C B T O P T I M A B AT C H N O V E M B E R 2 0 1 9

I L M U P E N YA K I T M ATA
| DR. SEPRIANI | DR. YOLINA | DR. OKTRIAN | DR. REZA | DR. CEMARA |
| DR. AARON | DR. CLARISSA | DR. KAMILA | DR. EDWIN |
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w w w. o p t i m a p r e p . c o . i d
TO 1
1. Glaukoma Akut
 Glaukoma Akut: Faktor Risiko
• Riwayat keluarga dengan
glaukoma
• Usia:
– prevalen di usia tua (>40
tahun)
• Beberapa etnis tertentu:
– PACG (primary angle closure
glaucoma) lebih sering pada
Asia tenggara, Cina, India.
– Sementara POAG (primary
open angle glaucoma) lebih
sering pada golongan
Hispanik.
https://www.aafp.org/afp/2016/0415/p668.html
• Faktor risiko lain: hipertensi, DM,
kelainan refraktif
– Miopia: meningkatkan risiko
POAG
– Hipermetropia: meningkatkan
risiko PACG
• Pasien hipermetropia memiliki
bola mata lebih pendek (narrow
eyes)  iris lebih mudah
menghambat aliran aqueous
humor  glaukoma sudut
tertutup
 Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006

Tatalaksana Glaukoma Akut

• Tujuan : merendahkan tekanan bola mata secepatnya
kemudian bila tekanan normal dan mata tenang → operasi
• Supresi produksi aqueous humor
– Beta bloker topikal: Timolol maleate 0.25% dan 0.5%, betaxolol
0.25% dan 0.5%, levobunolol 0.25% dan 0.5%, metipranolol
0.3%, dan carteolol 1% dua kali sehari dan timolol maleate 0.1%,
0.25%, dan 0.5% gel satu kali sehari (bekerja dalam 20 menit,
reduksi maksimum TIO 1-2 jam stlh diteteskan)
– Pemberian timolol topikal tidak cukup efektif dalam
menurunkan TIO glaukoma akut sudut tertutup.
– Apraclonidine: 0.5% tiga kali sehari
– Brimonidine: 0.2% dua kali sehari
– Inhibitor karbonat anhidrase:
• Topikal: Dorzolamide hydrochloride 2% dan brinzolamide 1% (2-3
x/hari)
• Sistemik: Acetazolamide 500 mg iv dan 4x125-250 mg oral (pada
glaukoma akut sudut tertutup harus segera diberikan, efek mulai
bekerja 1 jam, puncak pada 4 jam)
 Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007.

Tatalaksana Glaukoma Akut

• Fasilitasi aliran keluar aqueous humor
– Analog prostaglandin: bimatoprost 0.003%, latanoprost 0.005%, dan
travoprost 0.004% (1x/hari), dan unoprostone 0.15% 2x/hari
– Agen parasimpatomimetik: Pilocarpine
– Epinefrin 0,25-2% 1-2x/hari
• Pilokarpin 2% setiap menit selama 5 menit,lalu 1 jam selama 24 jam
– Biasanya diberikan satu setengah jam pasca tatalaksana awal
– Mata yang tidak dalam serangan juga diberikan miotik untuk mencegah
serangan
• Pengurangan volume vitreus
– Agen hiperosmotik: Dapat juga diberikan Manitol 1.5-2MK/kgBB dalam larutan
20% atau urea IV; Gliserol 1g/kgBB badan dalam larutan 50%
– isosorbide oral, urea iv
• Extraocular symptoms:
– analgesics
– antiemetics
– Placing the patient in the supine position → lens falls away from the iris
decreasing pupillary block
– Pemakaian simpatomimetik yang melebarkan pupil berbahaya
 2. Optic neuropathy
• optic neuropathy refers to damage to the optic nerve due to any cause.
• the principal cause of optic neuropathy is glaucoma and the other is non-
glaucomatous optic neuropathy (NGON).
• The etiology of a NGON:
– Inflammatory- optic neuritis (ON)  the most common cause of optic nerve
disease in younger adults
– Ischemic  the most common etiology in elderly patients
– compressive- infiltrative,
– hereditary,
– toxic,
– nutritional deficiency,
– post- traumatic,
– post- radiotherapy, or
– associated with intracraneal hypertension (ICH) ON is while
Etiology of optic neuropathy
 Optic neuritis
• Optic neuritis is an inflammation of the eye’s optic
nerve
• Optic neuritis may occur in one or both eyes.
• The symptoms may get worse with heat or exhaustion,
particularly when exercising or taking a bath.
• Classic classification of optic neuritis:
– Anterior (or papilitis)  inflammation of the optic disc and
can be seen in the fundus examination as a peripapillary
edema
– Posterior (retrobulbar)  inflammation in any portion
between the eye and the optic chiasm and can be only
seen in neuroimaging test
• Optic neuritis is associated
with various diseases and
conditions, such as:
– mumps;
– measles;
– influenza;
– multiple sclerosis;
– Leber’s optic neuropathy (a
rare eye condition that runs
in families);
– vascular occlusions of the
optic nerve.
• In most cases, however,
optic neuritis occurs with no
known cause.
• Symptoms may appear
suddenly or slowly (over a
few days) and may include:
– blurred vision;
– dim vision (as if someone
turned down the lights);
– abnormal color vision (colors
appear dull and faded);
– pain in the back of the eye
socket;
– pain when moving the eyes.
 Examination

• Pupillary reflex
• Funduscopy
• Perimetri
• Color visual test
• CT scan, MRI, or visual
brain wave recording
 Diseases Definition/characteristics
Neuritis optik (1) Peradangan optic disc
ditandai dgn disc swelling,
unilateral
Neuritis retrobulbar Bagian dari neuritis optik,
peradangan terjadi jauh
dibelakang optic disc,
unilateral
Neuropati optik Iskemia optic disc akibat
iskemik (2) aterosklerosis, hipertensi,
diabetes
Atrofi papil (3) Etiologi bisa vaskuler,
degeneratif, metabolik,
glaukomatosa
(1) (2)
Ophthalmoscopic findings
Nyeri bola mata dgn gerakan
tertentu, afferent pupil reflex
(-), hiperemia optic disc
Nyeri bola mata dgn gerakan
tertentu, afferent pupil reflex
(-), funduskopi normal
Optic disc swelling dan pucat,
splinter hemorrhage pd
daerah peripapila
Penurunan visus perlahan,
gangguan penglihatan warna,
defek lapang pandang
(3)
 Papilledema Papillitis (optic Retrobulbar neuritis Optic Disc Edema
neuritis) (Edema papil)
Definition Swelling of optic Inflammation or Inflammation of orbital Swelling of optic disc
nerve head due to infarction of optic portion of optic nerve secondary to lacl or
increased ICP nerve head systemic cause (other
than increased ICP)

Unilateral/bilate Bilateral Unilateral Unilateral Bilateral or unilateral

ral

Vision Enlarged blind spot Central/paracentral Central/paracentral Enlarged blind spot

impairment scotoma to complete scotoma to complete
blindness blindness

Fundus Hyperemic disk Hyperemic disk Normal Normal

appearance
Vessel Engorged, tortuous Engorged vessels Normal Normal
appearance veins
Hemorrhages? Around disk, not Hemorrhages near Normal Rare
periphery or on optic head
Pupillary light Not affected Depressed Depressed Not affected
reflex
Treatment Normalize ICP Corticosteroids if Corticosteroids with Based on the cause
cause known caution condition

Optic Disc Edema From Papilledema. INTERNATIONAL OPHTHALMOLOGY CLINICS Volume 54, Number 1, 13–26. 2014, Lippincott Williams &
Wilkins
Jung, J. J., Baek, S. H., & Kim, U. S. (2011). Analysis of the causes of optic disc swelling. Korean journal of ophthalmology : KJO, 25(1), 33-6.
 3. Pterigium
• Berasal dari Bahasa Yunani, yaitu pterygos yang
artinya sayap kecil.
• Pertumbuhan fibrovaskular yang bersifat
degenerative dan invasive – biasanya
berbentuk segitiga, tumbuh dari bagian nasal
atau temporal konjungtiva yang meluas hingga
ke area kornea sehingga puncak segitiga berada
di kornea.
• Faktor risiko:
– Radiasi ultraviolet (terutama UV-B)
– Genetik
– Pajanan debu atau iritan
 Pterigium: Patosiologi

Radiasi  mutasi pada P53 tumor suppressor

gene

Focal limbal damage: Proliferasi abnormal pada

limbal epithelium (limbal basal stem cell; LSC)

Sel-sel bermigrasi menuju kornea dan terjadi

angiogenesis  degenerasi kolagen dan terlihat
jaringan subepitelial fibrovaskular

LSC deficiency: konjungtivalisasi dari segala arah

 Pterigium: Tanda dan Gejala

• Pada tahap awal biasanya asimtomatik,

namun bisa juga teradapat tanda-tanda dry
eye:
– mata merah,
– perasaan mengganjal pada mata
• Progresif  jaringan fibrovaskular semakin
besar, terlihat jelas, astigmatisma
 Pterigium: Grading

• Grade I: Terbatas pada limbus kornea

• Grade II: Melewati limbus, bias mencapai kornea tetapi <2 mm
• Grade III: Melewati kornea >2mm tetapi tidak melebihi
pinggir pupil
• Grade IV: Melewati pupil  gangguan penglihatan
 Pterigium: Manajemen
• Pencegahan
– Mengurangi aktivitas di luar ruangan
– Pelindung kepala atau mata
• Tatalaksana
– Grade I atau II tanpa gangguan pengelihatan 
simtomatik; tear subsituent, vasokontriktor, steroid
jangka pendek
– Grade III atau IV  bedah
• Indikasi: tajam penglihatan berkurang, ancaman aksis
visual terganggu, gejala iritasi berat, dan indikasi
kosmetik.
 Pterigium vs Pinguekula

• as
 4. Katarak Komplikata
• Pembagian katarak berdasarkan usia:
– Katarak kongenital  usia < 1 thn
– Katarak juvenil  sesudah usia 1 thn
– Katarak senilis  > 50 thn
• Katarak komplikata
• akibat penyakit mata lain, mis: radang, glaukoma, tumor, dll.
Dpt jg disebabkan oleh peny.sistemik endokrin (mis: DM) dan
keracunan obat (mis: steroid lokal lama)
• Katarak traumatik
• akibat trauma, plg sering disebabkan oleh cedera benda asing
atau trauma tumpul bola mata
• Katarak sekunder
• tjd sesudah operasi katarak atau sesudah suatu trauma yg
memecah lensa
Sumber: - Ilmu Penyakit Mata. Sidarta Ilyas. 2000.
- General opthalmology. Vaughan, et al. 17th edition
KATARAK TRAUMATIK

Typical stellate/rosette/flower-shaped cortical

lens opacity
 Katarak traumatik
• akibat cedera benda asing di lensa atau trauma
tumpul pada bola mata.
• terdapat gambaran bintang pada kapsula
posterior
• tatalaksana
– Benda asing intraokular harus segera dikeluarkan
– Antibiotik sistemik dan topikal
– Kortikosteroid topikal
– Atropin sulfat 1%, 1 tetes 3 kali sehari untuk
mencegah sinekia posterior
 5. UVEITIS
•Uveitis :
–inflamasi di uvea
yaitu iris, badan siliar
dan koroid yang
dapat menimbulkan
kebutaan.
–Di negara maju,
10% kebutaan pada
populasi usia
produktif adalah
akibat uveitis
 Klasifikasi
• The International Uveitis Study Group (IUSG) dan The
Standardization of Uveitis Nomenclatur (SUN) membagi uveitis
berdasarkan anatomi, etiologi, dan perjalanan penyakit
• Anatomi :
– uveitis anterior, uveitis intermediet, uveitis posterior, dan panuveitis
• Etiologi:
– infeksi (bakteri, virus, jamur, dan parasit), non-infeksi, dan idiopatik.
• Perjalanan penyakit
– Akut (onset mendadak dan durasi kurang dari empat minggu),
– Rekuren (episode uveitis berulang),
– Kronik (uveitis persisten atau kambuh sebelum tiga bulan setelah
pengobatan dihentikan), dan
– Remisi (tidak ada gejala uveitis selama tiga bulan atau lebih)

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis anterior
• Inflamasi di iris (iritis) dan badan siliar (siklitis).
Bila inflamasi meliputi iris dan badan siliar maka
disebut iridosiklitis
• Etiologi :
– kelainan sistemik seperti spondiloartropati, artritis
idiopatik juvenil, sindrom uveitis fuchs, kolitis ulseratif,
penyakit chron, penyakit whipple, tubulointerstitial
nephritis and uveitis
– Infeksi yang sering menyebabkan uveitis anterior
adalah virus herpes simpleks (VHS), virus varisela
zoster (VVZ), tuberkulosis, dan sifilis.

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Diagnosis Uveitis Anterior
• Gejala Klinis : • Tanda
– mata merah – injeksi siliar akibat
– visus turun akibat kekeruhan vasodilatasi arteri siliaris
cairan akuos dan edema posterior longus dan arteri
kornea walaupun uveitis tidak siliaris anterior yang
selalu menyebabkan edema memperdarahi iris serta
kornea badan siliar.
– Nyeri tumpul berdenyut, dan – Bilik mata depan : pelepasan
fotofobia akibat spasme otot sel radang, pengeluaran
siliar dan sfingter pupil protein (cells and flare) dan
– Jika disertai nyeri hebat, endapan sel radang di endotel
perlu dicurigai peningkatan kornea (presipitat keratik).
tekanan bola mata. – Presipitat keratik halus 
– Spasme sfingter pupil inflamasi nongranulomatosa;
mengakibatkan miosis dan – Presipitat keratik kasar 
memicu sinekia posterior. inflamasi granulomatosa

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis Intermediet
• Peradangan di pars plana yang sering diikuti vitritis dan uveitis posterior.
• Penyakit tersebut biasanya terjadi pada usia dekade ketiga-keempat dan
20% terjadi pada anak.
• Etiologi:
– Idiopatik (69,1%), sarkoidosis (22,2%), multiple sclerosis (7,4%), dan lyme
disease (0,6%). Selain itu, dapat juga disebabkan oleh infeksi Mycobacterium
tuberculosis, Toxoplasma, Candida, dan sifilis.
• Gejala :
– Gejala biasanya ringan yaitu penurunan tajam penglihatan tanpa disertai nyeri
dan mata merah, namun jika terjadi edema makula dan agregasi sel di vitreus
penurunan tajam penglihatan dapat lebih buruk.
– Pars planitis berupa bercak putih akibat agregasi sel inflamasi dan jaringan
fibrovaskular (snowbank) yang menunjukkan inflamasi berat dan memerlukan
terapi agresif.
– Komplikasinya adalah edema makula (12-51%), glaukoma (20%), dan katarak
(15-50%)

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis Posterior
• Peradangan lapisan koroid yang sering melibatkan jaringan sekitar seperti
vitreus, retina, dan nervus optik.
• Etiologi:
– Infeksi paling sering disebabkan oleh T.gondii, M.tuberculosis, sifilis, VHS, VVZ,
cytomegalovirus (CMV), dan HIV.
– Non-infeksi, uveitis posterior disebabkan oleh koroiditis multifokal, birdshot
choroidopathy, sarkoidosis, dan neoplasma
• Gejala klinis :
– Penglihatan kabur yang tidak disertai nyeri, mata merah, dan fotofobia.
– Komplikasi dapat berupa katarak, glaukoma, kekeruhan vitreus, edema
makula, kelainan pembuluh darah retina, parut retina, ablasio retinae, dan
atrofi nervus optik.
– Prognosis uveitis posterior lebih buruk dibandingkan uveitis anterior karena
menurunkan tajam penglihatan dan kebutaan apabila tidak ditatalaksana
dengan baik.

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Panuveitis
• Peradangan seluruh uvea dan struktur
sekitarnya seperti retina dan vitreus.
• Etiologi:
– Penyebab tersering adalah tuberkulosis, sindrom
VKH, oftalmia simpatika, penyakit behcet, dan
sarkoidosis.
– Diagnosis panuveitis ditegakkan bila terdapat
koroiditis, vitritis, dan uveitis anterior

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 No. Jenis Keterangan
Pemeriksaan
Penunjang pada
Uveitis
1 Slit lamp menilai segmen anterior injeksi siliar dan episklera, skleritis,
edema kornea, presipitat keratik, bentuk dan jumlah sel di bilik
mata, hipopion serta kekeruhan lensa
2 Oftalmoskop menilai kelainan di segmen posterior seperti vitritis, retinitis, perdarahan
retina, koroiditis dan kelainan papil nervus optik

3 Pemeriksaan
laboratorium
4 Optical coherence
tomography (OCT)
5 USG B –scan
bermanfaat pada kelainan sistemik misalnya darah perifer lengkap, laju
endap darah, serologi, urinalisis, dan antinuclear antibody
merupakan pemeriksaan non-invasif yang dapat memperlihatkan edema
makula, membran epiretina, dan sindrom traksi vitreomakula
sangat membantu memeriksa segmen posterior mata pada keadaan
media keruh misalnya pada katarak dan vitritis

6 Fundus fluoresen
angiografi (FFA)
fotografi fundus yang dilakukan berurutan dengan cepat setelah injeksi
zat warna natrium fluoresen (FNa) intravena.
FFA memberikan informasi mengenai sirkulasi pembuluh darah retina dan
koroid, detail epitel pigmen retina dan sirkulasi retina serta menilai
integritas pembuluh darah saat fluoresen bersirkulasi di koroid dan retina.
 Penatalaksanaan Uveitis
• Prinsip penatalaksanaan uveitis
1. Menekan reaksi inflamasi
• Kortikosteroid topikal merupakan terapi pilihan untuk
mengurangi inflamasi : 1).prednisolon 0,5%,; 2).
prednisolon asetat 1%; 3). betametason 1% ; 4).
deksametason 0,1%, dan 5). fluorometolon 0,1%.
• Injeksi kortikosteroid periokular diberikan pada kasus yang membutuhkan
depo steroid dan menghindari efek samping kortikosteroid jangka panjang.
• Kortikosteroid sistemik diberikan untuk mengatasi uveitis berat atau uveitis
bilateral
• Imunosupresan dapat dipertimbangkan sebagai terapi lini pertama pada
penyakit behcet, granulomatosis wegener, dan skleritis nekrotik karena
penyakit tersebut dapat mengancam jiwa. Imunosupresan dibagi menjadi
golongan antimetabolit, supresor sel T, dan sitotoksik.
2. Mencegah dan memperbaiki kerusakan struktur,

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 3. Memperbaiki fungsi penglihatan
• Terapi bedah diindikasikan untuk memperbaiki penglihatan.
• Operasi dilakukan pada kasus uveitis yang telah tenang
(teratasi) tetapi mengalami perubahan permanen akibat
komplikasi seperti katarak, glaukoma sekunder, dan ablasio
retina.
• Kortikosteroid diberikan 1-2 hari sebelum operasi dan steroid
intraokular atau periokular dapat diberikan pasca-operasi
• Vitrektomi ditujukan untuk memperbaiki tajam penglihatan
bila kekeruhan menetap setelah pengobatan.
4. Menghilangkan nyeri dan fotofobia.
• NSAID digunakan untuk mengurangi nyeri dan inflamasi sedangkan
siklopegik diberikan untuk mencegah sinekia posterior.
• Obat yang diberikan adalah siklopentolat 0,5-2% dan homatropin

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
TO 2
 6. Blepharospasm
• Blepharospasm is a focal dystonia characterized
by repetitive, sustained contractions of the
orbicularis oculi and frontalis muscles.
• Clinical features of blepharospasm include
– involuntary eye closing aggravated by bright
lights,wind, pollution, smoke, emotional stress,
fatigue.
– This eye closing may interfere with reading, driving,
watching television, and other visual activities, and is
rarely associated with retro-orbital pain.
Blepharospasm
 Epicanthal Fold
• An epicanthal fold is a skin fold of the upper eyelid
covering the inner corner of the eye.
• It is often seen as a normal finding in very young children
and is also common in people of Asiatic decent.
• Epicanthal fold can be an important diagnostic finding in
conditions such as Down syndrome
 7. Ulkus kornea
ANAMNESIS

MATA MERAH MATA MERAH MATA TENANG

MATA TENANG VISUS
VISUS NORMAL VISUS TURUN VISUS TURUN
TURUN MENDADAK
• struktur yang PERLAHAN
mengenai media
bervaskuler 
refraksi (kornea, • uveitis posterior • Katarak
sklera konjungtiva •
uvea, atau perdarahan vitreous • Glaukoma
• tidak • Ablasio retina • retinopati
seluruh mata)
menghalangi • oklusi arteri atau vena penyakit sistemik
media refraksi retinal • retinitis
• neuritis optik pigmentosa
• Keratitis
• Konjungtivitis murni • neuropati optik akut • kelainan refraksi
• Keratokonjungtivitis
• Trakoma karena obat (misalnya
• Ulkus Kornea
• mata kering, etambutol), migrain,
• Uveitis
tumor otak
xeroftalmia • glaukoma akut
• Pterigium • Endoftalmitis
• Pinguekula • panoftalmitis
• Episkleritis
• skleritis
 Ulkus kornea
Konjungtivitis Keratitis Ulkus kornea Uveitis
Visus N <N <N N/<N
Sakit - ++ ++ +/++
Fotofobia - +++ - +++
Eksudat +/+++ -/+++ ++ -
Sekresi + - + +
Etiologi Bakteri/jamur/virus/a Bakteri/jamur/virus Infeksi, bahan kimia, Reaksi
lergi /alergi trauma, pajanan, imunologik
radiasi, sindrom lambat/dini
sjorgen, defisiensi
vit.A, obat-obatan,
reaksi
hipersensitivitas,
neurotropik
Tatalaksana Obat sistemik/topikal Obat Obat sesuai etiologi Steroid
sesuai etiologi sistemik/topikal
sesuai etiologi

