada mata yg•
ditutup atau dicegah
terbentuknya refleks fusi.
• Eksoforia kecil tanpa keluhan
sering terdapat pada anak”.
• Eksoforia besar sering sering
akan memberikan keluhan
astenopia
• Bila sudut penyimpangan pada
saat melihat jauh lebih besar 
disebabkan oleh ekses divergen.
Bila sudut penyimpangan pada
waktu melihat dekat lebih besar
 disebabkan oleh kelemahan
akomodasi.
Pengobatan secara umum:
– Bila ada kelainan refraksi 
dikoreki.
– Bila mungkin diberikan
latihan ortoptik
– Bila tidak berhasil, bisa
diberikan prisma base in
 Hiperforia / Strabismus Sursumvergen
Laten
• Suatu tendensi penyimpangan sumbu penglihatan ke arah
atas.
• Umumnya disebabkan o/ kerja berlebihan atau kelemahan
otot-otot rektus inferior & obliqus superior.
• Pengobatan dengan kacamata prisma & puncak di atas
(vertical base down) di depan mata yg sumbu penglihatannya
lebih tinggi.
• Dapat juga dilakukan operasi pada otot” rektus superior dan
inferior.
 Heterotropia
• Keadaan penyimpangan sumbu •
bola mata yg nyata di mana kedua
sumbu penglihatan tidak
berpotongan pada titik fiksasi.
• Dapat disebabkan oleh kelainan :
– Herediter
– Anatomik, kelainan otot luar,
kelainan ronggan orbita.
– Kelainan refraksi
– Kelainan persarafan, sensori
mototrik, keadaan yang
menggagalkan fusi.
Bentuk” heterotropia berdasarkan
kedudukan penyimpangannya :
– Bidang horizontal : eksotropia
& esotropia
– Vertikal : hipertrofi
– Sagital : insiklotropia (kornea
jam 12 berputar ke arah nasal)
& esiklotropia
• Pemeriksaan untuk menentukan
adanya heterotropia : uji tutup
mata, uji refleks korena
Hisrchberg, uji Krimsky, uji
Maddox rod.
 Esotropia / Strabismus Konvergen
Manifes
• Penyimpangan sumbu penglihatan • Penyebab :
dimana salah satu sumbu – Faktor refleks dekat,
penglihatan menuju titik fiksasi akomodatif estropia.
sedangkan sumbu penglihatan lain – Hipertoni rektus medius
menyimpang pada bidang kongenital.
horizontal ke arah medial.
– Hipotoni rektus lateral akuisita
• Bentuk” esotropia
– ↓ fungsi penglihatan satu mata
– Esotropia konkomitan (sudut pada bayi & anak.
penyimpangan sama besar
pada semua arah pandangan) • Pengobatan:
– Esotropia nonkomitan (besar – Memberikan lensa koreksi
sudut penyimpangan beda” untuk mengatas keadaan
pada arah pandang berbeda- miopinya.
beda) – Tindakan operatif
 Eksotropia / Strabismus divergen
manifes
• Penyimpangan sumbu
penglihatan dimana salah satu
sumbu penglihatan menuju titik
fiksasi sedangkan sumbu yg lain •
menyimpang pada bidang
horizontal ke arah lateral.
• Bentuk: Eksotropia konkomitan •
& nonkomitan
• Penyebab :
– Herediter
– Inervasi tapi tidak terdapat
abnormalitas yg berarti
dalam bidang sensorimotor
– Anatomi, kelainan rongga
orbita mis: pada penyakit
Crouzon
Pengobatan dgn koreksi refraksi
pada ekstropia harus dilakukan
dengan hati-hati.
Operasi pada eksotropia
tergantung pada jenis
eksotropianya, biasanya
dilakukan resesi otot rektus
lateral & reseksi otot rektus
medial mata yg sama pada yg
berdeviasi.
GLAUCOMA
 Glaucoma
• Glaucoma results from an imbalance between
the production of aqueous fluid and the
drainage of aqueous fluid.
• In open-angle glaucoma, there is apparent
free anatomic access to the trabecular
meshwork.
• In closed-angle glaucoma, there is a relative or
absolute anatomic barrier to the flow of
aqueous.