Ilmu Penyakit Mata, Sidarta Ilyas, 2005

 ULKUS KORNEA
• Ulkus kornea adalah hilangnya
sebagian permukaan kornea akibat
kematian jaringan kornea
• ditandai dengan adanya infiltrat
supuratif disertai defek kornea
bergaung, dan diskontinuitas
jaringan kornea yang dapat terjadi
dari epitel sampai stroma.
• Etiologi: Infeksi, bahan kimia,
trauma, pajanan, radiasi, sindrom
sjorgen, defisiensi vit.A, obat-
obatan, reaksi hipersensitivitas,
neurotropik
• Gejala Subjektif
– Eritema pada kelopak mata dan konjungtiva
– Sekret mukopurulen
– Merasa ada benda asing di mata
– Pandangan kabur
– Mata berair
– Bintik putih pada kornea, sesuai lokasi ulkus
– Silau
– Nyeri
– infiltat yang steril dapat menimbulkan sedikit
nyeri, jika ulkus terdapat pada perifer kornea
dan tidak disertai dengan robekan lapisan
epitel kornea.
• Gejala Objektif
– Injeksi siliar
– Hilangnya sebagian jaringan kornea, dan
adanya infiltrat
– Hipopion
 Typical clinical Feature
Bacterial Ulcer
• 1. History of trauma to the cornea, contact lens
wear
• 2. Pain, redness, watering,decrease in vision
• 3. Lid oedema (marked in gonococcal ulcer),
purulent discharge in gonococcal ulcer and bluish
green discharge in pseudomonas corneal ulcer
• 4. Round or oval in shape involving central or para
central part of the cornea. Rest of the cornea is
clear. Hypopyon may or may not be present.
• 5. In pneumococcal ulcer the advancing border will
have active infiltrate with undermined edges and
the trailing edge may show signs of healing. Most of
the pneumococcal ulcers will show leveled
hypopyon associated with Dacryocystitis.
• 6. Pseudomonas ulcer will have short duration,
marked stromal oedema adjacent to the ulcer with
rapid progression. If untreated, will perforate within
2-3 days. Advanced ulcer may involve the sclera
also.
• 7. Ulcers caused by Moraxella and Nocardia are
slowly progressive in immunocompromised hosts
WHO. Guidelines for the Management of Corneal Ulcer at Primary, Secondary & Tertiary Care health facilities in the South-East Asia Region. 2004
Fungal Ulcer
• 1. History of trauma with vegetable matter
• 2. Suspect fungal ulcer if patient reports
agriculture as main occupation.
• 3. Pain and redness are similar to bacterial
ulcer. But lid oedema is minimal even in
severe cases unless patients have received
native medicines or peri ocular injections.
• 4. Early fungal ulcer may appear like a
dendritic ulcer of herpes simplex virus. The
feathery borders are pathognomonic clinical
features. Satellite lesions, immune ring, and
unlevelled hypopyon may aid in diagnosis.
• 5. The surface is raised with greyish white
creamy infiltrates, which may or may not
appear dry.
• 6. Ulcer due to pigmented fungi will appear
as brown or dark; raised, dry, rough, leathery
plaque on the surface of the cornea
 ULKUS KORNEA
• Berdasarkan lokasi , dikenal ada 2:
1. Ulkus kornea sentral
– Ulkus kornea bakterialis
– Ulkus kornea fungi
– Ulkus kornea virus
– Ulkus kornea acanthamoeba
2.Ulkus kornea perifer
– Ulkus marginal
– Ulkus mooren (ulkus
serpinginosa kronik/ulkus
roden)
– Ulkus cincin (ring ulcer)
Penatalaksanaan :
– harus segera ditangani oleh
spesialis mata
– Pengobatan tergantung
penyebabnya, diberikan obat
tetes mata yang mengandung
antibiotik, anti virus, anti
jamur,
– sikloplegik
– Mengurangi reaksi
peradangan dengan steroid.
– Berikan analgetik jika nyeri
– Jangan menggosok-gosok
mata yang meradang
– Mencegah penyebaran infeksi
dengan mencuci tangan
 Ulkus kornea Bakterial
• Ulkus kornea pneumokokal
– Streptokokus pneumonia
– Muncul 24-48 jam setelah inokulasi
pd kornea yg abrasi
– Khas sebagai ulkus yang menjalar
dari tepi ke arah tengah kornea
(serpinginous).
– Ulkus bewarna kuning keabu-
abuan berbentuk cakram dengan
tepi ulkus yang menggaung.
– Ulkus cepat menjalar ke dalam dan
menyebabkan perforasi kornea,
karena eksotoksin yang dihasilkan
oleh streptokok pneumonia.
– Efek merambat  ulkus
serpiginosa akut
– Obat: mofifloxacin, gatifloxacin,
cefazolin
• Ulkus kornea stafilokokus
– Ulkus sering indolen, mungkin disertai
sedikit infiltrat dan hipopion
– Ulkus seringkali superfisial
– Obat: vankomisin
• Ulkus kornea pseudomonas
– Pseudomonas aeruginosa
– Awalnya berupa infiltrat kelabu/ kuning
di tempat yang retak
– Terasa sangat nyeri
– Menyebar cepat ke segala arah krn
adanya enzim proteolitik dr organisme
– Infiltrat dan eksudat mungkin berwarna
hijau kebiruan
– Berhubungan dengan penggunaan soft
lens
– Obat: mofifloxacin, gatifloxacin,
siprofloksasin, tobramisin, gentamisin
 Keratitis/ulkus Fungal
• Gejala  nyeri biasanya dirasakan diawal, namun lama-lama
berkurang krn saraf kornea mulai rusak.
• Pemeriksaan oftalmologi :
– Grayish-white corneal infiltrate with a rough, dry texture and feathery
borders; infiltrat berada di dalam lapisan stroma
– Lesi satelit, hipopion, plak/presipitat endotelilal
– Bisa juga ditemukan epitel yang intak atau sedikit meninggi di atas
infiltrat stroma
• Faktor risiko meliputi :
– Trauma mata (terutama akibat tumbuhan)
– Terapi steroid topikal jangka panjang
– Preexisting ocular or systemic immunosuppressive diseases

Sumber: American Optometric Association. Fungal Keratitis. / Vaughan Oftalmologi Umum 1995.
 Fungal Ulcer
• Faktor Resiko :
– Lokal
• Trauma-kornea akibat terkena tumbuhan atau benda – benda organik  55-
65 %
• Lensa Kontak 29 %
• Iatrogenic  setelah bedah katarak, operasi refraksi, LASIK, penetrating
keratoplasty
• Penggunaan steroid topical  4-30%. Penggunaan steroid dapat mengaktivasi
dan meningkatkan virulensi fungi
• Kelainan pada permukaan kornea  dry eye, bullous keratopathy, exposure
keratitis, allergic conjunctivitis
– Sistemik
• Diabetes-5%
• Malnutrisi-1%
• Alcoholism – jarang
• HIV – jarang
• Pasien ICU yang menderita penyakit kronik atau dirawat lama
 Keratitis/ ulkus Fungal
• Meskipun memiliki karakteristik, terkadang sulit membedakan
keratitis fungal dengan bakteri.
– Namun, infeksi jamur biasanya localized, dengan “button appearance”
yaitu infiltrat stroma yang meluas dengan ulserasi epitel relatif kecil.
• Pd kondisi demikian sebaiknya diberikan terapi antibiotik
sampai keratitis fungal ditegakkan (mis. dgn kultur, corneal
tissue biopsy).

Stromal infiltrate
 Ulkus kornea Jamur

Lesi satelit (panah merah) pada

keratitis jamur

Keratitis fungi bersifat indolen, dengan infiltrat kelabu, sering dengan hipopion,
peradangan nyata pada bola mata, ulserasi superfisial, dan lesi-lesi satelit (umumnya
infiltrat di tempat-tempat yang jauh dari daerah utama ulserasi).

Vaughan DG, dkk. Oftalmologi Umum Edisi 14. 1996.

 Management of
Supurative Keratitis
at the secondary
level of eye care
Penatalaksanaan
 8. Blefaritis Pedikulosis
DEFINISI
• Inflamasi yang terjadi pada
bagian kelopak mata (sering
kronik)
• Dapat terjadi di anterior
(folikel bulu mata) atau
posterior (kelenjar meibom)
• Klasifikasi :
1. Bakterial
2. Seboroik
3. Angularis
4. Pedikulosis Ebeigbe JA and Osaiyuwu AB - Pediculosis palpebrarum initially diagnosed as blepharitis. S

5. Meibomanitis Afr Optom 2009 68(2) 91-93

 8. Blefaritis Pedikulosis
DEFINISI GEJALA
• Infeksi pada kelopak mata • Kedua mata gatal terutama
yang disebabkan kutu kelopak mata
pedikulosis
• Penyebabnya : • Iritasi mata
1. Pedikulosis kapitis • Tampak kutu pada kelopak
(Pediculosis humanus var mata
capitis)
2. Pedikulosis korporis • Tampak lesi eritematosa
(Pediculus humanus var.
coporis) • Deposit coklat kemerahan
3. Pedikulosis pubis (Phthirus (feses kutu)
pubis penyebab paling sering
blefaritis)

Ebeigbe JA and Osaiyuwu AB - Pediculosis palpebrarum initially diagnosed as blepharitis. S

Afr Optom 2009 68(2) 91-93

 Blefaritis Pedikulosis
• Faktor risiko :
1. Jenis kelamin wanita
2. Usia anak-anak
3. Hidup pada lingkungan padat
4. Cuaca hangat
5. Riwayat hygiene buruk
6. Riwayat penggunaan barang bersama-sama

Ebeigbe JA and Osaiyuwu AB - Pediculosis palpebrarum initially diagnosed as blepharitis. S

Afr Optom 2009 68(2) 91-93

 Blefaritis Pedikulosis
Diagnosis Tatalaksana
• Melakukan pemeriksaan slit • Permetrin 1% lotion 
lamp • Malathion 0,5% lotion
• Menemukan kutu • Gameksan 1%
hidup/telur (berwarna abu-
abu atau mengkilat)

Ebeigbe JA and Osaiyuwu AB - Pediculosis palpebrarum initially diagnosed as blepharitis. S

Afr Optom 2009 68(2) 91-93

 Jenis Blefatis lain
Blefaritis Angularis Meibomanitis
• Infeksi staphyloccocus pada • Infeksi kelenjar meibom 
tepi kelopak atau kantus peradangan lokal

Putnam. Diagnosis and management of blepharitis: an optometrist’s perspective . Clinical Optometry.2016

 9. OKLUSI ARTERI RETINA
• Kelainan retina akibat sumbatan akut arteri retina
sentral yang ditandai dengan hilangnya penglihatan
mendadak.
• Predisposisi
– Emboli paling sering (hipertensi, aterosclerosis, penyakit
katup jantung, trombus pasca MCI, tindakan angiografi,
– Penyakit spasme pembuluh darah karena endotoksin
(keracunan alkohol, tembakau, timah hitam
– Trauma(frakturorbita)
– Koagulopati (kehamilan, oral kontrasepsi)
– Neuritis optik, arteritis, SLE

Kuliah SUB BAG. VITREORETINA

ILMU P. MATA FK.USU/RSUP H.ADAM MALIK MEDAN
 Gejala Klinis :
• Visus hilang mendadak tanda nyeri
• Amaurosis Fugax (transient visual loss)
• Lebih sering laki-laki diatas 60thn
• Fase awal setelah obstruksi gambaran fundus
normal.
• Setelah 30 menit retina polusposterior pucat
kecuali di daerah foveola dimana RPE dan koroid
dapat terlihat  Cherry Red Spot
• Setelah 4-6 minggu : fundus normal kembali
kecuali arteri halus, dan berakhir papil atropi

Kuliah SUB BAG. VITREORETINA

ILMU P. MATA FK.USU/RSUP H.ADAM MALIK MEDAN
Cherry red Spot

Kuliah SUB BAG. VITREORETINA

ILMU P. MATA FK.USU/RSUP H.ADAM MALIK MEDAN
 Penatalaksanaan :
• Tx berkaitan dengan • Gradient perfusion
penyakit sistemik pressure :
• Untuk memperbaiki visus – Parasentesis sumbatan di
harus waspada sebab 90 bawah 1 jam 0,1 – 0,4cc
menit setelah sumbatan – Masase bola mata (dilatasi
kerusakan retina arteri retina)
ireversible. – ß blocker
– acetazolamide
• Prinsip “gradient – Streptokinase (fibrinolisis)
perfusion pressure”
(menurunkan TIO secara – Mixtur O2 95% dengan
CO2 5% (vasodilatasi)
mendadak sehingga
terjadi referfusi dengan
menggeser sumbatan)

Kuliah SUB BAG. VITREORETINA

ILMU P. MATA FK.USU/RSUP H.ADAM MALIK MEDAN
 10.RETINOPATI DIABETIK
DM ophthalmic complications :
• Corneal abnormalities
• Glaucoma
• Iris neovascularization
• Cataracts
• Neuropathies
• Diabetic retinopathy →
most common and
potentially most blinding
• Diabetic Retinopathy :
Retinopathy (damage to the
retina) caused by
complications of diabetes,
which can eventually lead to
blindness.
• It is an ocular manifestation of
systemic disease which affects
up to 80% of all patients who
have had diabetes for 10 years
or more.
 10. RETINOPATI DIABETIK
Signs and Symptoms
• Seeing spots or floaters in the
field of vision
• Blurred vision
• Having a dark or empty spot in
the center of the vision
• Difficulty seeing well at night
• On funduscopic exam : cotton
wool spot, flame
hemorrhages, dot-blot
hemorrhages, hard exudates
Pemeriksaan :
• Tajam penglihatan
• Funduskopi dalam keadaan
pupil dilatasi : direk/indirek
• Foto Fundus
• USG bila ada perdarahan
vitreus
Tatalaksana :
• Fotokoagulasi laser
 RETINOPATI DIABETIK
• Riwayat DM yang lama, biasa > 20 tahun
• Mata tenang visus turun perlahan
• Pemeriksaan Oftalmoskop
– Mikroaneurisma (penonjolan dinding kapiler)
– Perdarahan dalam bentuk titik, garis, bercak yang letaknya dekat
dengan mikroaneurisma di polus posterior (dot blot hemorrhage)
– Dilatasi vena yang lumennya ireguler dan berkelok
– Hard exudate (infiltrasi lipid ke dalam retina akibat dari peningkatan
permeabiitas kapiler), warna kekuningan
– Soft exudate (cotton wall patches) adalah iskemia retina tampak
sebagai bercak kuning bersifat difus dan warna putih
– Neovaskularisasi
– Edema retina
 RETINOPATI DIABETIK - KLASIFIKASI

RETINOPATI DIABETIK NONPROLIFERATIF

• ditandai dengan kebocoran darah dan serum pada
pembuluh darah kapiler
• menyebabkan edema jaringan retina dan
terbentuknya deposit lipoprotein (hard exudates)
• Tidak menyebabkan gangguan penglihatan 
mengenai makula
• Edema makula  penebalan daerah makula
sebagai akibat kebocoran kapiler perifoveal
 Nonproliferative Diabetic Retinopathy
• Retinal vascular related abnormalities such as
microaneurysms, intraretinal hemorrhages, venous
dilatation, and cotton wool spot
• Increased retinal vascular permeability  result in
retinal thickening (edema) and lipid deposits (hard
exudate)
• Severe NPDR :
– Venous abnormalities (dilatation, beading and loops),
more severe and extensive vascular leackage (increased
retinal hemorrhage and exudation)
– This patient should be considered candidates for
treatment with panretinal photocoagulation

American Academy of Ophtalmology. Diabetic retinopathy. 2014

 RETINOPATI DIABETIK - KLASIFIKASI
RETINOPATI DIABETIK PROLIFERATIF
• ditandai dengan adanya proliferasi jaringan
fibrovaskular atau neovaskularisasi pada
permukaan retina & papil saraf optik serta vitreus
• Proliferasi  respon dari oklusi luas pembuluh
darah kapiler retina yang menyebabkan iskemia
retina
• menyebabkan gangguan penglihatan sampai
kebutaan melalui mekanisme;
– Perdarahan vitreus
– Tractional retinal detachment
– Glaukoma neovaskular
 Proliferative Diabetic retinopathy
• Neovascularization at the inner surface of retina
induced by more global retinal ischemia.
• Neovaskularisasi near the optic disc and
elsewhere are prone to bleed  vitreous
hemorrhage
• Neovaskularisasi undergo fibrosis and contraction
 epiretinal membrane formation, vitroretinal
traction band, retinal tears and traction or
rhegmatogenosa ablasio retina
American Academy of Ophtalmology. Diabetic retinopathy. 2014
 • Clinically significant macular edema (CSME)
describe retinal thickening and/or adjacent
hard exudates that etiher involve the center of
macula or threaten to invole it
– Center involving
– Non center involving

American Academy of Ophtalmology. Diabetic retinopathy. 2014

 KLASIFIKASI RETINOPATI DM
• Derajat I : Mikroaneurisama dengan atau
tanpa eksudat lemak pada fundus okuli
• Derajat II: Mikroaneurisma, perdarahan bintik
dan bercak dengan atau tanpa eksudat lemak
pada fundus okuli
• Derajat III: Mikroaneurisma, perdarahan bintik
dan bercak, neovaskularisasi
Pra Bukti oklusi (cotton wool spot). Vena menjadi iregular dan
Proliferatif(Non mungkin terlihat membentuk lingkaran.
proliferatif)
Proliferatif Perubahan oklusif menyebabkan pelepasan substansi
vasoproliferatif dari retina yang menyebabkan pertumbuhan
pembuluh darah baru di lempeng optik atau ditempat lain
pada retina. Penglihatan normal, mengancam penglihatan

Proliferatif Perubahan proliferatif dapat menyebabkan perdarahan pada

lanjut vitreus dan retina. Retina juga dapat tertarik dari epitel
pigmen di bawahnya oleh proliferasi fibrosa yang berkaitan
dengan pertumbuhan pembuluh darah baru. Penglihatan
berkurang, mengancam penglihatan
Dot blot hemorrhage
Flame-shaped hemorrhage

Microaneurysm / dot blot hemorrhage

Macular edema
Neovascularization
Proliferative diabetic retinopathy
 Penatalaksanaan :
1. Medical Treatment :
• Aldose reduktase inhibitor (sorbinil) 
Penelitian menurunkan proses retinopati
• Vascular Endothelial Growth factor Inhibitor
• Aminoguanidin (mengikat protein yang
mengalami glikolisis
• Pentoxypilin (memperbaiki sirkulasi perifer)
2. Laser Photocoagulation
• Early Treatment Diabetic Retinopathy Study
(ETDRS) : Fotokoagulasi dini menurunkan incident
ggn visus 50%
• Terapi pilihan utama pada retinopati diabetes
yang telah mengancam penglihatan
• Indikasi :
– Perdarahan vitreous atau preretinal terokalisasi
– Kontraksi progresif proliferasi fibrin
– Neovaskularisasi ekstensif di COA
 Anti-VEGF injection
• Initial treatment choice for center involving macular
edema with possible subsequent or deffered focal
treatment.
• The Diabetec Retinopathy Clinical Research Network
also showed that anti-VEGF with either prompt or
deffered laser photocoagulation was better than either
laser alone or laser combined with triamcinolone
acetonide.
• AntiVEGF theraphy using bevacizumab, ranibizumab, or
ablifibercept is an effective treatment for center
involving significant macular edema
3. Bedah Vitrektomi :
• Vitrektomi dini pada PDR dapat menyebabkan
regresi NVD dan NVE
• Indikasi :
– Vitrektomi dipertimbangkan dilakukan jika terjadi
rekurensi, kegagalan terapi dengan foto koagulasi,
ataupun perdarahan vitreus yang massif hingga polus
posterior tidak terlihat.
– Perdarahan vitreous yang lama (3 – 6 bln)
– PDR (retinopati diabetik proliferatif) yang aktif dengan
visus baik
– Adanya traksi pada papil, peripapil, makula
– Adanya ablasio retina yang melibatkan makula
– Penurunan tajam penglihatan dari 10/50 menjadi
10/100 atau lebih buruk
 Defini dan gejala
Oklusi arteri Penyumbataan arteri sentralis retina dapat disebabkan oleh radang arteri, thrombus dan
sentral emboli pada arteri, spsame pembuluh darah, akibat terlambatnya pengaliran darah, giant cell
retina arthritis, penyakit kolagen, kelainan hiperkoagulasi, sifilis dan trauma. Secara oftalmoskopis,
retina superficial mengalami pengeruhan kecuali di foveola yang memperlihatkan bercak
merah cherry (cherry red spot). Penglihatan kabur yang hilang timbul tanpa disertai rasa sakit
dan kemudian gelap menetap. Penurunan visus mendadak biasanya disebabkan oleh emboli

Oklusi vena Kelainan retina akibat sumbatan akut vena retina sentral yang ditandai dengan penglihatan
sentral hilang mendadak.
retina Vena dilatasi dan berkelok, Perdarahan dot dan flame shaped , Perdarahan masif pada ke 4
kuadran , Cotton wool spot, dapat disertai dengan atau tanpa edema papil

ARMD Degenerasi makula terkait usia. Penyebab pasti belum diketahui. Insidens meningkat pada usia
> 50 tahun. Predominansi pada wanita, riwayat keluarga, dan riwayat merokok. Gangguan
penglihatan sentral (mata kabur, distorsi atau skotoma). Ditandai oleh atrofi dan degenerasi
retina bagian luar, epitel pigmen retina, membran Bruch, dan koriokapilaris dengan derajat
bervariasi. Funduskopi: drusen (endapan putih, kuning, bulat, diskret tersebar di seluruh
makula dan kutub posterior)
Tatalaksana bisa berupa Antioksidan serta Fotokoagulasi laser

Retinopati suatu kondisi dengan karakteristik perubahan vaskularisasi retina pada populasi yang
hipertensi menderita hipertensi. Mata tenang visus turun perlahan dengan tanda AV crossing – cotton
wol spot- hingga edema papil; copperwire; silverwire
Amaurosis Kehilangan penglihatan tiba-tiba secara transient/sementara tanpa adanya nyeri, biasanya
Fugax monokular, dan terkait penyakit kardiovaskular
 11. Uveitis
Anterior Intermediate Posterior Panuveitis

Fuchs’ Sarcoidosis Toxoplasmosis Tuberculosis

heterochromic
uveitis
Posner Tuberculosis Acute retinal Sarcoidosis
Schlossman necrosis
syndrome
Infective uveitis Lyme’s disease Behcet’s disease

Arthritis Vogt-Koyanagi-
associated Harada
uveitis
Deepankur Mahajan, Pradeep Venkatesh, S.P. Garg ; Uveitis and glaucoma: a critical review : Journal of Current
Glaucoma Practise, September December 2011; 5(3): 14-30
 Behcet’s Disease

• Chronic, relapsing, occlusive systemic vasculitis

• Etiology unknown
• Affects both anterior & posterior segment
• Type:
– Neuro BD
– Ocular BD
– Intestinal BD
– Vascular BD
 Behçet disease
Oral or genital sores • Uveitis Anterior/Media/Posterior (Panuveítis)
Uveitis • HLA-B51+
Skin lesions

Criteria for Behçet's disease:

Mouth sores (oral ulcers) at least 3 times in 12 months
Any 2 of the following:
•Recurring genital sores/ulcers
•Uveitis
•Skin: Pustules or erythema nodosum
•Positive pathergy (skin prick test)
 Vogt-Koyanagi-Harada Syndrome
• Uncommon multisystem disease of Autoimmune etiology
• Chronic, bilateral, diffuse, granulamatous pan-uveitis
• Associated with Integumentary, Neurologic, Auditory involvement
• Commonly affects darkly pigmented ethnic groups
• History of the disease:
1. Prodromos flu-like-syndrome
2. Acute fase:
– Neurologic symptoms: meningismus, tinnitus, pleocytosis in CFS
– Uveitis
3. Convalescent phase: poliosis, skin/uveal discoloration,
poliosis, Sigiura sign (perilimbic discoloration), vitiligo,
alopecia areata
4. Chronic recurrent phase: recurrent anterior uveitis
 Vogt Koyanagi Harada syndrome
1. Prodromus
• Posterior uveitis with serous detachments
2. Neurologic symptoms+ Bilateral
uveitis
• Granulomatous bilateral uveitis
• Late: poliosis, Sigiura sign, sunset-glow fundus
3. Late cutaneous symptoms
 Posner- Schlossman syndrome
• Glaucomatocyclitic crisis
• Mild anterior uveitis with very
high IOP
• Discomfort, blurring of vision,
haloes, No pain, No redness
• PG level in aqueous
• unilateral recurrent episodes of
mild cyclitis and heterochromia.
• Its pathogenesis still remains
unknown, with suggested
possible associations including an
immunogenetic factor involving
HLA-Bw54, viral infections (HSV
and CMV)
CLINICAL FEATURES:
• mild ciliary flush
• a dilated or sluggishly reactive
pupil
• corneal epithelial edema
• open angles (No shallow AC)
• The IOP is in the range of 40 – 70
mmHg during an acute attack
• Minimal flare
• Few cells
• Few Keratic precipitate
• No pheripheral anterior
synechiae and posterior
synechiae
 Reiter syndrome/Reactive arthritis
Urethritis /gastroenteritis
1-5weeks before: • Keratoconjunctivitis+urethritis +arthritis
Ocular
yellowish serous papules at • Previously: urethritis ( can be seen as genital
soles and palms ulcer too) /gastroenteritis
HLAB27+

Infectious
agents: Chlamydiae, Salmonella, Shi
gella, Yersinia, Campylobacter
yellowish serous papules at soles
and palms even nails, scrotum,
scalp and trunk.
 Sympathetic Ophthalmia
• Definisi: inflamasi intraokular • Etiologi: belum jelas,
bilateral yang terjadi beberapa kemungkinan karena
hari atau bulan setelah autoimun terhadap antigen
pembedahan atau trauma okular.
penetrasi pada satu mata. • Faktor risiko: pembedahan
• Mata yang mengalami cedera viteroretina dan prosedur
atau menjalani pembedahan silodestruktif, trauma okular
disebut exciting eye, beberapa • Gejala: (pada mata yang
waktu kemudian terjadi sebelumnya sehat)
inflamasi di mata yang lain – Mata merah
yang sebelumnya tidak – Injeksi konjungtiva
mengalami keluhan apapun, – Penurunan visus
atau yang disebut dengan
sympathizing eye.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277011/
12. Glaukoma Akut
 Pemeriksaan Glaukoma Akut
• Tonometri • Perimetry
– Menilai tekanan intra – Pemeriksaan lapang
okular pandang
– Anestesi topikal pada mata – Dilakukan bila ada gejala
 probe tonometry akan gangguan lapang pandang,
diaplikasikan pada mata untuk menilai apakah
– Mudah, sederhana, tanpa peningkatan TIO
nyeri. memengaruhi lapang
– Nilai normal 12-22 mmHg. pandang
• Gonioskopi
– Dilakukan untuk menilai
adanya angle problems
(apakah open atau closure
angle)

https://emedicine.medscape.com/article/1205421-clinical#b4
 Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006

Tatalaksana Glaukoma Akut

• Tujuan : merendahkan tekanan bola mata secepatnya
kemudian bila tekanan normal dan mata tenang → operasi
• Supresi produksi aqueous humor
– Beta bloker topikal: Timolol maleate 0.25% dan 0.5%, betaxolol
0.25% dan 0.5%, levobunolol 0.25% dan 0.5%, metipranolol
0.3%, dan carteolol 1% dua kali sehari dan timolol maleate 0.1%,
0.25%, dan 0.5% gel satu kali sehari (bekerja dalam 20 menit,
reduksi maksimum TIO 1-2 jam stlh diteteskan)
– Pemberian timolol topikal tidak cukup efektif dalam
menurunkan TIO glaukoma akut sudut tertutup.
– Apraclonidine: 0.5% tiga kali sehari
– Brimonidine: 0.2% dua kali sehari
– Inhibitor karbonat anhidrase:
• Topikal: Dorzolamide hydrochloride 2% dan brinzolamide 1% (2-3
x/hari)
• Sistemik: Acetazolamide 500 mg iv dan 4x125-250 mg oral (pada
glaukoma akut sudut tertutup harus segera diberikan, efek mulai
bekerja 1 jam, puncak pada 4 jam)
 Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007.