Goldman-cecil medicine. 25th ed.

 CHRONIC OPEN-ANGLE GLAUCOMA
• The most common type of glaucoma in elderly
people
• The first symptom is loss of peripheral visual
field with retention of central visual function.
– The visual field may be reduced considerably
before the patient notes loss of function.
• The diagnosis of glaucoma is confirmed by
characteristic visual field loss as determined
by automated perimetry.

Goldman-cecil medicine. 25th ed.

• The treatment goal is to reduce intraocular
pressure, initially with pharmacologic agents:
– β-blockers (e.g., betaxolol drops 0.5% twice daily),
– carbonic anhydrase inhibitors (e.g., dorzolamide drops
twice daily),
– α-agonists (e.g., apraclonidine drops twice daily), and
– antiprostaglandins (e.g., latanoprost drops twice
daily).
• Generally, the drops are taken for a lifetime

Goldman-cecil medicine. 25th ed.

 ANGLE-CLOSURE GLAUCOMA
• Angle-closure glaucoma may occur over a short period of time and
cause extreme debilitating symptoms.
• Alternatively, symptoms may develop over a long period of time
with few specific symptoms.
• The risk factors for angle-closure glaucoma are based on the
anatomic configuration of the components of anterior chamber.
 Persons who are farsighted (hyperopia) have a shortened anterior-
to-posterior axis of the eye, indicated clinically by a shallow anterior
chamber
 As the crystalline lens increases in volume with time, the iris is
displaced anteriorly.
 At some point, the posterior surface of the iris may come in relatively
tight contact with the anterior surface of the lens.
 Aqueous flow is restricted, and fluid accumulates in the posterior
chamber, where it displaces the diaphanous peripheral iris anteriorly.

Goldman-cecil medicine. 25th ed.

• Initial treatment is with topical (e.g., timolol 0.5% in
one dose) and systemic pressure-lowering agents (e.g.,
carbonic acetazolamide, 250 to 500 mg intravenously
or two 250-mg tablets orally in one dose if intravenous
access or drug is not available),
• followed by creation of a fistula in the peripheral iris
with a laser (YAG laser iridectomy) between the
posterior chamber and the anterior chamber to bypass
the obstruction.
• Most patients require a laser iridectomy
prophylactically in the second eye to prevent angle-
closure glaucoma.

Goldman-cecil medicine. 25th ed.

 Retinal detachment
• A retinal detachment is a separation of the neural (sensory)
retina from the retinal pigment epithelium
• The two main types are:
– Rhegmatogenous, caused by a retinal hole, as may occur with a
posterior vitreous detachment
– Nonrhegmatogenous, caused by traction, such as in proliferative
diabetic retinopathy or by fluid accumulation under neural
retina in conditions such as malignant hypertension or
eclampsia of pregnancy.
• The classic symptoms are:
– A sensation of flashes of light,
– Floaters in the field of the involved eye owing to the causative
vitreous detachment, and
– A shadow.

Goldman-cecil medicine. 25th ed.

• Laser photocoagulation is used to treat small posterior
detachments, whereas cryotherapy is used for more
peripheral tears
• Intravitreal injection of 125 µg ocriplasmin (a recombinant
protease with activity against fibronectin and laminin,
which are components of the vitreoretinal interface) can
significantly improve outcomes in patients with
vitreomacular traction and macular holes.
• More extensive detachments may be treated with the
injection of air. The air bubble will locate in the superior
portion of the globe and tamponade the hole while it heals;
the patient’s head must be in the correct position for the
duration of treatment.

Goldman-cecil medicine. 25th ed.