Tatalaksana Glaukoma Akut

• Fasilitasi aliran keluar aqueous humor
– Analog prostaglandin: bimatoprost 0.003%, latanoprost 0.005%, dan
travoprost 0.004% (1x/hari), dan unoprostone 0.15% 2x/hari
– Agen parasimpatomimetik: Pilocarpine
– Epinefrin 0,25-2% 1-2x/hari
• Pilokarpin 2% setiap menit selama 5 menit,lalu 1 jam selama 24 jam
– Biasanya diberikan satu setengah jam pasca tatalaksana awal
– Mata yang tidak dalam serangan juga diberikan miotik untuk mencegah
serangan
• Pengurangan volume vitreus
– Agen hiperosmotik: Dapat juga diberikan Manitol 1.5-2MK/kgBB dalam larutan
20% atau urea IV; Gliserol 1g/kgBB badan dalam larutan 50%
– isosorbide oral, urea iv
• Extraocular symptoms:
– analgesics
– antiemetics
– Placing the patient in the supine position → lens falls away from the iris
decreasing pupillary block
– Pemakaian simpatomimetik yang melebarkan pupil berbahaya
 13. Conjunctivitis
• Inflammationor infection of the
conjunctiva  conjunctivitis
• Characterized by : dilatation of
the conjunctival vessels, resulting
in hyperemia and edema of the
conjunctiva, typically with
associated discharge
• Viral conjunctivitis is the most
common cause of infectious
conjunctivitis both overall and in
the adult population
• Bacterial conjunctivitis is the
second most common cause and
is responsible for the majority
(50%-75%) of cases in children
The conjunctiva is a thin membrane covering the sclera
(bulbar conjunctiva, labeled with purple) and the inside
of the eyelids (palpebral conjunctiva, labeled with blue

Azari A, Barney N. Conjunctivitis A Systematic Review of Diagnosis and Treatment. JAMA: 310(16).2013
Classification
• infectious and noninfectious
causes.
– Infectious : Viruses, bacteria  the
most common infectious causes.
– Noninfectious conjunctivitis :
allergic, toxic, and cicatricial
conjunctivitis, as well as
inflammation secondary to
immunemediated diseases and
neoplastic processes.1
• Acute, hyperacute, and chronic
according to the mode of onset
and the severity of the clinical
response.
• Primary or secondary to systemic
diseases such graft-vs-host
disease, and Reiter syndrome,
 Viral Conjunctivitis
• Etiology : Adenovirus (65-90% of
cases)
– produce 2 of the common clinical
entities associated with viral
conjunctivitis :
1. pharyngoconjunctival fever
• Abrupt onset of high
fever, pharyngitis,
bilateral conjunctivitis
and periauricular
lymphnode
enlargement
2. epidemic
keratoconjunctivitis
• More severe and presents
with watery discharge,
hyperemia, chemosis, and
ipsilateral
lymphadenopathy
• Viral conjunctivitis secondary to
adenoviruses  highly contagious,
and the risk of transmission 10% -
50%
• The virus spreads through direct
contact via contaminated fingers,
medical instruments, swimming pool
water,or personal items
• Incubation and communicability are
estimated to be 5 to 12 days and 10
to 14 days, respectively
• Treatment
– artificial tears, topical
antihistamines, or cold
compresses  alleviating some
of the symptoms
– Available antiviral medications
are not useful and topical
antibiotics are not indicated
 Follicularis vs Papillaris Conjunctivitis
Folicularis
• Seen ini variety condition:
inflamation caused by viruses,
atypical bacteria, toxin, topical
medication (glaucoma medication
 brimonidine)
• Follicle  small, dome shaped
nodules without prominent
central vessels. Pale on its
surface,red at base
• Most prominent in the inferior
palpebral and forniceal
conjunctiva
• Histology :
– Lymphoid follicle is situated in the
subepitelial region and consists of
germinal center  immature
proliferating lymphocyte
Papillaris
• Most commonly associated with
an allergic immune response (AKC
& VKC), response to foreign body
(CL, prosthetic ocular)
• Shows a cobblestone
arrangement of flattened nodules
with central vascular cores
– Papillae tarsal  Giant papillary
conjunctivitis
– Limbal papillae  horner trantas
dots in VKC
• Closely packed, flat topped
projections with numerous
eosinophil, lymphocyte, plasma
and mast cells.
• More red in surface, pale at base
Treatment
 14. Trichiasis
• Suatu kelainan dimana bulu mata
mengarah pada bola mata yang
akan menggosok kornea atau
konjungtiva
• Biasanya terjadi bersamaan
dengan penyakit lain seperti
pemfigoid, trauma kimia basa dan
trauma kelopak lainnya, blefaritis,
trauma kecelakaan, kontraksi
jaringan parut di konjungtiva dan
tarsus pada trakoma
• Gejala :
– Konjungtiva kemotik dan hiperemi,
keruh
– Erosis kornea, keratopati dan ulkus
– Fotofobia, lakrimasi dan terasa
seperti kelilipan
– blefarospasme
 Trichiasis
• Tatalaksana: • Tatalaksana bedah untuk
– Yang utama: bedah
– Lubrikan seperti artificial tears dan
trikiasis yg disebabkan
salep untuk mengurasi iritasi akibat krn kelainan anatomi:
gesekan – Entropion: dilakukan
– Atasi penyakit penyebab trikiasis, cth tarsotomi
SSJ, ocular cicatrical pemphigoid)
• Tatalaksana Bedah trikiasis – Posterior lamellar scarring:
segmental (fokal) Grafting
– Epilasi: dengan forsep dilakukan
pencabutan beberapa silia yang salah
letak, dilakukan 2-3 kali. Biasanya
dicoba untuk dilakukan epilasi
terlebih dahulu. Trikiasis bisa timbul
kembali.
– Elektrolisis/ elektrokoagulasi, ES: nyeri
– Bedah beku (krioterapi): banyak
komplikasi
– Ablasi denga radiofrekuensi: sangat
efektif, cepat , mudah, bekas luka
minimal
 15. Herpes Simplex oftalmikus
• HSV-1 infection occurs by direct contact of skin or
mucous membrane with virus-laden lesions or
secretions
• Occurs most commonly in the mucocutaneous
distribution of the trigeminal nerve
• After the primary infection, the virus travels in
retrograde fashion from the infected epithelial cells to
nearby sensory nerve endings and is transported along
the nerve axon to the cell body located in the
trigeminal ganglion, entering into a latent state.
• Interneuronal spread of HSV within the ganglion allows
patients to develop subsequent ocular disease without
ever having had primary ocular HSV infection
 Ocular Manifestation of HSV
• Periocular herpes simplex
• Blepharitis
• Conjunctivitis
• Scleritis
• Keratitis
• Iridocyclitis
• Retinitis
Herpes Simplex Keratitis
 Keratitis Herpes Simpleks

• Herpes simpleks virus (HSV) keratitis, sama dengan penyakit herpes simpleks
lainnya dapat ditemukan dalam dua bentuk: primer atau rekuren.
• Kebanyakan infeksi HSV pada kornea disebabkan oleh HSV tipe 1, namun
pada balita dan orang dewasa, dapat juga disebabkan oleh HSV tipe 2. Lesi
kornea yang disebabkan kedua virus tersebut tidak dapat dibedakan.
• Kerokan dari lesi epitel pada keratitis HSV mengandung sel-sel raksasa berinti
banyak.
• Virus dapat dibiakkan di dalam membran khorioallantoik embrio telur ayam
dan di dalam jaringan seperti sel-sel HeLa .
• Identifikasi akurat virus dilakukan menggunakan metode PCR

Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007
• Tanda dan gejala:
– Infeksi primer biasanya berbentuk
blefarokonjungtivitis vesikular, kadang disertai
keterlibatan kornea. Umumnya self-limmited tanpa
menyebabkan kerusakan mata yang signifikan.
– Iritasi, fotofobia, peningkatan produksi air mata,
penurunan penglihatan, anestesi pada kornea,
demam.
– Kebanyakan unilateral, namun pada 4-6% kasus dapat
bilateral
– Lesi: Superficial punctate keratitis -- stellate erosion --
dendritic ulcer -- Geographic ulcer
• Dendritic ulcer: Lesi yang paling khas pd keratitis HSV.
Berbentuk linear, bercabang, tepi menonjol, dan memiliki
tonjolan di ujungnya (terminal bulbs), dapat dilihat dengan
tes flurosensi.
• Geographic ulcer. Lesi defek epitel kornea berbentuk spt
amuba
Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007
 Keratitis herpes Treatment
• The treatment of herpes simplex keratitis is dependent upon whether the episode of
disease is caused by active viral replication or immune response to past infection.
• We recommend NOT using topical glucocorticoids when active HSV epithelial disease
is present (Grade 1C).
• We recommend that patients with epithelial herpes simplex keratitis receive antiviral
agents (Grade 1B).
– Oral and topical antivirals are equally effective, but oral agents are more convenient to use.
Trifluorothymidine 1% (trifluridine) is given one drop every two hours (eight or nine doses daily) for two
weeks.
– Ganciclovir 0.15% gel is given one drop five times daily until epithelial healing occurs and then three
times daily for seven days. Oral acyclovir is given 400 mg five times daily.
• We suggest treatment of stromal keratitis with a combination of an oral antiviral agent
and a topical glucocorticoid (Grade 2A).
– We suggest that patients with recurrent episodes of significant keratitis receive ongoing suppressive oral
antiviral therapy with either valacyclovir or acyclovir (Grade 2B).
– Valacyclovir is given 500 mg once daily and acyclovir 400 mg two times a day.
– Suppressive therapy may not be cost-effective for patients with mild recurrent disease, and its effect
does not persist when the drug is discontinued.
• Patients who have significant vision impairment due to corneal scarring from keratitis
may require corneal transplantation. Oral acyclovir improves corneal graft survival.
 Keratitis herpes treatment
• Treatment options for primary ocular herpes infection
include the following:
– Ganciclovir ophthalmic gel 0.15% - 5 times daily
– Trifluridine 1% drops - 9 times daily
– Vidarabine 3% ointment - 5 times daily
– Oral acyclovir 400 mg - 5 times daily for 10 days [20] ; oral
acyclovir is the preferred treatment in patients unable to
tolerate topical medications and with good renal function
• equivalent to topical treatment and avoids corneal epithelial
toxicity
– A cycloplegic agent may be added to any of the above
regimens for comfort from ciliary spasm.
Keratitis herpes zoster
• Bentuk rekuren dari keratitis Varicella
• Lesi pseudodenditik: lesi epitel yang menonjol dengan ujung
mengerucut, sedikit tonjolan pada ujungnya (terminal bulbs)

Keratitis varicella
• Bentuk infeksi primer pada mata dari virus Varicella
• Ciri khas: lesi pseudodendritik disertai lesi pada stroma kornea
dan uveitis

Keratitis marginal
• Keratitis non infeksius, sekunder setelah konjungtivitis bakteri, terutama Staphylococcus
• Keratitis ini merupakan hasil dari sensitisasi tubuh terhadap produk bakteri. Antibodi dari
pembuluh darah di limbus bereaksi dgn antigen yang terdifusi ke dalam epitel kornea

Keratitis bakteri
• Biasanya unilateral, terjadi pd org dengan penyakit mata sebelumnya atau mata
org yang menggunakan kontak lens
• Infiltrat stroma berwarna putih, edema stroma, pembentukan hipopion
 Herpes Zooster Ophtalmicus
• First described by Hutchinson in 1865
• Involves the reactivation of VZV in the
trigeminal ganglia with ophthalmic
involvement
• Accounts for 10%-25% of zoster episodes
– Nasociliary branch of the ophthalmic nerve
innervates the skin of the eyelids, conjunctiva,
sclera, cornea, iris, choroid, and the tip of the
nose
• Hutchinson’s sign
– Presence of vesicles at the
side of the tip of the nose
– Indicator of nasociliary
involvement
– Associated with a 50-76%
chance of ocular
complications
– The risk lowers to 34%
without nasociliary
involvement
Signs
• External
– Lid edema and vesicles
– Conjunctival hyperemia
– Episcleritis and scleritis
– Cornea
• Punctate epithelial keratitis
• Pseudodendrites
• Anterior stromal infiltrates
• Keratouveitis
• Uveitis
 Figure 1A

Shaikh S, Cristopher N. Evaluation and Management of Herpes zooster ophtalmicus. (Am Fam Physician 2002;66:1723-30,1732.
 16. GLAUKOMA SEKUNDER
• Glaucoma sekunder merupakan glaukoma yang diketahui
penyebab yang menimbulkannya. Hal tersebut disebabkan
oleh proses patologis intraokular yang menghambat aliran
cairan mata (cedera, radang, tumor, penyakit sistemik)
• Glaukoma sekunder bisa terjadi akibat lensa seperti :
 Luksasi lensa anterior, dimana terjadi gangguan pengaliran cairan mata ke
sudut bilik mata, COA dangkal
 Katarak imatur, dimana akibat mencembungnya lensa akan menyebabkan
penutupan sudut bilik mata, COA dangkal (glaukoma fakomorfik)
 Katarak hipermatur, dimana bahan lensa keluar dari lensa sehingga menutupi
jalan keluar cairan mata, COA normal/dalam (glaukoma fakolitik)
 Phacoanaphylactic glaucoma, COA dalam
 Lens particle glaucoma, COA dalam

Ilyas, Sidarta., 2004. Ilmu Penyakit Mata, Fakultas Kedokteran Universitas Indonesia, Jakarta.
 Glaucoma phacomorphic

• Cataract maturation is associated

with anteroposterior lens
diameter increase  Progressive
enlargement of the lens 
peripheral iridotrabecular
apposition.

• When the iridotrabecular

apposition raises the intraocular
pressure (IOP) enough to cause
the signs and symptoms of an
acute attack of secondary angle-
closure glaucoma  acute
phacomorphic angle-
closure/phacomorhpic glaucoma
 Diagnosis
• IOP above 21 mmHg
• secondary form of angleclosure, findings include : injection,
corneal edema, mid-dilated pupil, shallow anterior
chamber, and a mature cataract.
• 71% complained of eye pain
• 16% described it as a headache
• Nausea was reported by 8%.
• Biometry as diagnostic criteria, requiring a lens thickness of
at least 5 mm and an anterior chamber depth less than 2
mm.
• A vital part of the exam is gonioscopy to confirm a closed
angle.

Kaplowitz KB, Kapoor KG (2012) An Evidence-Based Approach to Phacomorphic Glaucoma. J Clinic Experiment Ophthalmol S1:2011
 Treatment
• The goal in treating phacomorphic angle-closure is to
reduce the IOP before the onset of acute glaucomatous
optic neuropathy
• The only definitive treatment is cataract extraction
• However, to avoid operating on an inflamed eye with
high pressure (increasing the risk of suprachoroidal
hemorrhage from rapid IOP fluctuations), with a
limited view from corneal edema and an extremely
shallow chamber  the initial goal is to stabilize the
eye by breaking the acute attack and lowering the IOP
using either medical or laser treatment.

Kaplowitz KB, Kapoor KG (2012) An Evidence-Based Approach to Phacomorphic Glaucoma. J Clinic Experiment Ophthalmol S1:2011
 Medical treatment
• Several studies relied on a standard treatment algorithm; timolol,
acetazolamide and intravenous mannitol were among the most common
medications used
• Pilocarpine should be avoided because it causes a forward shift of the iris-
lens diaphragm which would worsen the angle-closure, and can increase
the amount of inflammation
• Topical treatment alone may be insufficient to break the attack
• The presence of at least 180 degrees of peripheral anterior synechiae
(PAS) at presentation an indication that topical treatment will be
insufficient to break the attack
• If topical treatment fails to bring the IOP into a tolerable range until
cataract extraction can be performed, there are 3 options :
– The first is oral or intravenous medicine such as acetazolamide or mannitol.
– Argon laser peripheral iridoplasty (ALPI)
– peripheral iridotomy

Kaplowitz KB, Kapoor KG (2012) An Evidence-Based Approach to Phacomorphic Glaucoma. J Clinic Experiment Ophthalmol S1:2011
 17. Hifema
Darah di bilik mata anterior

• Komplikasi tersering dari trauma tumpul atau

penetrasi mata
– Anak  Tersering trauma tumpul (ex: bola)
– Remaja & Dewasa  Tersering karena
trauma dengan energi tinggi (ex: pukulan,
KLL)
• Pada sebagian besar kasus, visus kembali
normal.
• Penurunan visus permanen bila:
– Hifema luas
– Hemolgobinopati, ex: sickle cell disease
– Risiko perdarahan, ex:hemofilia, obat
antikoagulan
• Disertai ruptur bola mata  emergensi Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Hifema
Patofisiologi Hifema Traumatik
• Trauma tumpul  peningkatan TIO,
stretching bola mata & tekanan dari
posterior disalurkan ke sekitar iris
 “robekan” stuktur pada sudut
COA  perdarahan badan siliar
atau iris
• Trauma Penetrasi  kerusakan
langsung daerah iris
• Hifema spontan  bisa
perdarahan spontan atau trauma
minor pada pasien risiko
perdarahan, seperti:
• DM
• Melanoma iris,
retinoblastoma, tumor lainnya
• Gangguan pembekuan darah
• Obat yang mengganggu fungsi
platelet
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Hifema
Gejala&Tanda: • Kerusakan struktur sekitar:
• + darah COA dan peningkatan TIO  Abrasi kornea
• Penurunan visus  Anisokoria dan iridodialisis
• Nyeri mata dengan konstriksi pupil  Subluksasi lensa & gangguan
pada penyinaran cahaya langsung mobilitas lensa (fakodonesis)
dan konsensual  fotofobia  Gangguan sudut mata 
glaukoma sudut
• Tanda ruptur bola mata  terbuka/tertutup
emergency!!!  sinekia
– Penurunan visus signifikan
– Pupil eksentrik
– Penurunan/Peningkatan kedalaman
bilik mata depan signifikan
– Keluarnya vitreous
– Prolaps eksternal uvea atau struktur
internal lainnya
– Perdarahan subkonjungtiva luas
– Seidel’s sign  menilai kebocoran COA
dengan fluoresensi
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Hifema
• Diagnostik
– Inspeksi visual 
penlight dan slit lamp
– Cek Faktor predisposisi:
sickle cell
hemoglobinopathy,
gangguan pembekuan
darah, dll
– Imaging:
• CT orbital  curiga open
globe, benda asing,
fraktur orbita
• Ultrasound
biomicroscopy
© 2019 American Academy of Ophthalmology
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Tata Laksana Hifema Traumatik
• Tangani
– life-threatening (pada kasus trauma)
– Vision-theatening:
• Orbital Compartment Syndrome  proptosis, penurunan visus
signifikan, perdarahan subkonjungtiva luas, kelopak mata tegang,
defek pupil aferen, kimosis, penurunan retropulsi  Canthotomy
• Ruptur bola mata  tutup bola mata, obat anti nyeri dan anti mual-
muntah untuk mencegah keluarnya isi okular  Operasi repair
• Tutup mata + lampu redup  cegah akomodasi berlebih
• Bedrest & Elevasi kepala 30 derajat
• Pemberian sikloplegia (bila tidak ada ruptur bola mata) 
mengurangi nyeri, mencegah sinekia serta disfungsi iris
• Cegah mual-muntah  menghindari peningkatan TIO
• Obat nyeri topikal (ex: proparacaine 0,5%), bila kurang
dapat ditambahkan antinyeri sistemik
• Tetes mata glukokortikoid  menurunkan risiko
perdarahan ulang  ex: prednisolone asetat 1% atau
dexamethasone sodium fosfat 0,1% Andreoli CM, Gardiner MF. Traumatic hyphema:
Management. Uptodate: 2018.
• Tata Laksana Lanjutan
– Monitor TIO harian  bila hipertensi, terapi menekan
aliran aquous humor, ex: beta adrenergik bloker
topikal (timolol) dan karbonik anhidrase inhibitor
topikal (dorzolamide) atau tambahkan oral
asetazolamide/methazolamide bila efek topikal tidak
adekuat
• Rujuk untuk intervensi dan pemberian manitol bila
hipertensi intraokular tidak terkontrol:
– > 50 mmHg selama 5 hari atau
– >35 mmHg selama 7 hari atau
– Pasien dengan hemoglobinopati
– >25 mmHg selama >24 jam
• Hipertensi intraokular, hifema Grade III dan IV lebih dari
10 hari, early corneal blood staining  evakuasi clot
dengan pembedahan
• Rujuk  pada sindrom kompartemen orbital, ruptur bola
mata, hifema grade III-IV, hifema pada pasien risiko
perdarahan, hifema dengan peningkatan TIO
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 18. Ocular Foreign body
• An ocular foreign body :
– common condition, in which a small particle (such as a
piece of grit or small rust particle) becomes stuck on eye.
• Corneal foreign body  CA stuck on the eye ;
• sub-tarsal foreign body  the object is stuck under your lid
scratches to the surface of your cornea.
– Symptoms
• painful, red, watery and light sensitive and ↓ vision
• Subconjunctival hemorrhage
• Corneal laceration and abrasion  heal within 48 hours after
removal
• if CA is metal, a small ring of rust may form around it  a dark
spot on the white of eye and can cause a scar that may affect
vision
 Benda Asing superfisial
• Anamnesis dan catat tajam penglihatan
• Berikan anastesi topikal untuk mengontrol nyeri
• Jika tidak terdapat luka tembus, eversikan
kelopak untuk mencari benda asing di
konjungtiva tarsal
• Lakukan irigasi dan swab benda asing dengan lidi
kapas steril
• Bila benda asing tetap ada, segera rujuk ke SpM
 19. TRAUMA KIMIA MATA
• Klasifikasi :
• Merupakan trauma yang mengenai
bola mata akibat terpaparnya bahan
kimia baik yang bersifat asam atau
basa yang dapat merusak struktur bola
mata tersebut
• Keadaan kedaruratan oftalmologi
karena dapat menyebabkan cedera
pada mata, baik ringan, berat bahkan
sampai kehilangan penglihatan
• Etiologi : 2 macam bahan yaitu yang
bersifat asam (pH < 7) dan yang
bersifat basa (pH > 7,6)
• Pemeriksaan Penunjang :
 Kertas Lakmus : cek pH berkala
 Slit lamp : cek bag. Anterior mata dan lokasi
luka
 Tonometri
 Funduskopi direk dan indirek
http://samoke2012.files.wordpress.com/2012/10/trauma-kimia-pada-mata.pdf
 Derajat 1: kornea jernih dan tidak
ada iskemik limbus (prognosis
sangat baik)
 Derajat 2: kornea berkabut
dengan gambaran iris yang masih
terlihat dan terdapat kurang dari
1/3 iskemik limbus (prognosis
baik)
 Derajat 3: epitel kornea hilang
total, stroma berkabut dengan
gambaran iris tidak jelas dan
sudah terdapat 1/2 iskemik
limbus (prognosis kurang)
 Derajat 4: kornea opak dan
sudah terdapat iskemik lebih dari
1/2 limbus (prognosis sangat
buruk)
 TRAUMA KIMIA MATA
TRAUMA BASA LEBIH BERBAHAYA DIBANDINGKAN ASAM; gejala: epifora, blefarosasme, nyeri

Trauma Asam : Trauma Basa :

• Bahan asam mengenai mata maka
akan segera terjadi koagulasi protein
epitel kornea yang mengakibatkan
kekeruhan pada kornea, sehingga bila
konsentrasi tidak tinggi maka tidak
akan bersifat destruktif
• Biasanya kerusakan hanya pada
bagian superfisial saja
• Bahan kimia bersifat asam : asam
sulfat, air accu, asam sulfit, asam
hidrklorida, zat pemutih, asam
asetat, asam nitrat, asam kromat,
asam hidroflorida
http://samoke2012.files.wordpress.com/2012/10/trauma-kimia-pada-mata.pdf
• Bahan kimia basa bersifat koagulasi sel
dan terjadi proses safonifikasi, disertai
dengan dehidrasi
• Basa akan menembus kornea, kamera
okuli anterior sampai retina dengan
cepat, sehingga berakhir dengan
kebutaan.
• Pada trauma basa akan terjadi
penghancuran jaringan kolagen kornea.
• Bahan kimia bersifat basa: NaOH, CaOH,
amoniak, Freon/bahan pendingin lemari
es, sabun, shampo, kapur gamping,
semen, tiner, lem, cairan pembersih
dalam rumah tangga, soda kuat.
 Fluorescein test
• Fluorescein staining helps identify a corneal epithelial
defect.
• Step by step :
– A drop of topical anesthetic (proparacaine 0.5%) is applied
directly into the eye or on a fluorescein strip.
– The patient’s lower lid is pulled down, and the fluorescein
strip is lightly touched to the bulbar conjunctiva.
– The dye spreads over the cornea as the patient blinks, and
stains any exposed basement membrane of the
epithelium.
– In normal light, an abrasion may stain yellow
– Illumination with cobalt blue light shows the defect as
green
– Cobalt blue filters are present in many ophthalmoscopes,
as well as in slit lamps and Wood lamps.
• Interpretation
– Traumatic corneal
abrasions typically have
linear or geographic
shapes.
– contact lenses  the
abrasion may have
several punctate lesions
that coalesce into a
round, central defect. In normal light
– A branching (dendritic)
appearance suggests
herpetic keratitis and
warrants immediate
referral
– Multiple vertical lines on
the superior cornea
suggest a foreign body
under the upper eyelid
Viewed with cobalt blue light
 TRAUMA KIMIA MATA - TATALAKSANA

Tatalaksana Emergensi : Tatalaksana Medikamentosa :

 Irigasi : utk meminimalkan  Steroid : mengurangi
durasi kontak mata dengan inflamasi dan infiltrasi
bahan kimia dan neutrofil
menormalkan pH mata; dgn  Siklopegik : mengistirahatkan
larutan normal saline (atau iris, mencegah iritis (atropine
setara) atau scopolamin) → dilatasi
 Double eversi kelopak mata : pupil
utk memindahkan material  Antibiotik : mencegah infeksi
 Debridemen : pada epitel oleh kuman oportunis
kornea yang nekrotik

http://samoke2012.files.wordpress.com/2012/10/trauma-kimia-pada-mata.pdf; Ilmu Penyakit Mata, Sidarta Ilyas

 TRAUMA KIMIA MATA -
TATALAKSANA

• Removing the offending agent

– Immediate copious irrigation
• With a sterile balanced buffered solution
normal saline solution or ringer's lactate
solution
• Until the ph (acidity) of the eye returns to
normal
– Pain relief → Topical anesthetic
• Promoting ocular surface(epithelial)healing
– artificial tears
– Ascorbate → collagen remodeling
– Placement of a therapeutic bandage contact
lens until the epithelium has regenerated
• Controlling inflammation
– Inflammatory inhibits reepithelialization
and increases the risk of corneal ulceration
and perforation
– Topical steroids
– Ascorbate (500 mg PO qid)
• Preventing infection
– Prophylactic topical antibiotics
• Controlling IOP
– In initial therapy and during the later
recovery phase, if IOP is high (>30 mm Hg)
• Control pain
– Cycloplegic agents → ciliary spasm
– Oral pain medication
 Chemical Eye injury treatment
• Immediate Action
– in any known or even suspected chemical injury of the eye, immediate treatment with
irrigation precedes patient evaluation
– The most readily available nontoxic liquid is used to flush the area of the face, eyes,
and any other areas of contact. Tap water is usually the most readily available, but
using iced tea, milk, or any neutral liquid is better than delaying treatment
– Medical treatment begins by irrigating with 2 L of normal saline or lactated Ringer’s
solution over 20 to 30 minutes.
– These injuries are painful and result in blepharospasm and squeezing of the eyelid 
need topical anastethic in severe pain
– After irrigation is completed, the pH of the eye is measured with pH paper or a urine
dipstick
– After sufficient irrigation, the eyes and ocular adnexa are inspected for particulate
matter
– Five minutes after the end of irrigation, the pH is again measured
• If the pH is nearly normal  irrigation is temporarily suspended, particulate
matter removed, and the examination portion begun.
• If the pH is not normal, irrigation is again performed with an additional 2 L of fluid
• Acute Phase Treatment
– Once the emergency treatment and evaluation are
completed  The major treatment goals that are
important throughout the healing phases are
• (a) the reestablishment and maintenance of an intact and
healthy corneal epithelium,
• (b) control of the balance between collagen synthesis and
collagenolysis, and
• (c) minimizing the adverse sequelae that often follow a
chemical injury.
– This triad of care for casualties with ocular chemical
injuries takes place in the acute (urgent) phase of
treatment
TO 3
20
6. CRVO
 Central Retinal Vein Occlusion (CRVO)

• Kelainan retina akibat sumbatan akut vena sentral yang

ditandai dengan pengelihatan yang hilang mendadak.

Faktor Risiko
• Usia > 50 th
• Hipertensi sistemik
• DM & kolesterol
• TIO >>
• Periphlebitis (Sarcoidosis, Behcet disease)
• Sumbatan trombus vena retina sentralis pada daerah
posterior lamina cribrosa
 CRVO: Klasifikasi
Tipe Noniskemik
Gejala lebih ringan
Vena dilatasi ringan dan
sedikit berkelok
Perdarahan dot dan flame
shaped
Dengan atau tanpa edema
papil
Tipe Iskemik
Gejala lebih ekstensif
Vena dilatasi lebih nyata
Perdarahan masif pada
keempat kuadran
Cotton wool spot
Perdarahan vitreous,
neovaskularisasi pada iris
(rubeosis iridis)
Edema retina dan makula
 Central Retinal Vein Occlusion (CRVO)

Pemeriksaan
• Fundus florescein angiography (FFA)
• Electroretinogram (ERG)
• Tonometri

Tatalaksana
• Memperbaiki underlying disease
• Fotokoagulasi laser
• Vitrektomi
Central Retinal Vein Occlusion (CRVO)
 6. Central Retinal Vein Occlusion (CRVO)

Pemeriksaan
• Fundus florescein angiography (FFA)
• Electroretinogram (ERG)
• Tonometri

Tatalaksana
• Memperbaiki underlying disease
• Fotokoagulasi laser
• Vitrektomi
 6. Central Retinal Vein Occlusion (CRVO)

Pemeriksaan
• Fundus florescein angiography (FFA)
• Electroretinogram (ERG)
• Tonometri

Tatalaksana
• Memperbaiki underlying disease
• Fotokoagulasi laser
• Vitrektomi
 21. Jaras Penglihatan
• N. Optikus  N. II
– Mulai dari optic disc dan
berlanjut hingga kiasma
optikum
– Terdiri atas 4 bagian
• Intraocular – 1 mm
• Intraorbital – 30 mm (di dekat
foramina optikum, dikelilingi
oleh Annulus of Zinn)
• Intracanalicular – 6‐9 mm
(terdapat arteri ophthalmic di
bagian inferolateralnya, sinus
ethmoid posterior dan spenoid
terletak di bagian medialnya)
• Intracranial – 10 mm (terletak di
atas sinus cavernous sinus and
menyatu dengan bagian
kontralateralnya membentuk
chiasma)
• Kiasma optikum
– Berbentuk pipih
berukuran 12mm
horizontally dan 8mm
anteroposterior
– Dibungkus oleh pia
mater dan dikelilingi
oleh CSF
– Variasi lokasi dari kiasma
• central chiasma
• prefixed chiasma
• post fixed chiasma
 Gangguan Lapang Pandang:
Hemianopia
• Hemianopia, also known as Hemianopsia is
loss of vision in either the right or left sides
of both eyes
 22. RETINOPATI HIPERTENSI
• Kelainan retina dan pembuluh darah retina akibat tekanan darah tinggi  arteri
besarnya tidak teratur, eksudat pada retina, edema retina, perdarahan retina
• Kelainan pembuluh darah dapat berupa : penyempitan umum/setempat, percabangan
yang tajam, fenomena crossing, sklerose
• Pada retina tampak :
 warna pembuluh darah lebih pucat
 kaliber pembuluh lebih kecil
 akibat sklerose (refleks copper wire/silver wire, lumen pembuluh irreguler, fenomena crossing)
 perdarahan atau eksudat retina (gambaran seperti bintang, cotton wool patches)
 perdarahan vena (flame shaped)

Ilmu Penyakit Mata, Sidarta Ilyas, 2005

 Retinopati Hipertensi
• Pemeriksaan rutin:
 Pemeriksaan tajam
penglihatan
 Pemeriksaan biomikroskopi
 Pemeriksaan fundus
• Pemeriksaan penunjang:
 Foto fundus
 Fundus Fluorescein
Angiography
• Tatalaksana :
 Kontrol tekanan darah dan
faktor sistemik lain (konsultasi
penyakit dalam)
 Bila keadaan lanjut terjadi
pendarahan vitreous dapat
dipertimbangkan Vitrektomi.

Panduan Praktik Klinik RSCM Kirana

• Dinding arteriol normalny tidak terlihat;
arteri terlihat sebagai “erythrocyte
column” / “pipa merah” dengan “central • Penebalan yg progresif akan
light reflex” pada funduskopi  terjadi menutup gambaran “pipa
penebalan dinding pada retinopati HT  merah” sepenuhnya
“central light reflex” lebih difus dan lebar menjadi silver wire
memberikan gambaran dinding arteriol yg
kekuningan/copper wire appearance. • Bersamaan dengan itu,
terjadi fenomena
arteriovenous crossing (AV
crossing)  vena yang
berjalan bersilangan di
bawah arteri yang
mengalami arterosklerosis
mengalami deformitas,
berbelok, bulging,
menyempit seperti jam
pasir, atau tampak seperti
terputus akibat penekanan
dari arteri.
Schema of ophthalmoscopic grading of arteriolar sclerosis. (Scheie HG:
Evaluation of ophthalmoscopic changes of hypertension and arteriolar
sclerosis. Arch Ophthalmol 49:117, 1953) http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v3/v3c013.html

http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v3/ch013/005f.html
 Retinopati Hipertensi

https://westjem.com/articles/grade-iii-or-grade-iv-hypertensive-retinopathy-with-
severely-elevated-blood-pressure.html
http://www.theeyepractice.com.au/optometrist-sydney/high_blook_pressure_and_eye_disease
Hypertensive Retinopathy
 Funduskopi: AMD dan Retinitis
Pigmentosa

Age related macular degeneration Retinitis Pigmentosa

(Drusen (+)) (deposit bercak kehitaman,
spikula (+))
ARMD
 Funduskopi Retinopati Diabetik

• Terdapat venous bleeding • Neovaskularisasi

• Dot blot haemorrhage
• Hard exudate
23. Gambar di Soal
 Perdarahan subkonjungtiva
• Perdarahan • Perdarahan
subkonjungtiva adalah subkonjungtiva akan
perdarahan akibat hilang atau diabsorpsi
rupturnya pembuluh dalam 1- 2 minggu tanpa
darah dibawah lapisan diobati.
konjungtiva yaitu • Pengobatan penyakit
pembuluh darah yang mendasari bila ada.
konjungtivalis atau
episklera.
• Dapat terjadi secara
spontan atau akibat
trauma.
 Subconjunctival hemorrhage
• Subconjunctival hemorrhage (or subconjunctival haemorrhage)
also known as hyposphagma, is bleeding underneath the
conjunctiva.
• Occur after sudden severe venous congestion to the head, such as
in a Valsalva maneuver, whooping cough, vomiting, sneezing,
weight lifting, crush injuries, or spontaneously
• A subconjunctival hemorrhage initially appears bright-red
underneath the transparent conjunctiva.
• Later, the hemorrhage may spread and become green or yellow, like
a bruise.
• In general a subconjunctival hemorrhage is a painless and harmless
condition
• however, it may be associated with high blood pressure, trauma to
the eye, or a base of skull fracture if there is no posterior border of
the hemorrhage visible.
 Subconjunctival hemorrhage
Causes
• Eye trauma
• Whooping cough or other
extreme sneezing or coughing
• Severe hypertension
• Postoperative subconjunctival
bleeding
• Acute hemorrhagic
conjunctivitis (picornavirus)
• Leptospirosis
• Increased venous pressure
(straining, vomiting, choking,
or coughing)
Management
• Self-limiting that requires
no treatment in the absence
of infection or significant
trauma.
• Artificial tears may be
applied four to six times a
day.
• Cold compress in the 1st
hour may stop the bleeding
 Penanganan Subconjunctival
Hemorrhage
• Artificial tears dapat meringankan rasa tidak enak
pada mata, tetapi tetap tidak memperbaiki
pembuluh darah yang pecah
• Jika pasien memakai obat seperti aspirin atau
antikoagulan lainnya, perlu dihentikan untuk
sementara
• Menghindari menggosok mata karena
meningkatkan resiko perdarahan ulang
• Perdarahan subconjunctiva dapat menghilang
dalam 7-10 hari, area yang terkena dapat
berubah warna menjadi kebiruan, seperti memar.
https://www.aao.org/eye-health/diseases/subconjunctival-hemorrhage-treatment
 24. Ablasio Retina
• Definition :
– Multilayer neurosensory retina separates from the underlying retinal pigment
epithelium and choroid.
• This separation can occur passively due to accumulation of fluid between these
two layers, or it may occur actively due to vitreous traction on the retina, such as
with diabetic traction retinal detachment.
• Separation between the neurosensory retina and the underlying choroidal
circulation results in ischemia and rapid and progressive photoreceptor
degeneration
 Pathophysiology
• Retinal detachments can be :
– Rhegmatogenous (caused by a break in the retina; “rhegma” is Greek
for tear)
– Nonrhegmatogenous (caused by leakage or exudation from beneath
the retina [exudative retinal detachment]
– Vitreous traction pulling on the retina [traction retinal detachment]).
• On occasion the retina appears to be detached but is actually not;
this is termed pseudo retinal detachment.

• A full-thickness retinal break may exist as a:

– round retinal hole,
– linear break, or
– horseshoe-shaped retinal tear.
• In all of these cases, there is a discontinuity in the retina that
allows vitreous fluid to pass through the retinal break into the
subretinal space, resulting in retinal detachment.
 Rhegmatogenous
• Rhegmatogenous retinal detachments are the most common type of
retinal detachment.
• Caused by a full-thickness retinal hole or retinal tear.
• Holes and tears can be asymptomatic or symptomatic;
– asymptomatic breaks in the retina are much more common than symptomatic
breaks but much less likely to lead to retinal detachment.
– Thus, most retinal holes or tears found in an asymptomatic patient do not
result in retinal detachment
– Whereas symptomatic retinal breaks often result in retinal detachment.
• Etiology Of Holes and Tears:
– Posterior vitreous detachment (PVD)
– Traumatic retinal detachment
• Risk factors :
– myopia,
– focal thinning of the periphery of the retinal called lattice degeneration, and
– a family history of retina tears or detachments
 Pathogenesis Myopia Tinggi menjadi
Retinal Detachment

Myopia yang tinggi menyebabkan kelengkungan bola mata yang ekstrim sehingga menyebabkan
Robekan di retina, robekan tersebut terisi oleh cairan vitreous yang terus menerus yang menggese
Lapisan retina dan membuat robekan semakin luas
Shroff Eye Centre. 2012
• Posterior Vitreous
Detachment
• the most common cause of retinal
holes and tears lead to
rhegmatogenous retinal
detachment
• The vitreous slowly liquefies
throughout life  break through
the posterior vitreous face 
cause PVD from the retina.
• Typically occurs in patients
between the ages of 50 and 75
years.
• However, it can occur earlier in
patients who are myopic, have had
a history of ocular trauma, or have
had ocular inflammation, all of
which lead to a more rapid vitreous
liquefaction.
• Traumatic Retinal Detachment
• Patients who sustain an ocular injury also can develop a
full-thickness retinal break or retinal dialysis.
• These may lead to subretinal migration of liquid vitreous
and the development of a retinal detachment
• This is much less common than spontaneous
rhegmatogenous detachment
 Nonrhegmatogenous retinal detachment

Traction retinal detachment

• the vitreous has an abnormally strong attachment to the
retina and contracts, thus pulling the retina off the back of
the eye.
• Typically seen in patients with :
– Proliferative diabetic retinopathy,
– vitreomacular traction syndrome,
– retinopathy of prematurity, or
– sickle cell retinopathy
– retinal neovascularization  The areas of neovascularization
and fibrosis between the retina and the vitreous create a strong
adhesion between these two tissues  . With vitreous
contraction, the retina is pulled away from the back of the eye
and a traction retinal detachment is created
Exudative retinal detachment
• Occurs in patients who do not have a full-
thickness retinal break but rather have an
accumulation of fluid beneath the retina.
• Often associated with :
– inflammatory conditions
– may occur spontaneously as with central serous
chorioretinopathy,
– In association with choroidal neoplasms/metastases
 Ablasio Retina
• Anamnesis: • Funduskopi : adanya
– Riwayat trauma robekan retina, retina yang
– Riwayat operasi mata terangkat berwarna keabu-
– Riwayat kondisi mata abuan, biasanya ada fibrosis
sebelumnya (cth: uveitis, vitreous atau fibrosis
perdarahan vitreus, miopia preretinal bila ada traksi.
berat) Bila tidak ditemukan
– Durasi gejala visual & robekan kemungkinan suatu
penurunan penglihatan
ablasio nonregmatogen
• Gejala & Tanda:
– Fotopsia (kilatan cahaya) 
gejala awal yang sering
– Defek lapang pandang 
bertambah seiring waktu
– Floaters
 Tatalaksana
• Ablasio retina 
kegawatdaruratan mata
• Tatalaksana awal:
– Puasakan pasien u/ persiapan
operasi
– Hindari tekanan pada bola
mata
– Batasi aktivitas pasien sampai
diperiksa spesialis mata
– Segera konsultasi spesialis
retina  konservatif (untuk
nonregmatogen), pneumatic
retinopexy, bakel sklera,
vitrektomi tertutup

Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17 th ed. Philadephia: McGraw-Hill, 2007.
 25. UVEITIS
•Uveitis :
–inflamasi di uvea
yaitu iris, badan siliar
dan koroid yang
dapat menimbulkan
kebutaan.
–Di negara maju,
10% kebutaan pada
populasi usia
produktif adalah
akibat uveitis
 Klasifikasi
• The International Uveitis Study Group (IUSG) dan The
Standardization of Uveitis Nomenclatur (SUN) membagi uveitis
berdasarkan anatomi, etiologi, dan perjalanan penyakit
• Anatomi :
– uveitis anterior, uveitis intermediet, uveitis posterior, dan panuveitis
• Etiologi:
– infeksi (bakteri, virus, jamur, dan parasit), non-infeksi, dan idiopatik.
• Perjalanan penyakit
– Akut (onset mendadak dan durasi kurang dari empat minggu),
– Rekuren (episode uveitis berulang),
– Kronik (uveitis persisten atau kambuh sebelum tiga bulan setelah
pengobatan dihentikan), dan
– Remisi (tidak ada gejala uveitis selama tiga bulan atau lebih)

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis anterior
• Inflamasi di iris (iritis) dan badan siliar (siklitis).
Bila inflamasi meliputi iris dan badan siliar maka
disebut iridosiklitis
• Etiologi :
– kelainan sistemik seperti spondiloartropati, artritis
idiopatik juvenil, sindrom uveitis fuchs, kolitis ulseratif,
penyakit chron, penyakit whipple, tubulointerstitial
nephritis and uveitis
– Infeksi yang sering menyebabkan uveitis anterior
adalah virus herpes simpleks (VHS), virus varisela
zoster (VVZ), tuberkulosis, dan sifilis.