 Uveitis
• Inflammation of any part or parts of the uveal
tract (iris, ciliary body, and choroid) may be
called anterior or posterior uveitis, iritis,
iridocyclitis, or choroiditis.
• Symptoms include a red eye, decreased vision,
and photophobia
• Treatment with topical corticosteroids (e.g.,
prednisolone acetate 1%, one drop in the
affected eye or eyes every 1 to 6 hours while
awake) is usually sufficient to control the ocular
disease.
 Myopia
• Myopia usually progresses until the eye is fully developed,
typically by age 20 to 25 years
• Myopia is usually fully correctable with glasses.
• Laser in situ keratomileusis (LASIK) is one of the refractive
surgical procedures that may be used in adults to correct
myopia and other refractive errors, with 95% of patients
achieving visual acuity of 20/40 or better
– Complications of LASIK include glare symptoms, dry eye, and
undercorrection or overcorrection.
• Pathologic myopia is a heritable condition causing
progressive weakening of the posterior sclera and
resulting increases in the axial length of the eye. The
posterior radius of curvature of the eye increases
(posterior staphyloma).
ANATOMI
 Orbit
• bony cavities in the facial skeleton that resemble
hollow quadrangular pyramids
– bases directed anterolaterally
– Apices directed posteromedially
• medial walls of the two orbits, separated by the
ethmoidal sinuses and the upper parts of the
nasal cavity, are parallel, whereas their lateral
walls are nearly at a right (90°) angle
• axes of the orbits diverge at approximately 45°
• The optical axes (axes of gaze, the direction or
line of sight) for the two eyeballs, are parallel
• The pyramidal orbit has a base, four walls, and an
apex
– Base
• outlined by the orbital margin that surrounds the orbital
opening
– Superior wall
• approximately horizontal and is formed mainly by the orbital
part of the frontal bone
• Near the apex of the orbit, the superior wall is formed by the
lesser wing of the sphenoid
• Anterolaterally, a shallow depression in the orbital part of
the frontal bone, called the fossa for the lacrimal gland
– Medial wall
• formed primarily by the ethmoid bone, along with
contributions from the frontal, lacrimal, and sphenoids
• Anteriorly, the medial wall is indented by the lacrimal groove
and fossa for the lacrimal sac
• “Paper thin”
– Inferior wall
• formed mainly by the maxilla and partly by the zygomatic
and palatine bones
• inferior wall is demarcated from the lateral wall of the orbit
by the inferior orbital fissure
– Lateral wall
• formed by the frontal process of the zygomatic bone and the
greater wing of the sphenoid
• strongest and thickest wall
– Apex  at the optic canal in the lesser wing of the
sphenoid just medial to the superior orbital fissure
 Eyelids
• cover the eyeball anteriorly, thereby protecting it from injury and
excessive light
• keep the cornea moist by spreading the lacrimal fluid
• covered externally by thin skin and internally by transparent
mucous membrane, the palpebral conjunctiva
• part of the conjunctiva is reflected onto the eyeball, where it is
continuous with the bulbar conjunctiva
• lines of reflection of the palpebral conjunctiva onto the eyeball
form deep recesses  superior and inferior conjunctival fornices
• conjunctival sac  space bound by the palpebral and bulbar
conjunctivae
–  enables the eyelids to move freely over the surface of the eyeball
as they open and close
 Lacrimal apparatus
• Lacrimal glands
– secrete lacrimal fluid, a watery physiological saline containing
the bacteriocidal enzyme lysozyme
– moistens and lubricates the surfaces of the conjunctiva and
cornea
– provides some nutrients and dissolved oxygen to the cornea
• Lacrimal ducts
– convey lacrimal fluid from the lacrimal glands to the conjunctival
sac
• Lacrimal canaliculi
– commence at a lacrimal punctum on the lacrimal papilla & drain
lacrimal fluid from the lacrimal lake to the lacrimal sac
• Nasolacrimal duct
 The eyeball
• contains the optical apparatus of the visual system and
occupies most of the anterior portion of the orbit
– The loose connective tissue layer 
• Anterior : bulbar conjunctiva
• Posterior : bulbar fascia
• The layers of the eyeball
– Fibrous layer (outer coat),
• consisting of the sclera and cornea
– Vascular layer (middle coat),
• consisting of the choroid, ciliary body, and iris
– Inner layer (inner coat),
• consisting of the retina that has both optic and non-visual parts
 Inner layer
• Retina
– Optic part  sensitive to visual light rays
• neural layer: light receptive
• pigment cell layer: reinforces the light-absorbing
property of the choroid in reducing the scattering of
light in the eyeball
– Non-visual retina
• anterior continuation of the pigment cell layer and a
layer of supporting cells over the ciliary body (ciliary
part of the retina)
• posterior surface of the iris (iridial part of the retina)
• Fundus
–  posterior part of the eyeball
• optic disc: sensory fibers and vessels conveyed by the optic nerve
• macula lutea: small oval area of the retina with special
photoreceptor cones that is specialized for acuity of vision
• fovea centralis: the area of most acute vision