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Diagnosis Uveitis Anterior
• Gejala Klinis : • Tanda
– mata merah – injeksi siliar akibat
– visus turun akibat kekeruhan vasodilatasi arteri siliaris
cairan akuos dan edema posterior longus dan arteri
kornea walaupun uveitis tidak siliaris anterior yang
selalu menyebabkan edema memperdarahi iris serta
kornea badan siliar.
– Nyeri tumpul berdenyut, dan – Bilik mata depan : pelepasan
fotofobia akibat spasme otot sel radang, pengeluaran
siliar dan sfingter pupil protein (cells and flare) dan
– Jika disertai nyeri hebat, endapan sel radang di endotel
perlu dicurigai peningkatan kornea (presipitat keratik).
tekanan bola mata. – Presipitat keratik halus 
– Spasme sfingter pupil inflamasi nongranulomatosa;
mengakibatkan miosis dan – Presipitat keratik kasar 
memicu sinekia posterior. inflamasi granulomatosa

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis Intermediet
• Peradangan di pars plana yang sering diikuti vitritis dan uveitis posterior.
• Penyakit tersebut biasanya terjadi pada usia dekade ketiga-keempat dan
20% terjadi pada anak.
• Etiologi:
– Idiopatik (69,1%), sarkoidosis (22,2%), multiple sclerosis (7,4%), dan lyme
disease (0,6%). Selain itu, dapat juga disebabkan oleh infeksi Mycobacterium
tuberculosis, Toxoplasma, Candida, dan sifilis.
• Gejala :
– Gejala biasanya ringan yaitu penurunan tajam penglihatan tanpa disertai nyeri
dan mata merah, namun jika terjadi edema makula dan agregasi sel di vitreus
penurunan tajam penglihatan dapat lebih buruk.
– Pars planitis berupa bercak putih akibat agregasi sel inflamasi dan jaringan
fibrovaskular (snowbank) yang menunjukkan inflamasi berat dan memerlukan
terapi agresif.
– Komplikasinya adalah edema makula (12-51%), glaukoma (20%), dan katarak
(15-50%)

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis Posterior
• Peradangan lapisan koroid yang sering melibatkan jaringan sekitar seperti
vitreus, retina, dan nervus optik.
• Etiologi:
– Infeksi paling sering disebabkan oleh T.gondii, M.tuberculosis, sifilis, VHS, VVZ,
cytomegalovirus (CMV), dan HIV.
– Non-infeksi, uveitis posterior disebabkan oleh koroiditis multifokal, birdshot
choroidopathy, sarkoidosis, dan neoplasma
• Gejala klinis :
– Penglihatan kabur yang tidak disertai nyeri, mata merah, dan fotofobia.
– Komplikasi dapat berupa katarak, glaukoma, kekeruhan vitreus, edema
makula, kelainan pembuluh darah retina, parut retina, ablasio retinae, dan
atrofi nervus optik.
– Prognosis uveitis posterior lebih buruk dibandingkan uveitis anterior karena
menurunkan tajam penglihatan dan kebutaan apabila tidak ditatalaksana
dengan baik.

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Bercak Yellow Placoid pada Uveitis
Posterior

https://www.semanticscholar.org/paper/Focal-chorioretinitis-in-Thailand.-Pathanapitoon-Kunavisarut/1ffcb5442a82835d913a416d82bb785088654328/figure/1
 Panuveitis
• Peradangan seluruh uvea dan struktur
sekitarnya seperti retina dan vitreus.
• Etiologi:
– Penyebab tersering adalah tuberkulosis, sindrom
VKH, oftalmia simpatika, penyakit behcet, dan
sarkoidosis.
– Diagnosis panuveitis ditegakkan bila terdapat
koroiditis, vitritis, dan uveitis anterior

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 No. Jenis Keterangan
Pemeriksaan
Penunjang pada
Uveitis
1 Slit lamp menilai segmen anterior injeksi siliar dan episklera, skleritis,
edema kornea, presipitat keratik, bentuk dan jumlah sel di bilik
mata, hipopion serta kekeruhan lensa
2 Oftalmoskop menilai kelainan di segmen posterior seperti vitritis, retinitis, perdarahan
retina, koroiditis dan kelainan papil nervus optik

3 Pemeriksaan
laboratorium
4 Optical coherence
tomography (OCT)
5 USG B –scan
bermanfaat pada kelainan sistemik misalnya darah perifer lengkap, laju
endap darah, serologi, urinalisis, dan antinuclear antibody
merupakan pemeriksaan non-invasif yang dapat memperlihatkan edema
makula, membran epiretina, dan sindrom traksi vitreomakula
sangat membantu memeriksa segmen posterior mata pada keadaan
media keruh misalnya pada katarak dan vitritis

6 Fundus fluoresen
angiografi (FFA)
fotografi fundus yang dilakukan berurutan dengan cepat setelah injeksi
zat warna natrium fluoresen (FNa) intravena.
FFA memberikan informasi mengenai sirkulasi pembuluh darah retina dan
koroid, detail epitel pigmen retina dan sirkulasi retina serta menilai
integritas pembuluh darah saat fluoresen bersirkulasi di koroid dan retina.
 Penatalaksanaan Uveitis
• Prinsip penatalaksanaan uveitis
1. Menekan reaksi inflamasi
• Kortikosteroid topikal merupakan terapi pilihan untuk
mengurangi inflamasi : 1).prednisolon 0,5%,; 2).
prednisolon asetat 1%; 3). betametason 1% ; 4).
deksametason 0,1%, dan 5). fluorometolon 0,1%.
• Injeksi kortikosteroid periokular diberikan pada kasus yang membutuhkan
depo steroid dan menghindari efek samping kortikosteroid jangka panjang.
• Kortikosteroid sistemik diberikan untuk mengatasi uveitis berat atau uveitis
bilateral
• Imunosupresan dapat dipertimbangkan sebagai terapi lini pertama pada
penyakit behcet, granulomatosis wegener, dan skleritis nekrotik karena
penyakit tersebut dapat mengancam jiwa. Imunosupresan dibagi menjadi
golongan antimetabolit, supresor sel T, dan sitotoksik.
2. Mencegah dan memperbaiki kerusakan struktur,

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 3. Memperbaiki fungsi penglihatan
• Terapi bedah diindikasikan untuk memperbaiki penglihatan.
• Operasi dilakukan pada kasus uveitis yang telah tenang
(teratasi) tetapi mengalami perubahan permanen akibat
komplikasi seperti katarak, glaukoma sekunder, dan ablasio
retina.
• Kortikosteroid diberikan 1-2 hari sebelum operasi dan steroid
intraokular atau periokular dapat diberikan pasca-operasi
• Vitrektomi ditujukan untuk memperbaiki tajam penglihatan
bila kekeruhan menetap setelah pengobatan.
4. Menghilangkan nyeri dan fotofobia.
• NSAID digunakan untuk mengurangi nyeri dan inflamasi sedangkan
siklopegik diberikan untuk mencegah sinekia posterior.
• Obat yang diberikan adalah siklopentolat 0,5-2% dan homatropin

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Gambaran Sifilis Pada Mata Luar
• Pada bagian
terluar mata,
syphilis dapat
menyebabkan:
– konjungtivitis,
– skleritis dan
– episkleritis,
atau
– keratitis
interstitial.
Primary and secondary syphilis--United States, 2003-2004. MMWR Morb Mortal Wkly Rep 2006;55:269-73.
 Gambaran Sifilis Pada Bilik
Mata Dalam
• Uveitis, unilateral atau bilateral
– manifestasi sifilis yang paling umum
• Gambaran granulomatosa seperti
keratik presipitat yang besar dan
nodul iris dapat muncul.
• Pelebaran pembuluh darah iris(iris
roseolae)
– jarang terlihat tapi sangat spesifik
untuk sifilis.
• Sifilis juga dapat meningkatkan
tekanan intraocular
– disebut juga Inflammatory Ocular
Hypertension Syndrome.
Reddy S, Cubillan LD, Hovakimyan A, Cunningham ET Jr. Inflammatory ocular hypertension syndrome
(IOHS) in Patients with Syphilitic Uveitis. Br J Ophthalmol 2007; 91: 1610-2. Epub 2007 May 23.
 Gambaran Sifilis pada segmen
posterior mata
• Sifilis dapat menyebabkan chorioretinitis,
retinitis, vasculitis, vitritis and panuveitis
• Chorioretinitis manifestasi paling umum.
– “Ground glass" retinitis
• merupakan retinal vasculitis
• salah satu karakteristik sifilis
• Acute syphilitic posterior placoid
chorioretinopathy (ASPPC)
– terjadi akibat infeksi sifilis pada epitel pigmen retina
pada macula atau regio peripapillary
– Seperti namanya, gambarannya berupa plak-plak
kekuningan.
Tran TH, Cassoux N, Bodaghi B. Syphilitic uveitis in patients infected with human immunodeficiency virus. Graefe's Arch Clin Exp
Ophthalmol 2005;243:863-9.
 Gambaran Sifilis Pada
Segmen Posterior Mata
 26. Konjungtivitis Alergi
• Allergic conjunctivitis may be divided into 5
major subcategories.
• Seasonal allergic conjunctivitis (SAC) and
perennial allergic conjunctivitis (PAC) are
commonly grouped together.
• Vernal keratoconjunctivitis (VKC), atopic
keratoconjunctivitis (AKC), and giant papillary
conjunctivitis (GPC) constitute the remaining
subtypes of allergic conjunctivitis.
 Konjungtivitis Atopi
• Biasanya ada riwayat atopi • Terapi topikal jangka
• Gejala + Tanda: sensasi panjang: cell mast stabilizer
terbakar, sekret mukoid • Antihistamin oral
mata merah, fotofobia • Steroid topikal jangka
• Terdapat papila-papila halus pendek dapat meredakan
yang terutama ada di tarsus gejala
inferior
• Jarang ditemukan papila
raksasa
• Karena eksaserbasi datang
berulanga kali 
neovaskularisasi kornea,
sikatriks
 Konjungtivitis Atopik

Papila halus pada konjungtiva

tarsal superior dan inferior

Keratokonjungtivitis atopik disertai

vaskularisasi  tindakan:
transplantasi kornea
 Etiologi Diagnosis Karakteristik
Viral Konjungtivitis folikuler Merah, berair mata, sekret minimal, folikel sangat
akut mencolok di kedua konjungtiva tarsal
Klamidia Trachoma Seringnya pd anak, folikel dan papil pd konjungtiva
tarsal superior disertai parut, perluasan pembuluh
darah ke limbus atas
Konjungtivitis inklusi Mata merah, sekret mukopurulen (pagi hari), papil
dan folikel pada kedua konjungtiva tarsal (terutama
inferior)
Alergi/hiper- Konjungtivitis vernalis Sangat gatal, sekret berserat-serat, cobblestone pd
sensitivitas konjungtiva tarsal superior, horner-trantas dots
(limbus)
Konjungtivitis atopik Sensasi terbakar, sekret berlendir, konjungtiva
putih spt susu, papil halus pada konjungtiva tarsal
inferior
Konjungtivitis Reaksi hipersensitif tersering akibat protein TB,
fliktenularis nodul keabuan di limbus atau konjungtiva bulbi,
mata merah dan berair mata
Autoimun Keratokonjungtivitis sicca Akibat kurangnya film air mata, tes shcirmer
abnormal, konjungtiva bulbi hiperemia, sekret
mukoid, semakin sakit menjelang malam dan
berkurang pagi
 Tatalaksana Konjungtivitis Alergi
• Self-limiting • Jangka panjang & prevensi
• Akut: sekunder:
• Antihistamin topikal
• Steroid topikal (+sistemik • Stabilisator sel mast Sodium
kromolin 4%: sebagai
bila perlu), jangka pengganti steroid bila gejala
pendek  mengurangi sudah dapat dikontrol
gatal (waspada efek • Tidur di ruangan yang sejuk
dengan AC
samping: glaukoma, • Siklosporin 2% topikal (kasus
katarak, dll.) berat & tidak responsif)

• Vasokonstriktor topikal • Desensitisasi thdp antigen

(belum menunjukkan hasil
• Kompres dingin & ice baik)
pack

Vaughan & Asbury General Ophtalmology 17th ed.

 KONJUNGTIVITIS VERNAL
• Nama lain:
– spring catarrh/seasonal conjunctivitis/warm weather conjunctivitis
– Disebut vernal karena exaserbasi paling sering pada musim semi
(spring)
• Etiologi: reaksi hipersensitivitas bilateral (alergen sulit diidentifikasi)
• Epidemiologi:
– Dimulai pada masa prepubertal, bertahan selama 5-10 tahun sejak
awitan
– Laki-laki > perempuan
– Paling sering pada Afrika Sub-Sahara & Timur Tengah
– Temperate climate > warm climate > cold climate (hampir tidak ada)
– Terkait dengan manifestasi atopi lainnya seperti asma dan rinitis alergi
pada setengah kasus

Vaughan & Asbury General Ophtalmology 17th ed.

 Pathogenesis of Vernal Conjunctivitis
• Classic IgE mediated Hypersensitivity
– Evidence supporting an atopic origin :
• Seasonal incidence, eosinofil and mast cells in conjunctiva,
Play a
igE serum and tears, response to major role
mast cells stabilazer
• Th2 cells mediated respone
• Ig G mediated response
• Basofilic hypersensitivity
• Cellular delayed type hypersensitivity
(Hypersensitivity Type IV)
• Gejala & tanda:
– Rasa gatal yang hebat, dapat
disertai fotofobia
– Sekret ropy
– Riwayat alergi pada RPD/RPK
– Tampilan seperti susu pada
konjungtiva
– Gambaran cobblestone
(papila raksasa berpermukaan
rata pada konjungtiva tarsal)
– Tanda Maxwell-Lyons (sekret
menyerupai benang &
pseudomembran fibrinosa
halus pada tarsal atas, pada • Komplikasi:
pajanan thdp panas) • Blefaritis & konjungtivitis
– Bercak Trantas (bercak stafilokokus
keputihan pada limbus saat
fase aktif penyakit)
– Dapat terjadi ulkus kornea
superfisial
Vaughan & Asbury General Ophtalmology 17th ed.
 Tatalaksana
• Self-limiting
• Akut:
• Steroid topikal (+sistemik
bila perlu), jangka pendek
 mengurangi gatal
(waspada efek samping:
glaukoma, katarak, dll.)
• Vasokonstriktor topikal
• Kompres dingin & ice
pack
• Jangka panjang & prevensi
sekunder:
• Antihistamin topikal
• Stabilisator sel mast Sodium
kromolin 4%: sebagai
pengganti steroid bila gejala
sudah dapat dikontrol
• Tidur di ruangan yang sejuk
dengan AC
• Siklosporin 2% topikal (kasus
berat & tidak responsif)
• Desensitisasi thdp antigen
(belum menunjukkan hasil
baik)
Vaughan & Asbury General Ophtalmology 17th ed.
 Table. Major Differentiating Factors Between VKC and AKC

Characteristics VKC AKC

Age at onset Generally presents at a younger age -
than AKC
Sex Males are affected preferentially. No sex predilection
Seasonal variation Typically occurs during spring months Generally perennial
Discharge Thick mucoid discharge Watery and clear discharge
Conjunctival - Higher incidence of
scarring conjunctival scarring
Horner-Trantas Horner-Trantas dots and shield ulcers Presence of Horner-Trantas
dots are commonly seen. dots is rare.
Corneal Not present Deep corneal
neovascularization neovascularization tends to
develop
Presence of Conjunctival scraping reveals Presence of eosinophils is
eosinophils in eosinophils to a greater degree in less likely
conjunctival VKC than in AKC
scraping
 27. ASTIGMATISME - DEFINISI
• Ketika cahaya yang
masuk ke dalam
mata secara paralel
tiudak membentuk
satu titik fokus di
retina.

http://www.mastereyeassociates.com/Portals/60407/images//astig
Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry matism-Cross_Section_of_Astigmatic_Eye.jpg
 ASTIGMATISME
• Kornea seharusnya berbentuk hampir sferis
sempurna (bulat)  pada astigmat kornea
berbentuk seperti bola rugby.
• Bagian lengkung yang paling landai dan yang
paling curam mengakibatkan cahaya
direfraksikan secara berbeda dari kedua
meridian  mengakibatkan distorsi bayangan
• Kekuatan refraksi pada horizontal plane
memproyeksikan gambar/ garis vertikal.
• Kekuatan refraksi pada vertical plane
memproyeksikan gambar/ garis horizontal.
• The amount of astigmatism is equal to the
difference in refracting power of the two
principal meridians

http://www.improveeyesighthq.com/Corrective-Lens-Astigmatism.html
 KLASIFIKASI :
ETIOLOGI
• Astigmatisme korneal: When
the cornea has unequal curvature
on the anterior surface – 90% PLACIDO
penyebab astigmatisme  bisa
dites dgn tes Placido
(keratoscope)
• Astigmatisme lentikular: When
the crystalline lens has an
unequal on the surface or in its
layers
• Astigmatigma total: The sum of
corneal astigmatism and Astigmatisme korneal akibat trauma
lenticular astigmatism pada kornea. Perhatikan iregularitas
bayangan placido
Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry http://oelzant.priv.at/~aoe/images/galleries/narcism/med/hornhautabrasion/
 KLASIFIKASI : HUBUNGAN ANTAR BIDANG MERIDIAN

ASTIGMATISME REGULER

• Kedua bidang meridian

utamanya saling tegak lurus. • Kebanyakan kasus
(meredian di mana terdapat astigmatisme adalah
daya bias terkuat dan terlemah astigmatisme reguler
di sistem optis bolamata).
• Cth: • 3 tipe:
– jika daya bias terkuat berada – are with-the-rule
pada meredian 90°, maka daya – against-the-rule
bias terlemahnya berada pada
meredian 180° – oblique astigmatism
– Jika daya bias terkuat berada
pada meredian 45°, maka daya
bias terlemah berada pada
meredian 135°.
Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry
KLASIFIKASI : HUBUNGAN ANTAR BIDANG MERIDIAN

ASTIGMATISME IREGULER

• When the two principal

meridians are not
perpendicular to each
other
• Curvature of any one
meridian is not uniform
• Associated with trauma,
disease, or degeneration
• VA is often not correctable
to 20/20

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

 BASED ON FOCAL POINTS
RELATIVE TO THE RETINA
• SIMPLE ASTIGMATISM
– When one of the principal meridians is focused on the retina and
the other is not focused on the retina (with accommodation
relaxed)
– Terdiri dari
• astigmatisme miopikus simpleks
• astigmatisme hipermetrop simpleks
• COMPOUND ASTIGMATISM
– When both principal meridians are focused either in front or
behind the retina (with accommodation relaxed)
– Terdiri dari
• astigmatisme miopikus kompositus
• astigmatisme hipermetrop kompositus
• MIXED ASTIGMATISM
– When one of the principal meridians is focused in front of the
retina and the other is focused behind the retina (with
accommodation relaxed)
 BASED ON FOCAL POINTS RELATIVE TO
THE RETINA
1. Simple Myopic Astigmatism
• When one of the principal
meridians is focused in
front of the retina and the
other is focused on the
retina (with accommodation
relaxed)
• Astigmatisme jenis ini, titik A
berada di depan retina,
sedangkan titik B berada tepat
pada retina.

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

 BASED ON FOCAL POINTS RELATIVE TO
THE RETINA
2. Simple Hyperopic Astigmatism
• When one of the principal
meridians is focused behind
the retina and the other is
focused on the retina (with
accommodation relaxed)
• Astigmatisme jenis ini, titik A
berada tepat pada retina,
sedangkan titik B berada di
belakang retina.

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

 BASED ON FOCAL POINTS RELATIVE TO
THE RETINA
3. Compound Myopic Astigmatism
• When both principal
meridians are focused in
front of the retina (with
accommodation relaxed)

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

 BASED ON FOCAL POINTS RELATIVE TO
THE RETINA
4. Compound Hyperopic Astigmatism

• When both
principal
meridians are
focused behind
the retina (with
accommodation
relaxed)
Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry
 BASED ON FOCAL POINTS RELATIVE TO
THE RETINA
5. MIXED ASTIGMATISM

• When one of the

principal meridians is
focused in front of the
retina and the other is
focused behind the
retina (with
accommodation relaxed)

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

http://www.improveeyesighthq.com/Corrective-Lens-Astigmatism.html
 BASED ON RELATIVE LOCATIONS OF PRINCIPAL MERIDIANS OR AXES WHEN
COMPARING THE TWO EYES

SYMMETRICAL ASTIGMATISM

• The principal meridians • Example

or axes of the two eyes – OD: pl -1.00 x 175
are symmetrical (e.g., – OS: pl -1.00 x 005
both eyes are WTR or • Both eyes are WTR
ATR) astigmatism, and the sum of
the two axes equal
• Ciri yang mudah dikenali approximately 180
adalah axis cylindris mata
kanan dan kiri yang bila
dijumlahkan akan bernilai
180° (toleransi sampai 10-
15°).

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

 BASED ON RELATIVE LOCATIONS OF PRINCIPAL MERIDIANS OR AXES WHEN
COMPARING THE TWO EYES

ASYMMETRICAL ASTIGMATISM

• The principal meridians • Example:

or axes of the two eyes – OD: pl -1.00 x 180
are not symmetrical – OS: pl -1.00 x 090
(e.g., one eye is WTR – One eye is WTR
while the other eye is astigmatism, and the
ATR) other eye is ATR
astigmatism, and the
• The sum of the two sum of the two axes do
axes of the two eyes not equal approximately
does not equal 180
approximately 180

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry

Toric/Spherocylinder lens pada koreksi
Astigmatisme

They have a different focal power in different meridians.

http://www.oculist.net/downaton502/prof/ebook/duanes/graphics/figures/v1/051a/010f.gif
http://vision.zeiss.com/content/dam/Vision/Vision/International/images/image-text/opticaldesigns_asphere_atorus_atoroidal-surface_500x375.jpg
 TIPS & TRIK
• Rumus hapalan ini bisa digunakan untuk menentukan jenis jenis
astigmatisme berdasarkan kedudukannya di retina kalau disoal
diberikan rumus astigmatnya sbb
1. sferis (-) silinder (-)  pasti miop kompositus
2. Sferis (+); silinder (+)  pasti hipermetrop kompositus
3. Sferis (tidak ada); silinder (-) pasti miop simpleks
4. Sferis (tidak ada); silinder (+)  pasti hipermetrop simpleks

• Agak sulit dijawab jika di soal diberikan rumus astigmat sbb:

1. Sferis (-) silinder (+)
2. Sferis (+) silinder (-)
 BELUM TENTU astigmatisme mikstus!!
Harus melalui beberapa tahap penjelasan untuk menemui
jawabannya
 cara menentukan jenis astigmatisme berdasarkan kedudukannya di
retina kalau disoal diberi rumus S(-) Cyl(+) atau S(+) Cyl(-)

• PERTAMA, rumus kacamata astigmat adalah

SFERIS ± X SILINDER ±Y x AKSIS Z

• Sferis tidak harus selalu ada, kadang jika tidak ada,
nilai sferis akan dihilangkan penulisannya menjadi
C (silinder) ± .… x …..°
atau menjadi
pl (plano) C (silinder) ± …. x …..°
 KEDUA, TRANSPOSISI
• Transposisi itu artinya: notasi silinder bisa ditulis dalam nilai minus atau
plus
• Rumus ini bisa ditransposisikan (dibolak-balik) tetapi maknanya sama.
Cara transposisi:
• To convert plus cyl to minus cyl:
– Add the cylinder power to the sphere power
– Change the sign of the cyl from + to –
– Add 90 degrees to the axis is less than 90 or subtract 90 if the original axis is
greater than 90.
• To convert minus cyl to plus cyl:
– add the cylinder power to the sphere
– Change the sign of the cylinder to from - to +
– Add 90 to the axis if less than 90 or subtract if greater than 90

• Misalkan pada soal OD ∫-4,00 C-1,00 X 1800minus cylinder notation yang

jika ditransposisi maknanya sama dengan ∫-5,00 C+1,00 X 900 (plus cylinder
notation)
 KETIGA, CARA MEMBACA
• OD ∫-4,00 C-1,00 X 1800 artinya adalah kekuatan
lensa pada aksis 180 adalah -4.00 D. Kemudian
kita transposisikan menjadi ∫-5,00 C+1,00 X 900
artinya kekuatan lensa pada 90 adalah -5,00 D

• OS ∫-5,00 C-1,00 X 900 artinya adalah kekuatan

lensa pada aksis 90 adalah -5.00 D dan
Kemudian kita transposisikan menjadi ∫-6,00
C+1,00 X 1800 artinya kekuatan lensa pada 180
adalah -6,00 D
 KEEMPAT, MENENTUKAN JENIS ASTIGMATISME BERDASARKAN
KEDUDUKANNYA DI RETINA

• Prinsipnya: selalu lihat besarnya sferis di kedua rumus baik

rumus silinder plus maupun silinder minus (makanya
kenapa harus tahu transposisi)
• Contoh: OD rumusnya ∫-4,00 C+1,00 X 1800  sferis= -4D
(MIOP di aksis 180) dan rumus satu lagi ∫-3,00 C-1,00 X 90
 sferis= -3D (MIOP di aksis 90) untuk mata kanan.
• Bayangan di kedua aksis jatuh di depan retina maka jenis
astigmatnya miopik kompositus, bukannya astigmat mikstus
 Analisa Soal
• Mata kanan pasien OD S-2.50 C-1.50 180o
artinya astigmatus miop kompositus
• Transposisi pada mata kiri OS S-2.00 C +0.50
120o menjadi S-1.50 C-0.5 300.
• Dengan demikian, astigmatus yang dialami
pasien adala astigmatus miop kompositus
ODS.
 28. Keratitis Exposure
• Berkurangnya lubrikasi permukaan mata karena
penutupan kelopak mata yang inadekuat 
keratitis exposure
• Gejala dan tanda:
– Nyeri, rasa mengganjal seperti benda asing, fotofobia,
epifora, visus turun
– Kedipan mata berkurang, lagoftalmos, ↓ meniskus air
mata, pembentukan filamen kornea, erosi epitelial
pungtata,
– Kasus yang berat  edema kornea, penipisan ataupun
ulkus pada kornea
• Diagnosis :
– Diagnosis ditegakkan
berdasarkan riwayat dan
pemeriksaan fisik
• Palpebra : entropion,
ektropion, Bell`s palsy,
traksi congenital
coloboma, trauma
palpebra
• Proptosis :
• Herpetic keratopathy atau
kelainan nervus V
• Penatalaksanaan :
– Lubrikasi :
• Salep antibiotik
(eritromisin) ; gel artificial
tears
– Steroid
• Weak topical steroid
– Amniotic membrane
– Tarssoraphy
 Eyelid trauma
• Eyelid is specialized tissue • Eyelid margin has slightly
characterized by skin on rounded anterior edge and
anterior surface and mucous sharp posterior edge.
membrane – tarsal conjunctiva – Mucocutaneous junction
on its posterior. – Meibomian gland orifices
• Eyelid skin is thinnest in the – Gray line
body. – Eyelash follicles
• It has loose attachment and
absence of fat in corium.
• Lid contains muscle, glands,
blood vessels and nerves.
• The firmness to the lid is
provided with tarsus which is
dense fibrous tissue and not a
cartilage

Vichare N. Management of Eyelid Lacerations. DOS Times - Vol. 20, No. 8 February, 2015
 Repair of eyelid trauma
• Repairing of eyelid injuries
requires knowledge and
meticulous approach.
• Gentle tissue handling and proper
alignment should be done.
• Aim should be to achieve best
possible functional and cosmetic
outcome
• Timing of repair
– Every effort must be made to
reconstruct the injured
tissues as soon as possible.
– Primary repair can be done
even after 24 -48 hrs after the
patient is stabilized.
• Preoperative evaluation
– Detailed history is obtained to determine
time, course and circumstances of injury.
– Management of ocular injury starts after
traumatized patient is stabilized and life
threatening injuries are addressed
– Detailed ocular examination includes visual
acuity, ocular movements, intra ocular
pressure, pupillary reactions and posterior
segment examination.
– Eyelid trauma can be associated with
hyphema, angle recession or retinal
detachment.
– Globe injuries should be attended before lid
injuries.
– Systemic antibiotics should be started. 
Intravenous antibiotics are preferable for
severely contaminated wounds.
– Wounds are irrigated thoroughly to remove
all debris.
– Tetanus toxoid must be given to non-
immunized patients.
29. Classification of Scleral
inflammation

Lalit Varma. Scleral Inflammations: An update. 2013

 Scleritis
• Sclera is a relatively avascular structure except for
some vessels that pass through the emissary
canals.
• The low vascularity of sclera can be explained by
the low metabolic demand of the tissue because
of the slow turnover rate of its collagen and cells.
• Scleritis occurs more commonly anterior to the
equator because of the more abundant anterior
vascular supply.
• The circulation overlying the sclera can be divided
into three vascular layers
Lalit Varma. Scleral Inflammations: An update. 2013
Lalit Varma. Scleral Inflammations: An update. 2013
 Scleritis
• Scleritis is a severe infl ammation of the scleral
tissue.
• Characterized by edema and cellular infiltration
of the sclera and episclera.
• Scleritis affects women more often than men,
with a peak incidence in the fifth decade.
• It frequently starts in one eye and becomes
bilateral in more than half of the cases.
• Bilaterality is more commonly encountered in
scleritis associated with systemic rheumatic
disorders. Lalit Varma. Scleral Inflammations: An update. 2013
 Etiology
1. Idiopathic:
– These autoimmune reactions are usually idiopathic and mostly mediated by type IV delayed
type of hypersensitivity reaction.
2. Systemic rheumatic diseases or collagen vascular disorders:
– Half of patients with scleritis have evidence of an underlying systemic disease.
– Rheumatoid arthritis is the most common systemic condition associated with scleritis.
– Scleral inflammations in such systemic rheumatic disorders are mostly due to vascular
involvement which results from deposition of circulating immune complexes in superfi cial
and deeper episcleral vessels.
3. Infectious:
– Endogenous spread of microorganisms can give rise to scleral infections.
– Neurotropic viruses like Herpes viruses can invade the scleral nerves and causes scleral infl
ammation.
4. Surgery induced scleritis (SINS)
– rare but serious complication of ocular surgery
– SINS typically occurs after surgery as intense scleral infl ammation associated with necrosis
near the site of scleral incision.
 Scleritis: Diagnosis
• Symptoms
– Redness and pain  The onset is usually gradual,
• Signs
extending over several
– sine qua non of scleritis
– Ocular pain is severe and typically dull and boring
(piercing) in nature, exacerbated by eye is the presence of scleral
movement, and occasionally may worsen at night
and waken the patient from sleep.
edema and congestion
– The pain often radiates to the ear, scalp, face, of the deep episcleral
temple and jaw.
plexus
– The extraocular muscles insert into the sclera, thus
ocular movements exacerbate the pain associated
with scleral inflammation.
– Additionally, patients may report headache;
watering of the eye; ocular redness, particularly in
patients with non-necrotizing anterior scleritis; and
photophobia, which is variably present.
– When there is tissue necrosis in severe disease,
there is loss of peripheral innervation which leads
to "paradoxic" lessening of symptoms:
 Scleritis: Subtype
• Anterior scleritis is the most common form of scleral infl
ammation.
• Anterior scleritis can be broadly divided into nonnecrotizing
scleritis and necrotizing scleritis.
• Non-necrotizing scleritis is the most common form of anterior
scleritis, which can be further divided into nodular and diffuse
varieties.

Lalit Varma. Scleral Inflammations: An update. 2013

 Diffuse anterior scleritis
• the most common and least severe form of scleritis, accounting for
nearly 50 percent of cases
• Most cases respond to relatively mild therapies and do not recur.
• Clinical Manifestation :
– Associated with widespread ocular erythema and scleral edema
but no nodules or areas of necrosis
– Only a small number of patients with diffuse anterior scleritis
have disease that progresses to more aggressive forms.
 Nodular Anterior Scleritis
• Nodular anterior scleritis is the second most common
form of anterior scleritis, accounting for 20 to 40 percent
of cases
• Multiple attacks of scleritis occur in approximately 50
percent of patients.
• Clinical Manifestation :
– Localized areas of firm, tender edema associated
with intense dilation of the deep episcleral vessels
may be found in nodular anterior scleritis
– With treatment, the pain and scleral tenderness
resolve rapidly; however, the nodules may persist for
months.
Necrotizing anterior scleritis with inflammation

• It is the most severe of all the types and carries a potential threat to visual
loss.
• It is often seen in patients with rheumatoid arthritis.
• The condition has been found to be due to vasculitides secondary to
immune complex deposition and results in shut down of the episcleral
vascular bed
• Clinical manifestation :
– bilateral in 60% of cases
– severe pain and tenderness out of proportion to inflammatory signs.
– Examination reveals :
• white, avascular areas of localized scleral edema and congestion, the edges of these
lesions are more inflamed than the center (Figure 8).
• Gradually underlying uveal tissue becomes visible as the sclera becomes thin and
translucent.
• Because of the ectasia of the sclera, staphylomas are frequently seen.
• If not treated, the necrotizing scleritis may spread to the equator and
circumferentially and can involve the entire globe

Lalit Varma. Scleral Inflammations: An update. 2013

 Necrotizing anterior scleritis without
inflammation (Scleromalacia perforans)
• Necrotizing anterior scleritis without signs of infl ammation occurs
predominantly in patients with long-standing rheumatoid arthritis
• Though rare, the condition is vision threatening.
• Clinical manifestation:
– minimal signs of inflammation and absence of pain.
– In early phase of the disease, patient may present with blurred vision
because of astigmatism due to thinning and distortion of the globe.
– As the disease progresses, the sclera progressively thins and the
underlying dark uveal tissue becomes visible (fi gure 9).
– Staphylomas can develop during the course of scleral thinning.
– Peripheral corneal thinning is often seen, though direct corneal
involvement is rare.
– Spontaneous perforation is rare but these eyes are prone to rupture
with minimal trauma because of the extreme thinning of sclera.

Lalit Varma. Scleral Inflammations: An update. 2013

Scleritis vs episcleritis
 30. Normal Tension Glaukoma
• Normal Tension Glaukoma yang terdapat pada satu ujung
spektrum glaukoma sudut terbuka kronis merupakan bentuk yang
tersering menyebabkan pengecilan lapangan pandang bilateral
progressif asimptomatik yang muncul perlahan dan sering tidak
terdeteksi sampai terjadi pengecilan lapangan pandang yang
ekstensif.
• Tipe glaukoma dimana nervus optic rusak dan kehilangan
kemampuan melihat dan lapangan pandang, muncul pada
glaukoma sudut terbuka namun tekanan intra okuler yang normal
(<22 mmHg)

Vaughn DG, Oftalmologi Umum, ed.14

Normal tension Glaucoma Diagnostic Criterias
Diagnostic criteria Diagnostic tests
1. Intraocular tension Tonometry
2. Optic nerve head changes Ophthalmoscopy
3. Visual field defects Perimetry
4. Angle of ant. Chamber Gonioscopy
 OPTIC NERVE HEAD CHANGES
Early Changes
• Vertically oval cup
• Asymmetry of C:D ratio
between two eyes(>0.2)
• Enlarged C:D Ratio (>0.5)
• Pallor Areas
Increased C:D Ratio
Advanced Changes:
• Notch/Thinning of
neuroretinal rim
• Pallor of neuroretinal rim
• Superficial disc haemorrhages
• Cupping of disc
• Bayonetting Sign
• Lamellar Dot Sign
Glaucomatous optic atrophy:
• Neural disc is destroyed
• Optic nerve head appears
white and deeply excavated
Cupping of discs and Bayonetting sign

Thinning of neuroretinal rim

Bayonetting sign
Atrofi Papil dan Papiledema
Papil Atrophy Papil Edema

Columbia University Department of Opthalmology

 Treatment
• ↓IOP remains important in the pathogenesis of
NTG  the use of topical anti-glaucoma drugs
remains the mainstay of treatment.
• The CNTGS demonstrated that lowering IOP by
30% from baseline, to an average of 11mmHg,
reduced the risk of progression nearly three-
fold.19
• That each 1mmHg IOP reduction reduced the risk
of glaucoma damage by 10% emphasized the
importance of vigilant monitoring, and that ‘last
millimeter of mercury of effect
 31. GLAUKOMA SEKUNDER
• Glaucoma sekunder merupakan glaukoma yang diketahui
penyebab yang menimbulkannya. Hal tersebut disebabkan
oleh proses patologis intraokular yang menghambat aliran
cairan mata (cedera, radang, tumor, penyakit sistemik)
• Glaukoma sekunder bisa terjadi akibat lensa seperti :
 Luksasi lensa anterior, dimana terjadi gangguan pengaliran cairan mata ke
sudut bilik mata, COA dangkal
 Katarak imatur, dimana akibat mencembungnya lensa akan menyebabkan
penutupan sudut bilik mata, COA dangkal (glaukoma fakomorfik)
 Katarak hipermatur, dimana bahan lensa keluar dari lensa sehingga menutupi
jalan keluar cairan mata, COA normal/dalam (glaukoma fakolitik)
 Phacoanaphylactic glaucoma, COA dalam
 Lens particle glaucoma, COA dalam

Ilyas, Sidarta., 2004. Ilmu Penyakit Mata, Fakultas Kedokteran Universitas Indonesia, Jakarta.
 Glaukoma Fakolitik
• Glaukoma yang terjadi akibat penutupan sudut bilik mata oleh bagian
lensa yang lisis ini disebut glaukoma fakolitik,
• Pasien mengeluh sakit kepala berat, mata sakit, tajam pengelihatan hanya
tinggal proyeksi sinar.
• Examination reveals a markedly elevated IOP, microcystic corneal
edema, prominent cell and flare reaction without keratic precipitates
(KP), and an open anterior chamber angle.
• The lack of KP (keratic Precipitate) helps distinguish phacolytic glaucoma
from phacoantigenic glaucoma.
• Management Patients with phacolytic glaucoma should be treated initially
with topical cycloplegia, topical steroids (to reduce inflammation), and
aqueous suppressants (to reduce intraocular presure).
• Cataract extraction is the definitive treatment for phacolytic glaucoma
 Lens particle glaucoma
• Pathophysiology Lens particle glaucoma, in contrast to phacolytic
glaucoma, is secondary to a "disruption of the lens capsule”
• may occur after cataract surgery, penetrating lens injury, or laser
posterior capsulotomy.
• The disrupted lens releases lens particle material in the anterior
chamber leading to the obstruction of the aqueous outflow
• Diagnosis
– The presentation is usually delayed for a few weeks after the
precipitating event, but it may occur months or years later.
– A history of surgery or trauma is an important
– Clinical findings include elevated intraocular pressure and evidence of
cortical lens material in the anterior chamber.
– Other possible signs are corneal edema, synechiae, and cell/flare
reaction in the anterior chamber.
 Phacoanaphylactic
glaucoma/Phacoantigenic Glaucoma
• Pathophysiology Phacoantigenic
glaucoma is a granulomatous
inflammatory reaction directed
against own lens antigens leading to
obstruction of the trabecular
meshwork and increased intraocular
pressure
• Phacoanaphylaxis is not the correct
name of this condition since it is not
an allergy.
• The mechanism causing the reaction
seems to be an Arthus-type immune
complex reaction mediated by IgG
and the complement system
• Diagnosis Phacoantigenic glaucoma
usually occurs between one and
fourteen days after cataract surgery
or trauma.
• Pain is often slow in onset and is
associated with signs of
granulomatous uveitis (eg, keratic
precipitates) in contrast to the acute,
severe pain that is typical of PG,
which shows no signs of chronic
inflammation.
• Clinical findings include "keratic
precipitates", anterior chamber
cell/flare reaction, synechiae and
residual lens material.
• Management Initial therapy is to
control the intraocular pressure with
IOP-lowering medications and to
reduce the inflammation with topical
steroids.
• If medical treatment is unsuccessful,
surgical removal of residual lens
material is indicated
 32. HORDEOLUM
• Peradangan supuratif kelenjar kelopak mata
• Infeksi staphylococcus pada kelenjar sebasea
• Gejala: kelopak bengkak dengan rasa sakit dan mengganjal,
merah, nyeri bila ditekan, ada pseudoptosis/ptosis akibat
bertambah berat kelopak
• Gejala
– nampak adanya benjolan pada kelopak mata bagian atas atau
bawah
– berwarna kemerahan.
– Pada hordeolum interna, benjolan akan nampak lebih jelas
dengan membuka kelopak mata.
– Rasa mengganjal pada kelopak mata
– Nyeri takan dan makin nyeri saat menunduk.
– Kadang mata berair dan peka terhadap sinar.
Ilmu Penyakit Mata, Sidharta Ilyas
 • 2 bentuk :
 Hordeolum internum: infeksi kelenjar Meibom di dalam
tarsus. Tampak penonjolan ke daerah kulit kelopak, pus
dapat keluar dari pangkal rambut
 Hordeolum eksternum: infeksi kelenjar Zeiss atau Moll.
Penonjolan terutama ke daerah konjungtiva tarsal

http://www.huidziekten.nl/zakboek/dermatosen/htxt/Hordeolum.htm

Hordeolum Eksterna Hordeolum Interna

Ilmu Penyakit Mata, Sidharta Ilyas
• Pengobatan
– Self-limited dlm 1-2 mingu
– Kompres hangat selama sekitar 10-15 menit, 4x/hari
– Antibiotik topikal (salep, tetes mata), misalnya:
Gentamycin, Neomycin, Polimyxin B,
Chloramphenicol
– Jika tidak menunjukkan perbaikan : Antibiotika oral
(diminum), misalnya: Ampisilin, Amoksisilin,
Eritromisin, Doxycyclin
– Insisi bila pus tidak dapat keluar
• Pada hordeolum interna, insisi vertikal terhadap margo
palpebra supaya tidak memotong kelenjar meibom lainnya
• Pada hordeolum eksterna, insisi horizontal supaya kosmetik
tetap baik
 Diagnosis Banding
• Kalazion
– Inflamasi idiopatik, steril, dan kronik dari kelenjar Meibom
– Ditandai oleh pembengkakan yang tidak nyeri, muncul
berminggu-minggu.
– Dibedakan dari hordeolum oleh ketiadaan tanda-tanda inflamasi
akut
– Jika sangat besar, kalazion dapat menekan bola mata,
menyebabkan astigmatisma
• Blefaritis
– Radang kronik pada kelopak mata, disebabkan peradangan
kronik tepi kelopak mata (blefaritis anterior) atau peradangan
kronik kelenjar Meibom (blefaritis posterior)
– Gejala: kelopak mata merah, edema, nyeri, eksudat lengket,
epiforia, dapat disertai konjungtivitis dan keratitis
• Selulitis palpebra
– Infiltrat difus di subkutan dengan tanda-tanda radang akut,
biasanya disebabkan infeksi Streptococcus.
Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007.
 33. Blepharitis
• Inflammation of the eyelids Physical examination:
• Signs and symptoms: • Skin → erythema, papules,
– Redness/irritation pustules (rosacea)
– Burning/tearing • Eyelids → abnormal eyelid
– Itching position,hyperemia, ulceration,
– Crusting of eyelashes scaling, scarring
– Loss of eyelashes (madarosis_ • Eyelashes → malposition/
– Eyelid sticking misdirection, loss, pediculosis
– Blurring/fluctuating vision nits, cylindrical sleeves,
– Contact lens intolerance collarettes
– Photophobia • Tarsal conjunctiva →
– Increased frequency of blinking dilation/inflammation of
meibomian glands, capping of
meibomian orifices,
papillary/folicular reaction
• Bulbar conjunctiva → hyperemia,
phylctenules, follicles
• Cornea → epithelial defect,
edema, infiltrates

Clinical Ophthalmology. Kanski. 7th ed.

 Treatment
• Warm compresses to soften adherent scurf and scales, warm the
meibomian secretions → once or twice daily
• Eyelid cleansing, including eyelid massage in cases of MGD → once or
twice daily
• Antibiotics (topical and/or systemic)
– Topical bacitracin or erythromycin on eyelid margins
– Metronidazole gel if unresponsive to antibiotic treatment (off-label)
– Patients with MGD → oral + topical
– Doxycycline 100 mg or tetracycline 1000 mg in divided doses, tapered to
doxycycline 40-50 mg or tetracycline 250 mg after clinical improvement
– Alternative: erythromycin 250-500 mg daily or azithromycin 250-500 mg one
to three times a week
• Topical corticosteroid → for ocular surface inflammation eg severe
conjunctival infection, marginal keratitis, or phlyctenules. Applied several
times daily to the eyelids or ocular surface.
• Artificial tears

Clinical Ophthalmology. Kanski. 7th ed.

 Treatment
• Good lid hygiene is the mainstay of treatment for all forms of blepharitis.
• The goal is to alleviate symptoms and to develop a maintenance regimen
to prevent or minimize future exacerbations.
• Mild to moderate symptoms : can generally be managed with
symptomatic measures, including warm compresses, lid massage, lid
washing, and artificial tears.
• Severe or refractory symptoms : may require additional therapies such as
topical or oral antibiotics, topical glucocorticoids, or typical cyclosporine.
– Because of the potential for systemic side effects with oral drugs, topical
therapy is usually tried first.
– Antibiotic ointment (eg, bacitracin, erythromycin) is placed directly onto the
lid margin once daily at bedtime.
– Once symptoms improve (generally one to two weeks), treatment can be
stopped, but lid hygiene measures should be continued.
– Oral antibiotic therapy (eg, doxycycline, tetracycline, azithromycin) can be
given if the response to topical therapy is inadequate.
• All patients should be advised to eliminate or limit potential triggers or
exacerbating factors (eg, allergens, cigarette smoking, contact lenses).

Uptodate.com
 Blepharitis Complication
• Dry eye disease is a frequent complication of
blepharitis, occurring in 25 to 40 percent of
patients
• Keratitis
 Definisi
Blefaritis superfisial Infeksi kelopak superfisial yang
diakibatkan Staphylococcus
Hordeolum Peradangan supuratif kelenjar
kelopak mata
Blefaritis Blefaritis diseratai skuama atau
skuamosa/seboroik krusta pada pangkal bulu mata
yang bila dikupas tidak terjadi luka
pada kulit, berjalan bersamaan
dengan dermatitis sebore
Meibomianitis Infeksi pada kelenjar meibom
(blefaritis posterior)
Blefaritis Angularis Infeksi Staphyllococcus pada tepi
kelopak di sudut kelopak atau
kantus
Ilmu Penyakit Mata, Sidharta Ilyas
Gejala
Terdapat krusta dan bila
menahun disertai dengan
meibomianitis
Kelopak bengkak, sakit, rasa
mengganjal, merah, nyeri bila
ditekan
Etiologi: kelainan metabolik
atau jamur. Gejala: panas,
gatal, sisik halus dan
penebalan margo palpebra
disertai madarosis
Tanda peradangan lokal pada
kelenjar tersebut
Gangguan pada fungsi
pungtum lakrimal, rekuren,
dapat menyumbat duktus
lakrimal sehingga mengganggu
fungsi lakrimalis
Tatalaksana
Salep antibiotik
(sulfasetamid dan
sulfisoksazol), pengeluaran
pus
Kompres hangat, drainase
nanah, antibiotik topikal
Membersihkan tepi kelopak
dengan sampo bayi, salep
mata, dan topikal steroid
Kompres hangat, penekanan
dan pengeluaran pus,
antibiotik topikal
Dengan sulfa, tetrasiklin,
sengsulfat
TO 4
 34. Trauma Duktus Lakrimalis

Tann TM and Long JA. Eyelid and Lacrimal Trauma. In: Ocular Trauma
Principles and Practice. New York. 2002 : 371-381.
 Trauma Duktus Lakrimalis

Tann TM and Long JA. Eyelid and Lacrimal Trauma. In: Ocular Trauma
Principles and Practice. New York. 2002 : 371-381.
 Trauma Duktus Lakrimalis

Tann TM and Long JA. Eyelid and Lacrimal Trauma. In: Ocular Trauma
Principles and Practice. New York. 2002 : 371-381.
 Trauma Duktus Lakrimalis
Mekanisme penyebab :
1. Kontak dengan objek tajam (Kaca atau logam)
• Partial thickness laceration (kulit & subkutan)
• Full thickness laceration (posterior, tarsesus,
konjnungtiva)

2. Trauma avulsi oleh benda tumpul

 Kanalikuli  struktur kompleks sehingga repair
dilakukan untuk kanalis lakrimalis dan jaringan
sekitarnya

Kanski JJ. Eyelid Trauma In : Clinical Ophthalmology. London. 2004 : 659-661.