• Arteries & veins

– retina is supplied by the central artery of the retina, a
branch of the ophthalmic artery
– corresponding system of retinal veins unites to form the
central vein of the retina
 Refractive Media of the Eyeball
• Cornea
– circular area of the anterior part of the outer fibrous
layer of the eyeball
– largely responsible for refraction
– Transparent; regular arrangement of its collagen fibers
– Avascular
– Sensitive to touch
– nourishment is derived from the capillary beds at its
periphery, the aqueous humor, and lacrimal fluid
– Innervated by N. V1
• Aqueous humor
– produced in the posterior chamber by the ciliary
processes of the ciliary body 
– passing through the pupil into the anterior chamber

– drains into the scleral venous sinus/canal of Schlemm
at iridocorneal angle 
– removed by the limbal plexuses 
– vorticose and the anterior ciliary veins

– provides nutrients for the avascular cornea and lens

• Lens
– posterior to the iris and anterior to the vitreous humor of the
vitreous body
– transparent, biconvex structure enclosed in a capsule
– anchored by the zonular fibers (suspensory ligament of the lens)
to the ciliary body and encircled by the ciliary processes
– ciliary muscle in the ciliary body changes the shape of the lens

• Vitreous humor
– watery fluid enclosed in the meshes of the vitreous body;
transparent jelly-like substance in the posterior four fifths of the
eyeball posterior to the lens
– holds the retina in place and supports the lens
 Extraocular muscles of the orbit
• Levator Palpebrae Superioris
– broadens into a wide bilaminar aponeurosis as it
approaches its distal attachments
• superficial lamina attaches to the skin of the superior eyelid
• deep lamina to the superior tarsus
– opposed most of the time by gravity
– antagonist of the superior half of the orbicularis oculi,
the sphincter of the palpebral fissure
– The deep lamina includes smooth muscle fibers, the
superior tarsal muscle  additional widening of the
palpebral fissure during a sympathetic response (e.g.,
fright)
 Fascial Sheath of the Eyeball
• ~fascia bulbi, Tenon capsule
• envelops the eyeball from the optic nerve nearly
to the corneoscleral junction, forming the actual
socket for the eyeball
• is pierced by the tendons of the extraocular
muscles and is reflected onto each of them as a
tubular muscle sheath
• The muscle sheaths of the levator and superior
rectus muscles are fused; thus, when the gaze is
directed superiorly, the superior eyelid is further
elevated out of the line of vision
• Triangular expansions from the sheaths of the medial and
lateral rectus muscles, called the medial and lateral check
ligaments, are attached to the lacrimal and zygomatic
bones  limit abduction and adduction
• blending of the check ligaments with the fascia of the
inferior rectus and inferior oblique muscles forms a
hammock-like sling  suspensory ligament of the eyeball
• potential episcleral space between the eyeball and the
fascial sheath allows the eyeball to move inside the cup-like
sheath
• similar check ligament from the fascial sheath of the
inferior rectus  retracts the inferior eyelid when the gaze
is directed downward
 Daftar Pustaka
• Juncqueira LC, Cerneceiro J, Kelley RO. Basic
histology 8th ed. Connecticut: Appleton &
Lange, 1995
• Sidarta Ilyas. Ilmu Penyakit mata. Edisi
keempat. Jakarta: FKUI, 2007