 Trauma Duktus Lakrimalis
Diagnosis Tatalaksana
• Anamnesa riwayat trauma • Awal  Diberikan eye patch lalu rujuk
pada kelopak mata • Tindakan dalam 24-48 jam
• Pemeriksaan oftalmologi  • Dilakukan kanalisasi (stent/ selang
silikon) untuk memperbaiki drainase
melihat kerusakan dalam sistim kanalis lakrimalis
mata, derajat luka dan • Stent diangkat 2-3 bulan
perkiraan jaringan yang
hilang
• Tes Anel  laserasi saluran
lakrimalis
• CT Scan – curiga fraktur
orbita

Kanski JJ. Eyelid Trauma In : Clinical Ophthalmology. London. 2004 : 659-661.

 Lacerations involving the tear
drainage system
• If not repaired appropriately, a lacerating injury to the tear drainage
system can result in permanent tearing.
• Lacerations involving the medial aspect of the eyelids mandate
particularly close inspection to exclude damage to the lacrimal
system.
• trauma to the canalicular system should be suspected when a
laceration occurs medially to the punctum on the upper or lower
eyelid.
• Definitive determination of canalicular involvement requires
ophthalmologic consultation. The ophthalmologist may use special
instruments to probe and irrigate the laceration in order to
establish whether the laceration involves the tear drainage system.
• Lacerations involving the canaliculi require placement of silicone
tubes to maintain patency of the drainage system while the
laceration heals
 35. Blepharitis
• Inflammation of the eyelids
• Signs and symptoms:
– Redness/irritation
– Burning/tearing
– Itching
– Crusting of eyelashes
– Loss of eyelashes (madarosis_
– Eyelid sticking
– Blurring/fluctuating vision
– Contact lens intolerance
– Photophobia
– Increased frequency of blinking
Clinical Ophthalmology. Kanski. 7th ed.
Physical examination:
• Skin  erythema, papules, pustules
(rosacea)
• Eyelids  abnormal eyelid position,
hyperemia, ulceration, scaling,
scarring
• Eyelashes  malposition/
misdirection, loss, pediculosis nits,
cylindrical sleeves, collarettes
• Tarsal conjunctiva 
dilation/inflammation of meibomian
glands, capping of meibomian
orifices, papillary/folicular reaction
• Bulbar conjunctiva  hyperemia,
phylctenules, follicles
• Cornea  epithelial defect, edema,
infiltrates
 Blepharitis
• Terdiri dari blefaritis anterior dan
posterior
• Blefaritis anterior: radang
bilateral kronik di tepi palpebra
– Blefaritis stafilokokus: sisik
kering, palpebra merah,
terdapat ulkus-ulkus kecil
sepanjang tepi palpebra, bulu
mata cenderung rontok 
antibiotik stafilokokus
– Blefaritis seboroik: sisik
berminyak, tidak terjadi
ulserasi, tepi palpebra tidak
begitu merah
– Blefaritis tipe campuran
• Tx blefaritis seboroik: perbaikan
hygiene mata dengan cara:
– kompres hangat untuk evakuasi
dan melancarkan sekresi kelenjar
– tepi palpebra dicuci + digosok
perlahan dengan shampoo bayi
untuk membersihkan skuama
– pemberian salep antibiotik
eritromisin (bisa digunakan
kombinasi antibioti-KS)
• Blefaritis posterior:
• peradangan palpebra akibat difungsi
kelenjar meibom bersifat kronik dan
bilateral
• Kolonisasi stafilokokus
• Terdapat peradangan muara meibom,
sumbatan muara oleh sekret kental
Blepharitis
 Staphylococcal anterior blepharitis
• Hardscales and crusting around
bases of the lashes (collarettes;
figure A)
• Mild papillary conjunctivitis and
chronic conjunctival
hyperaemia
• Chronic cases  scarring and
notching (tylosis) of lid margin Seborrhoeic blepharitis:
(figure B), madarosis, trichiasis, • Hyperaemic and greasy anterior lid margins
and poliosis with sticking together of lashes (figure C)
• Secondary changes  marginal • Scales are soft and located anywhere on the
keratitis, phlyctenulosis lid margin and lashes
• Tear film instability and dry eye
syndrome

Posterior blepharitis/Meibomian gland dysfunction (MGD)

• Excessive and abnormal meibomian gland secretion manifest as
capping of meibomian gland orifices with oil globules (Fig. 1)
• Plugging of the meibomian gland orifices (Fig. 2)
• Hyperaemia and telangiectasis of the posterior lid margin.
1 2 • Pressure on the lid margin results in expression of meibomian
fluid that may be turbid or toothpaste-like (Fig. 3)
• Lid transillumination may show gland loss and cystic dilatation
of meibomian ducts.
• The tear film is oily and foamy, and froth may accumulate on
the lid margins or inner canthi.
• Secondary changes include papillary conjunctivitis and inferior
3 corneal punctate epithelial erosions.

Clinical Ophthalmology. Kanski. 7th ed.

 Definisi
Blefaritis superfisial Infeksi kelopak superfisial yang
diakibatkan Staphylococcus
Hordeolum Peradangan supuratif kelenjar
kelopak mata
Blefaritis Blefaritis diseratai skuama atau
skuamosa/seboroik krusta pada pangkal bulu mata
yang bila dikupas tidak terjadi luka
pada kulit, berjalan bersamaan
dengan dermatitis sebore
Meibomianitis Infeksi pada kelenjar meibom
(blefaritis posterior)
Blefaritis Angularis Infeksi Staphyllococcus pada tepi
kelopak di sudut kelopak atau
kantus
Ilmu Penyakit Mata, Sidharta Ilyas
Gejala
Terdapat krusta dan bila
menahun disertai dengan
meibomianitis
Kelopak bengkak, sakit, rasa
mengganjal, merah, nyeri bila
ditekan
Etiologi: kelainan metabolik
atau jamur. Gejala: panas,
gatal, sisik halus dan
penebalan margo palpebra
disertai madarosis
Tanda peradangan lokal pada
kelenjar tersebut
Gangguan pada fungsi
pungtum lakrimal, rekuren,
dapat menyumbat duktus
lakrimal sehingga mengganggu
fungsi lakrimalis
Tatalaksana
Salep antibiotik
(sulfasetamid dan
sulfisoksazol), pengeluaran
pus
Kompres hangat, drainase
nanah, antibiotik topikal
Membersihkan tepi kelopak
dengan sampo bayi, salep
mata, dan topikal steroid
Kompres hangat, penekanan
dan pengeluaran pus,
antibiotik topikal
Dengan sulfa, tetrasiklin,
sengsulfat
 Treatment
• Warm compresses to soften adherent scurf and scales, warm the
meibomian secretions  once or twice daily
• Eyelid cleansing, including eyelid massage in cases of MGD  once
or twice daily
• Antibiotics (topical and/or systemic)
– Topical bacitracin or erythromycin on eyelid margins
– Metronidazole gel if unresponsive to antibiotic treatment (off-label)
– Patients with MGD  oral + topical
• Doxycycline 100 mg or tetracycline 1000 mg in divided doses, tapered
to doxycycline 40-50 mg or tetracycline 250 mg after clinical
improvement
• Alternative: erythromycin 250-500 mg daily or azithromycin 250-500
mg one to three times a week
• Topical corticosteroid
– for ocular surface inflammation eg severe conjunctival infection,
marginal keratitis, or phlyctenules. Applied several times daily to the
eyelids or ocular surface.
• Artificial tears
Bleoharitis. American Academy of Ophthalmology.
 Blefaritis Anterior

• Masalah pada kelenjar meibom akan menghasilkan

produksi kelenjar minyak yang berlebih,
menyebabkan kelopak mata teriritasi dan bengkak.
• Blefaritis sering disebabkan oleh infeksi bakteri,
terutama pada dasar bulu mata. Pertumbuhan
jumlah bakteri yang berlebih bisa menyebabkan sisik
dan ulkus sepanjang perbatasan bulu mata
• Faktor yang bisa menyebabkan pertumbuhan
bakteri: dandruff, dry skin, acne, diabetes, etc

https://www.nhcs.com.sg/patient-care/conditions-treatments/blepharitis/causes-risk-factors
36. Glaukoma Akut
 Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006

Tatalaksana Glaukoma Akut

• Tujuan : merendahkan tekanan bola mata secepatnya
kemudian bila tekanan normal dan mata tenang → operasi
• Supresi produksi aqueous humor
– Beta bloker topikal: Timolol maleate 0.25% dan 0.5%, betaxolol
0.25% dan 0.5%, levobunolol 0.25% dan 0.5%, metipranolol
0.3%, dan carteolol 1% dua kali sehari dan timolol maleate 0.1%,
0.25%, dan 0.5% gel satu kali sehari (bekerja dalam 20 menit,
reduksi maksimum TIO 1-2 jam stlh diteteskan)
– Pemberian timolol topikal tidak cukup efektif dalam
menurunkan TIO glaukoma akut sudut tertutup.
– Apraclonidine: 0.5% tiga kali sehari
– Brimonidine: 0.2% dua kali sehari
– Inhibitor karbonat anhidrase:
• Topikal: Dorzolamide hydrochloride 2% dan brinzolamide 1% (2-3
x/hari)
• Sistemik: Acetazolamide 500 mg iv dan 4x125-250 mg oral (pada
glaukoma akut sudut tertutup harus segera diberikan, efek mulai
bekerja 1 jam, puncak pada 4 jam)
Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asbury’s General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007.

Tatalaksana Glaukoma Akut

• Fasilitasi aliran keluar aqueous humor
– Analog prostaglandin: bimatoprost 0.003%, latanoprost 0.005%, dan
travoprost 0.004% (1x/hari), dan unoprostone 0.15% 2x/hari
– Agen parasimpatomimetik: Pilocarpine
– Epinefrin 0,25-2% 1-2x/hari
• Pilokarpin 2% setiap menit selama 5 menit,lalu 1 jam selama 24 jam
– Biasanya diberikan satu setengah jam pasca tatalaksana awal
– Mata yang tidak dalam serangan juga diberikan miotik untuk mencegah
serangan
• Pengurangan volume vitreus
– Agen hiperosmotik: Dapat juga diberikan Manitol 1.5-2MK/kgBB dalam larutan
20% atau urea IV; Gliserol 1g/kgBB badan dalam larutan 50%
– isosorbide oral, urea iv
• Extraocular symptoms:
– analgesics
– antiemetics
– Placing the patient in the supine position → lens falls away from the iris
decreasing pupillary block
– Pemakaian simpatomimetik yang melebarkan pupil berbahaya
 Pharmacologic therapy
No. Drugs class Mechanism of action
1. Prostaglandin Increase aquos humor outflow  increase in uveoscleral outflow, increase
(latanoprost, travoprost, trabecular outflow, regulate matrix metaloproteinase and remodelling of
bimatoprost) Extracellular matrix, widening connective tissue filled spaces and changes
in the shapes of cells.
Topical prostaglandin are chosen over topical beta blocker and other class
of medication as initial therapy in open angle glaucoma
2. Beta blocker (timolol, Decreasing aquos humor production --> blockade of symphatetic nerve
levobunolol, endings in the cilliary epithelium
metipranolo)
3. Alpha adrenergic Increasing aquos humor outflow and decresasing the production. Simillary
agonist effective to beta blockers but are associated with a number ocular side
effect including allergic conjunctivitis, ocular pruritus, and hyperemia
4. Carbonic anhidrase Decreasing aquos humor production. Systemic CAI have been replaced by
inhibitor newer topical drugs whic have fewer systemic side effects. Topical CAI
(Acetazolamide) don`t appear to be as effective in treating open angle glaucoma compared
to other topical drugs.
5. Cholinergic agonist Increasing aquos humor outflow. Have fewer systemic side effect
compared to beta blocker, but ocular side effect is higher (myopia, small
pupils, visual distrubance related to coexistent cataract)
 Iris Bombe dan
Glaukoma
• Sinekia posterior yang
substansial dapat menggangu
pergerakan cairan aqueous
dari posterior ke anterior
chamber, disebut juga iris
bombe Sinekia Posterior
• Saat tekanan menekan dari
posterior mata, iris terdorong
ke depan, menyebabkan
secondary angle closure
glaucoma.
• Sinekia anterior perifer juga
dapat menyebabkan
glaucoma sekunder bila
terjadi sinekia secara
sirkumferensial Sinekia Anterior
Lee JY, Kim YY, Jung HR. Distribution and characteristics of peripheral anterior synechiae in primary angle-closure
glaucoma. Korean J Ophthalmol. 2006 Jun;20(2):104-8.
 Iris Bombe dan
Glaukoma
• Sinekia posterior yang
substansial dapat menggangu
pergerakan cairan aqueous
dari posterior ke anterior
chamber, disebut juga iris
bombe Sinekia Posterior
• Saat tekanan menekan dari
posterior mata, iris terdorong
ke depan, menyebabkan
secondary angle closure
glaucoma.
• Sinekia anterior perifer juga
dapat menyebabkan
glaucoma sekunder bila
terjadi sinekia secara
sirkumferensial Sinekia Anterior
Lee JY, Kim YY, Jung HR. Distribution and characteristics of peripheral anterior
synechiae in primary angle-closure glaucoma. Korean J Ophthalmol. 2006
Jun;20(2):104-8.
Iris Bombe pada Sinekia Posterior
• Pada sinekia posterior terjadi
adhesi bagian posterior iris
dengan bagian anterior kapsul
lensa.
• Sinekia posterior yang berbentuk
bulat (annular) menghambat
sirkulasi aqueous humour dari
bilik mata posterior ke bilik mata
depan. Akibatnya, aqueous
tertumpuk di bagian belakang iris
hingga mendorongnya ke depan,
yang disebut dengan iris bombe
(tanda panah pada gambar).
• Kondisi ini kemudian diikuti
dengan peningkatan TIO
 37. Pseudopterygium
• Pseudopterygium
– adhesi dari conjunctiva ke
kornea perifer dan dapat
terjadi pad kuadran kornea
yang manapun
• Adhesi bersifat tidak
kokoh dan tampak seperti
massa menonjol lebar
pada permukaan kornea,
berbeda dengan
pterygium yang
berbentuk segitiga.
Columbia University Department of Opthalmology
 Pseudopterygium: Etiologi &
Tatalaksana
• Pseudopterygium dapat terjadi akibat:
– peripheral corneal ulcer
– inflamasi permukaan mata seperti cicatrizing
conjunctivitis
– trauma kimia
– friksi kronis dari kontak lensa
• Penanganan definitive dengan operasi sama
seperti pterygium

Columbia University Department of Opthalmology

 38. Thyroid Ophthalmopathy
• Inflammatory disorder of the eye
• Commonly complicates Graves’ disease but can also be
associated with Hashimoto’s thyroiditis, or in euthyroid
pts
• 50% of pts with Graves’ have clinical ophthalmopathy,
but up to 70% of the remaining half have
ophthalmopathy by imaging
• Prevalence of thyroid ophthalmopathy = 0.4%
• Most common cause of exophthalmos
– >50% of cases
– Of note, other causes of exophthalmos include primary
hyperadrenalism, longstanding steroid use or acromegaly.
 Pathogenesis
• Autoimmune process • Inflammatory cells activated
manifesting as: by TSH receptor antigen
– Extraocular m. myositis – TSH receptor mRNA and
• T-cell inflammatory infiltrate protein found in orbital
– Fibroblast proliferation fibroblasts and adipocytes
– Glycosaminoglycan – TSHR expression greater in
overproduction
retro-orbital tissues of Graves’
– Orbital congestion pt compared to other tissues.
• Increase in soft tissue mass – Correlation between severity of
within bony orbit due to ophthalmopathy and serum
extraocular muscle TSHR Ab concentrations
enlargement, increased orbital
fat and connective tissue
• Later in disease, inflammatory
infiltrate replaced by
widespread fibrosis
– “Inactive” phase
– Occurs about 8mo to 3yrs after
onset
 Initial Signs/Symptoms
• The clinical signs are haracteristic
and include a combination of eye
lid retraction, lid lag, globe lag,
proptosis, restrictive extraocular
myopathy and optic neuropathy

Note enlarged extraocular mm.

 Exophthalmometer
• Exophthalmometer is an instrument used for
measuring the degree of forward displacement of the
eye in exophthalmos.
• The device allows measurement of the forward
distance of the lateral orbital rim to the front of the
cornea.
• Exophthalmometers can also identify enophthalmos
• There are several types of exophthalmometers:
– Hertel exophthalmometer:
– Naugle exophthalmometer
– Luedde exophthalmometer
Exophtalmometry
Penilaian Derajat Beratnya Penyakit
• Derajat beratnya opthalmopathy ditentukan
menggunakan clinical activity score (CAS) yang
terdiri dari tujuh poin.
– Skor  3 menunjukkan pasien memiliki penyakit aktif
dan responsive terhadap terap imunomodulator,
seperti kortikosteroid.
• Tiga kriteria tambahan dalam CAS adalah:
– Peningkatan proptosis (2 mm)
– Penurunan gerakan bola mata ( 5 derajat)
– Penurunan tajam penglihatan (1 baris pada Snellen
chart)

https://www.uptodate.com/contents/clinical-features-and-diagnosis-of-graves-orbitopathy-ophthalmopathy#H14
 Histology

• Fluid and inflammatory cells separate the

muscle bundles of the extraocular muscles.
 Complications
• Optic nerve compression at orbital apex by enlarged muscles
– May present with blurry vision, color loss, afferent pupillary defect, or
visual field loss
– More likely when superior rectus is enlarged or if no exophthalmos
(form of self-decompression)

Optic neuropathy as result of optic nerve compression from enlargement of extraocular muscles
 Radiologic Evaluation
• Usually employed if cause of exophthalmos is unclear
(ie. normal thyroid lab studies, or hx/PE inconsistent
with thyroid disease)
• Also to determine optic nerve involvement if not
obvious by fundoscopic exam
• Distinct sparing of muscle tendons in thyroid
ophthalmopathy
• Non-contrast enhanced coronal orbital CT scan most
helpful to assess size of extraocular mm.
 Treatment
• TEARS mnemonic for remembering initial
management.
• T – Tobacco abstinence is immensely important
• E – Euthyroidism must be achieved and maintained
• A – Artificial tears are helpful for the majority of the
patients and can afford rapid relief from symptoms of
corneal exposure
• R – Referral to a specialist centre with experience and
expertise in treating thyroid eye disease is indicated in
all but the mildest of cases
• S – Self help groups can provide valuable additional
support
Pinto CN. Current Protocol for the Management of Thyroid Eye Disease (absent/present). All India Institute of Medical Sciences, New Delhi
 Medical care

• Inform patients that thyroid ophthalmopathy usually runs a self limited

but prolonged course over 1 or more years.
• Patient should realize that no immediate care is available
• Monitor for visual loss from corneal exposure and optic neuropathy and
for strabismus development.
– Visual field and colour vision testing may help in early detection of visual loss.
– If a patient has dry eye symptoms, consider using tears during the day,
lubricating ointment at night and punctual plugs.
– Morning lid edema may be reduced by sleeping on a bed with its head slightly
elevated.
– Patients should be encouraged to stop smoking in order to reduce the risk of
congestive orbitopathy
• Severe form of disease may need more aggressive management.
• Whereas patients with active and progressive disease may benefit from
immunosuppression, patients with inactive burnt out disease are only
amenable to surgical intervention
1. Radiotherapy
– This has a non specific anti- inflammatory effect and destroys the radiosensitive lymphocytes and reduces
glycosaminoglycans roduction.
2. Glucocorticoids
– These are highly effective in soft tissue changes and optic neuropathy, whereas decrease in proptosis and
ocular motility is less impressive
– Intravenous glucocorticoids seem to be associated with higher success rate and better tolerability as compared
to oral glucocorticoids.
– Patients may be treated with one gram of intravenous methyl prednisolone daily for three days followed by
oral steroids which may be tapered as condition improves.
3. Antioxidants
– Nicotineamide and allopurinol have been used in doses of 300mg daily. The effect was found to be more
pronounced in cigarette smokers.
– Though soft tissue inflammation responds well to treatment, effect on proptosis is not very impressive
4. Somatostatin analogues
– Somatostatin analogues are postulated to bind to certain somatostatin receptors on surface of various orbital
cells like lymphocytes, fibroblasts and muscle cells, thereby altering their immunologic and metabolic
activities.
5. Monoclonal antibodies
– Rituximab causes an immediate depletion of circulating b cells which usually lasts for 4-6 months but may last
upto 4 years
6. Immunosuppressive drugs
– Cyclosporine has a lower effectiveness than glucocorticoids but a combination may be more effective than
either treatment alone
– Low dose treatment with Methotrexate is being used with apparent success. Other drugs that have been tried
include Azathioprine and cyclophosphamide
 39. Defisiensi vitamin A
• Vitamin A meliputi retinol, retinil ester, retinal
dan asam retinoat. Provitamin A adalah semua
karotenoid yang memiliki aktivitas biologi β-
karoten
• Sumber vitamin A: hati, minyak ikan, susu &
produk derivat, kuning telur, margarin, sayuran
hijau, buah & sayuran kuning
• Fungsi: penglihatan, diferensiasi sel, keratinisasi,
kornifikasi, metabolisme tulang, perkembangan
plasenta, pertumbuhan, spermatogenesis,
pembentukan mukus

Kliegman RM. Nelson’s textbook of pediatrics, 19th ed. McGraw-Hill; 2011

• Konjungtiva normalnya memiliki sel goblet.
Hilangnya/ berkurangnya sel goblet secara
drastis bisa ditemukan pada xerosis
konjungtiva.
• Gejala defisiensi:
– Okular (xeroftalmia): rabun senja, xerosis
konjungtiva & kornea, keratomalasia, bercak Bitot,
hiperkeratosis folikular, fotofobia
– Retardasi mental, gangguan pertumbuhan,
anemia, hiperkeratosis folikular di kulit
 Xerophthalmia (Xo)
Stadium :
XN : night blindness (hemeralopia)
X1A : xerosis conjunctiva
X1B : xerosis conjunctiva (with bitot’s spot)
X2 : xerosis cornea
X3A : Ulcus cornea < 1/3
X3B : Ulcus cornea > 1/3, keratomalacea
XS : Corneal scar
XF : Xeroftalmia fundus
 Xeroftalmia
XN. NIGHT BLINDNESS
• Vitamin A deficiency can interfere with rhodopsin
production, impair rod function, and result in
night blindness.
• Night blindness is generally the earliest
manifestation of vitamin A deficiency.
• “chicken eyes” (chickens lack rods and are thus
night-blind)
• Night blindness responds rapidly, usually within
24—48 hours, to vitamin A therapy
 X1A, X1B. CONJUNCTIVAL XEROSIS
AND BITOT’S SPOT
• The epithelium of the • Conjunctival xerosis first
conjunctiva in vitamin A appears billateraly, in the
deficiency is transformed temporal quadrant, as an
from the normal columnar isolated oval or triangular
to the stratified squamous, patch adjacent to the
with loss of goblet cells, limbus in the interpalpebral
formation of a granular cell fissure.
layer, and keratinization of
the surface.
• Clinically, these changes are
expressed as marked
dryness or unwettability,
the affected area appears
roughened, with fine
droplets or bubbles on the
surface.
 X1A, X1B. CONJUNCTIVAL XEROSIS
AND BITOT’S SPOT
• In some individuals, keratin • Conjunctival xerosis and
and saprophytic bacilli Bitot’s spots begin to
accumulate on the xerotic resolve within 2—5 days,
surface, giving it a foamy or most will disappear within 2
cheesy appearance, known weeks.
as Bitot’s spots and they’re
easily wiped off)
• Generalized conjunctival
xerosis, involving the
inferior and/or superior
quadrants, suggests
advanced vitamin A
deficiency.
 X2 CORNEAL XEROSIS
• Corneal changes begin early in • Clinically, the cornea develops
vitamin A deficiency, long before classical xerosis, with a hazy,
they can be seen with the naked lustreless, dry appearance, first
eye which characteristic are observable near the inferior
superficial punctate lesions of the limbus
inferior—nasal aspects of the • Corneal xerosis responds within
cornea, which stain brightly with 2—5 days to vitamin A therapy,
fluorescein with the cornea regaining its
• Early in the disease the lesions normal appearance in 1—2 weeks
are visible only through a slit-
lamp biomicroscope
• With more severe disease the
punctate lesions become more
numerous, spreading upwards
over the central cornea, and the
corneal stroma becomes
oedematous
 X3A, X3B. Corneal
ulceration/keratomalacia
• Ulceration/keratomalacia • Superficial ulcers heal
indicates permanent with little scarring,
destruction of a part or all deeper ulcers, especially
of the corneal stroma, perforations, form dense
resulting in permanent peripheral adherent
structural alteration leukomas.
• Ulcers are classically • Localized keratomalacia is
round or oval “punched- a rapidly progressive
out” defects condition affecting the
• The ulceration may be full thickness of the
shallow, but is commonly cornea
deep
 XS. SCARS
• Healed sequelae of prior
corneal disease related to
vitamin A deficiency include
opacities or scars of varying
density (nebula, macula,
leukoma), weakening and
outpouching of the
remaining corneal layers
(staphyloma, and
descemetocele), and
phthisis bulbi.
XF. XEROPHTHALMIC FUNDUS
• The small white retinal
lesions described in some
cases of vitamin A
deficiency
• They may be accompanied
by constriction of the visual
fields and will largely
disappear within 2—4
months in response to
vitamin A therapy
• Gambaran funduskopi “
fenomena cendol”
 Pemeriksaan Penunjang
• A serum retinol study is a costly • The serum retinol level may be
but direct measure using high- low during infection because of a
performance liquid transient decrease in the RBP.
chromatography. • A zinc level is useful because zinc
– A value of less than 0.7 mg/L in deficiency interferes with RBP
children younger than 12 years is production.
considered low.
• A serum RBP study • An iron panel is useful because
iron deficiency can affect the
– easier to perform and less metabolism of vitamin A.
expensive than a serum retinol
study, because RBP is a protein and • Albumin levels are indirect
can be detected by an measures of vitamin A levels.
immunologic assay.
• Obtain a complete blood count
– RBP is also a more stable (CBC) with differential if anemia,
compound than retinol
– However, RBP levels are less
infection, or sepsis is a possibility.
accurate, because they are
affected by serum protein
concentrations and because types
of RBP cannot be differentiated.
 Therapy and Prevention
• For treatment of xerophthalmia, vitamin A is given in three doses at
the age-specific doses:
– Infants < 6 months of age: 50,000 international units orally
– Infants 6 to 12 months of age: 100,000 international units orally
– Children >12 months: 200,000 international units orally
– Adolescent and adults is 200,000 international units orally

• The first dose is given immediately on diagnosis, the second on the

following day, and the third dose at least two weeks later.

• Women of reproductive age or who are pregnant and have night

blindness should be treated with frequent small doses of vitamin A,
rather than high doses used for other adults
 Therapy & Prevention
• Vitamin A deficiency is common among populations
in resource-limited countries.
• For populations in which vitamin A deficiency is
endemic the World Health Organization (WHO)
recommends the following replacement approaches
• Universal periodic distribution — Periodic
supplementation is recommended for populations
endemic for vitamin A deficiency, at the following
doses (where 1 microgram retinol = 3.3 international
units)
– Infants 6 to 12 months of age: 100,000 international units
orally (30 mg retinol equivalent) – One dose
– Children 12 to 59 months of age: 200,000 international units
orally (60 mg retinol equivalent) – Dose repeated every four
to six months
 40. Ectopia Lentis
• Ectopia lentis adalah dislokasi atau perpindahan lensa
kristal alami.
• Lensa didefinisikan sebagai luksasi atau dislokasi ketika
terletak sepenuhnya di luar fossa hyaloid, mengambang
bebas di cairan vitreus, di ruang anterior, atau terletak
langsung di retina.
• Lensa dianggap subluks ketika sebagian bergeser tetapi
tetap berada dalam ruang lensa.
• Ectopia lentis dapat terjadi setelah trauma atau mungkin
berhubungan dengan penyakit mata atau sistemik.
• Ectopia Lentis dapat menyebabkan komplikasi besar pada
mata, termasuk perubahan bias yang signifikan, glaukoma
blok pupil, kerusakan retina, dan kebutaan.

https://eyewiki.aao.org/Ectopia_Lentis
 Ectopia Lentis
Penanganan dapat meliputi:
• Lensectomy/vitrectomy
with aphakic contact lens
or spectacles
• Iris-fixated intraocular
lens
• Scleral-sutured posterior
intraocular lens
• Implantation of in-the-
bag intraocular lens with
a capsular tension ring

American Academy of Ophthalmology. Cataract/Anterior Segment: Ectopia lentis Practicing Ophthalmologists

Learning System, 2017 - 2019 San Francisco: American Academy of Ophthalmology, 2017.
 41. Katarak Senilis
Katarak senilis adalah kekeruhan lensa yang terdapat pada usia lanjut,
yaitu usia di atas 50 tahun. Katarak ini merupakan katerak tersering
dari semua jenis katarak
Etiologi :
 Faktor biologi, yaitu karena usia tua dan pengaruh genetic
 Faktor fungsional, yaitu akibat akomodasi yang sangat kuat
mempunyai efek buruk terhadap serabu-serabut lensa.
 Faktor imunologik, Gangguan yang bersifat lokal pada lensa, seperti
gangguan nutrisi, gangguan
permeabilitas kapsul lensa, efek radiasi dan cahaya matahari.
 Gangguan metabolisme umum
• 4 stadium: insipien, imatur matur, hipermatur
• Gejala : distorsi penglihatan, penglihatan kabur/seperti
berkabut/berasap, mata tenang
• Penyulit : Glaukoma, uveitis
• Tatalaksana : operasi (ekstraksi intracapsular/ekstracapsular)

Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006

 Patofisiologi
Serabut protein nukleus
sentral pada lensa
semakin bertambah
usia akan terkompresi
dan mengeras (nuclear
sclerosis), yang
berakibat pada lensa
yang opak dan tidak
dapat ditembus cahaya

https://www.vincenzomaurino.co.uk/treatments/cataract-surgery/
Gambaran Progresif dari Katarak
Senilis

Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006

 42. UVEITIS
•Uveitis :
–inflamasi di uvea
yaitu iris, badan siliar
dan koroid yang
dapat menimbulkan
kebutaan.
–Di negara maju,
10% kebutaan pada
populasi usia
produktif adalah
akibat uveitis
 Klasifikasi
• The International Uveitis Study Group (IUSG) dan The
Standardization of Uveitis Nomenclatur (SUN) membagi uveitis
berdasarkan anatomi, etiologi, dan perjalanan penyakit
• Anatomi :
– uveitis anterior, uveitis intermediet, uveitis posterior, dan panuveitis
• Etiologi:
– infeksi (bakteri, virus, jamur, dan parasit), non-infeksi, dan idiopatik.
• Perjalanan penyakit
– Akut (onset mendadak dan durasi kurang dari empat minggu),
– Rekuren (episode uveitis berulang),
– Kronik (uveitis persisten atau kambuh sebelum tiga bulan setelah
pengobatan dihentikan), dan
– Remisi (tidak ada gejala uveitis selama tiga bulan atau lebih)

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis anterior
• Inflamasi di iris (iritis) dan badan siliar (siklitis).
Bila inflamasi meliputi iris dan badan siliar maka
disebut iridosiklitis
• Etiologi :
– kelainan sistemik seperti spondiloartropati, artritis
idiopatik juvenil, sindrom uveitis fuchs, kolitis
ulseratif, penyakit chron, penyakit whipple,
tubulointerstitial nephritis and uveitis
– Infeksi yang sering menyebabkan uveitis anterior
adalah virus herpes simpleks (VHS), virus varisela
zoster (VVZ), tuberkulosis, dan sifilis.

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Diagnosis Uveitis Anterior
• Gejala Klinis : • Tanda
– mata merah – injeksi siliar akibat
– visus turun akibat kekeruhan vasodilatasi arteri siliaris
cairan akuos dan edema posterior longus dan arteri
kornea walaupun uveitis tidak siliaris anterior yang
selalu menyebabkan edema memperdarahi iris serta
kornea badan siliar.
– Nyeri tumpul berdenyut, dan – Bilik mata depan : pelepasan
fotofobia akibat spasme otot sel radang, pengeluaran
siliar dan sfingter pupil protein (cells and flare) dan
– Jika disertai nyeri hebat, endapan sel radang di endotel
perlu dicurigai peningkatan kornea (presipitat keratik).
tekanan bola mata. – Presipitat keratik halus 
– Spasme sfingter pupil inflamasi nongranulomatosa;
mengakibatkan miosis dan – Presipitat keratik kasar 
memicu sinekia posterior. inflamasi granulomatosa

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Pemeriksaan Lab pada JIA
Pemeriksaan yang biasa dilakukan
• ANA - Autoantibodies, dapat 80% positif pada pasien dengan
keterlibatan mata
• Rheumatoid Factor – dapat positif atau negative, lebih ditemukan
pada orang dewasa dengan penyakit rheumatoid arthritis
• ESR atau CRP – untuk mendeteksi inflamasi

Lainya:
• HLA-B27 untuk mengeksklusi arthritis lainnya yang terutama
mempengaruhi tulang belakang (ankylosing spondylitis)
• Analisis cairan sendi untuk mendeteksi tanda-tanda infeksi pada
sendi
• Kultur darah untuk mengeksklusi infeksi.

American Association of Clinical Chemistry. Juvenile Idiopathic Arthritis. 2017

 43-44. Congenital Nasolacrimal Duct
Obstruction (CNDO)
• Embriology
– This condition affects nearly 20 % of all newborns
– The development of the lacrimal drainage system begins at
approximately 6 weeks of gestation
– Communication between the lacrimal drainage system and
the nose occurs at the end of the sixth month.
– Tears are normally produced a few weeks after birth;
hence nasolacrimal duct (NLD) obstruction may not be
recognised until several weeks after birth.

• Etiology :
– Most commonly, this is due to the presence of a
membrane at the level of the valve of Hasner, which is
present at the nasal opening of the nasolacrimal duct
Murthy R. Congenital Nasolacrimal Duct Obstruction (CNLDO). Kerala Journal of Ophthalmology. 2007.9:2
Congenital nasolacrimal duct obstruction

Epiphora and matting Infrequently acute dacryocystitis

 Treatment
• one third: bilateral
• Role out congenital glaucoma 
fotophobia
• Conservative management by
massage can be done safely upto 1
year of age;
• the reason being most of the cases
(96 %) will resolve within the first
year of life
• Massage of nasolacrimal duct: 10
strokes 4 times a day
• antibiotic drops 4 times daily for
mucopurulent discharge
• If no improvement - probe at 12
months
• Results - 90% cure by first probing
, 6% by repeated probing
 45. Horner Syndrome
• a classic neurologic
syndrome whose signs
include miosis, ptosis,
and anhidrosis.
• Also called
oculosympathetic paresis,
a Horner syndrome can
be produced by a lesion
anywhere along the
sympathetic pathway
that supplies the head,
eye, and neck.
No Terms Definition
1 Adie pupil ( is a neurological disorder that causes one or both pupils
Holmes-Adie to be abnormally dilated (mydriasis) with delayed
Syndrome) constriction in response to exposure to light. Patients
commonly present with areflexia of the knee and/or
ankles in addition to tonic pupil
2 Senile miosis the reduction in diameter occurs gradually with aging,
decreasing from a mean of 8 mm in the third decade to 6
mm in the seventh decade and 5 mm in the tenth decade
of life
Results from a relatively higher rate of aging atrophy in
the radial dilator muscles, which dilate the pupil,
compared to the sphincter constrictor muscles, which
constrict it  the sphincter is constantly dominant in the
elderly, causing persistent constriction.
3 Argyll Robertson irregular and smaller than normal in darkness and
pupil demonstrate lack of the pupillary light reflex with
preserved pupillary constriction during accommodation
and convergence for near objects.
 46. KONJUNGTIVITIS VERNAL
• Nama lain:
– spring catarrh/seasonal conjunctivitis/warm weather conjunctivitis
– Disebut vernal karena exaserbasi paling sering pada musim semi
(spring)
• Etiologi: reaksi hipersensitivitas bilateral (alergen sulit diidentifikasi)
• Epidemiologi:
– Dimulai pada masa prepubertal, bertahan selama 5-10 tahun sejak
awitan
– Laki-laki > perempuan
– Paling sering pada Afrika Sub-Sahara & Timur Tengah
– Temperate climate > warm climate > cold climate (hampir tidak ada)
– Terkait dengan manifestasi atopi lainnya seperti asma dan rinitis alergi
pada setengah kasus

Vaughan & Asbury General Ophtalmology 17th ed.

 Pathogenesis of Vernal Conjunctivitis
• Classic IgE mediated Hypersensitivity
– Evidence supporting an atopic origin :
• Seasonal incidence, eosinofil and mast cells in conjunctiva,
Play a
igE serum and tears, response to major role
mast cells stabilazer
• Th2 cells mediated respone
• Ig G mediated response
• Basofilic hypersensitivity
• Cellular delayed type hypersensitivity
(Hypersensitivity Type IV)
• Gejala & tanda:
– Rasa gatal yang hebat, dapat
disertai fotofobia
– Sekret ropy
– Riwayat alergi pada RPD/RPK
– Tampilan seperti susu pada
konjungtiva
– Gambaran cobblestone
(papila raksasa berpermukaan
rata pada konjungtiva tarsal)
– Tanda Maxwell-Lyons (sekret
menyerupai benang &
pseudomembran fibrinosa
halus pada tarsal atas, pada • Komplikasi:
pajanan thdp panas) • Blefaritis & konjungtivitis
– Bercak Trantas (bercak stafilokokus
keputihan pada limbus saat
fase aktif penyakit)
– Dapat terjadi ulkus kornea
superfisial
Vaughan & Asbury General Ophtalmology 17th ed.
 Tatalaksana
• Self-limiting
• Akut:
• Steroid topikal (+sistemik
bila perlu), jangka pendek
 mengurangi gatal
(waspada efek samping:
glaukoma, katarak, dll.)
• Vasokonstriktor topikal
• Kompres dingin & ice
pack
• Jangka panjang & prevensi
sekunder:
• Antihistamin topikal
• Stabilisator sel mast Sodium
kromolin 4%: sebagai
pengganti steroid bila gejala
sudah dapat dikontrol
• Tidur di ruangan yang sejuk
dengan AC
• Siklosporin 2% topikal (kasus
berat & tidak responsif)
• Desensitisasi thdp antigen
(belum menunjukkan hasil
baik)
Vaughan & Asbury General Ophtalmology 17th ed.
 47. KONJUNGTIVITIS NEONATAL
• Bacterial conjunctivitis contracted by newborns during delivery
• Cause:
– Neisseria gonorrhoeae ( inkubasi 2-7 hari)
– Chlamydia trachomatis (inkubasi 5-14 hari)
– S. Aureus (inkubasi nongonokokal dan nonklamidial 5-14 hari)
• Mucopurulent discharge
• Chlamydial  less inflamed  eyelid swelling, chemosis, and
pseudomembrane formation
• Complication in chlamydia infection  pneumonia (10-20% kasus)
• Blindness in chlamydia rare and much slower to manifes than
gonococcal  caused by eyelid scarring and pannus
• Terapi konj. Klamidial  oral erythromycin (50 mg/kg/d divided qid)
for 14 days (because of the significant risk for life-threatening
pneumonia)

http://emedicine.medscape.com/article
Neisseria gonorrhoeae
• manifests in the first five days of life
• marked bilateral purulent
• discharge
• local inflammation  palpebral
• edema
• Complication  diffuse epithelial
edema and ulceration, perforation of
the cornea and endophthalmitis
• Gram-negative intracellular
diplococci on Gram stain
• Culture  Thayer-Martin agar
Chlamydia trachomatis
• 5 to 12 days after birth
• Mucopurulent discharge
• less inflamed  eyelid swelling,
chemosis, and
• pseudomembrane formation
• Complication  pneumonitis
(range 2 weeks – 19 weeks after
delivery)
• Blindness rare and much
slower to menifest caused by
eyelid scarring and pannus
 Microscopic Findings

Etiology Findings
Chemical PMNs, few lymphocytes
Chlamydia PMNs, lymphocytes, plasma cells, Leber
cells, intracytoplasmic basophilic
inclusions
Bacteria PMNs, bacteria
Virus Lymphocytes, plasma cells,
multinucleated giant cells, intranuclear
eosinophilic inclusion

http://80.36.73.149/almacen/medicina/oftalmologia/enciclopedias/duane/pages/v4/v4c006.html
 KONJUNGTIVITIS GO
• Neisseria gonorrhoeae Gram-negative intracellular
diplococci on Gram stain
• Masa inkubasi: 1-7 hari
• manifests in the first five days of life
• Marked bilateral purulent discharge
• local inflammation  palpebral edema
• Complication  diffuse epithelial edema and ulceration,
perforation of the cornea and endophthalmitis  kebutaan
• Culture  Thayer-Martin agar
• Topical erythromycin/tetrasiklin ointment and IV or IM
third-generation cephalosporin. Topical kloramfenikol 0,5-
1%
Non-Infectious • Nasolacrimal duct obstruction may cause ‘sticky’ eyes.
• Corneal abrasion following trauma at delivery.
• Glaucoma (watch for corneal clouding or proptosis, is associated with portwine stains in the ophthalmic
region).
• Foreign body.

Infectious Organism Age of Onset Clinical Features Therapy

# Uncommon,
potential for serious
consequences - severe
keratitis and Staphylococcus aureus 2-5 days Unilateral, crusted purulent Topical soframycin drops qds for 5
endophthalmitis.
Requires early Streptococcus discharge days
recognition and
treatment. Needs pneumoniae,
blood and CSF culture.
Consider concomitant Haemophilus spp,
chlamydial infection if
poor response to Enterococci
cephalosporin.
Parents require
investigation and Neisseria gonorrhoeae # 3 days to 3 Bilateral, hyperaemic, Ceftriaxone 50mg/kg IV/IM as a
screening.
+ Risk of rapid Infants who are positive weeks chemosis, copious thick single dose (maximum 125mg),
progression from
purulent discharge to need to be evaluated for white discharge Saline irrigations hourly until exudate
denuding of corneal
epithelium, and disseminated infections resolves.
perforation of cornea.
The anterior chamber
can fill with fibrinous
exudate, iris can
Pseudomonas 5-18 days Oedema and erthyema of lid, IV anti-pseudomonal antibiotics.
adhere to cornea and
later blood vessel
aeruginosa + purulent discharge.
invasion. The late Topical Gentamicin.
ophthalmic
complications can be
followed by Chlamydia trachomatis * 5-14 days Unilateral or bilateral, mild PO erythromycin 50mg/kg/day x 14d
bacteraemia and
septic foci. conjunctivitis, copious (qid)Alternative, 5 days Azithromycin
* Most common
pathogen, 20-50% of purulent discharge. syrup
exposed infants will
develop chlamydia (= pertussis dosing 10mg/kg/day and
conjunctivitis, 10-20%
will develop 5mg/kg day 2-5)
pneumonia. If relapse
occurs repeat course
of erythromycin for Herpes simplex Conjunctivitis with vesicles Acyclovir 30mg/kg/day IV tid x 14-
further 14 days.
Parents require elsewhere 21d.
treatment.
Need ophthalmology review
within 24 hours. Topical acyclovir 3% 5 times daily.
http://www.adhb.govt.nz/newborn/guidelines/infection/neonatalconjunctivitis.htm
 Conjunctivits GO Treatment
• Infants with ophthalmic disease
– Infants with gonococcal ophthalmic disease should be
hospitalized and observed for response to therapy and for
disseminated disease.
– Treatment consists of:
• a single dose of ceftriaxone (25 to 50 mg/kg, not to exceed 125 mg,
intravenously [IV] or intramuscularly [IM])
• Where available, a single dose of cefotaxime (100 mg/kg, IV or IM) is
an alternative option and is preferred for neonates with
hyperbilirubinemia and those receiving calcium-containing IV
solutions (eg, parenteral nutrition)
• If cefotaxime is unavailable, ceftazidime is another alternative
• Topical antibiotic therapy alone is inadequate and is not necessary
when systemic treatment is provided.
• The eyes should be irrigated frequently with saline until the discharge
clears.
TO 5
 48. Dakriosistitis

Kumpulan faktor risiko penyakit kardiovaskular yang terjadi

secara bersamaan pada seorang individu, antara lain:
peningkatan GDP, obesitas sentral, dislipidemia, dan HT.
 Dakriosistitis

• Obstruksi parsial atau komplit dari duktus nasolakrimalis

dengan inflamasi yang disebabkan oleh infeksi, tumor,
benda asing, posttrauma atau penyakit granuloma.
 Dakriosistitis

• Treatment (selain AB): irigasi,

Dacryocystorhinotomy

• Diagnosis: Anel test (+)  bukan dakriosistitis, kemungkinan abses

kulit. Sedangkan bila (-) atau regurgitasi (+)  dakriosistitis.
• Saran lanjutan swab dan kultur
 Dakriosistitis

STAGING KRONIK
• Catharral: ntermittent conjunctival hyperaemia and
epiphora, with mucoid discharge (normally sterile).
• Lacrimal sac mucocele: stagnant tears collect, dilation of
the lacrimal sac (with mucoid content)
• Chronic suppurative: epiphora and chronic conjunctivitis,
erythema of the lacrimal sac, reflux of purulent material
with pressure
 Dakriosistitis

STAGING KRONIK
• Catharral: ntermittent conjunctival hyperaemia and
epiphora, with mucoid discharge (normally sterile).
• Lacrimal sac mucocele: stagnant tears collect, dilation of
the lacrimal sac (with mucoid content)
• Chronic suppurative: epiphora and chronic conjunctivitis,
erythema of the lacrimal sac, reflux of purulent material
with pressure
 49. CMV Retinitis
• Coinfection with CMV occurs in 75-85% of the patients with HIV
infection, of whom, more than a half develop CMV retinitis
• Cytomegalovirus retinitis is the most common ocular opportunistic
infection, representing 90% of the infectious retinitis, 20-30% of the
patients with AIDS develop CMV retinitis.
• It usually occurs in the late stages of the disease (about 18 months
after the declaration of the clinical onset) in patients with a lower
limit of CD4 levels of 50/mmc
• CMV infection classically produces a hemorrhagic, necrotic retinitis
that can destroy the entire retina if left untreated.
• Frequency of bilateral presentation of newly diagnosed CMV
retinitis varies among studies but seems to be between 35% and
45%.

WHO. Ophtalmic complication of HIV Infection

 Clinical Manifestation
• floaters,
• blurred vision,
• Visual field defects, and
• flashing lights/sparks.
• Even subtle changes, such
as a minor loss of
peripheral vision, can
indicate the development
of CMV retinitis.
• There is usually no pain
involved.
• Progressive CMV retinitis
include
– a dry-appearing, granular
border with little vitreous
inflammation.
– Edema and necrosis are
also known to cause
irregular patches of retinal
whitening.
– A “brushfire” pattern
emerges when a
photograph of the lesion is
enlarged
 50. Relative Afferent
Pupillary Defect (RAPD)
• The physiological basis of the RAPD test is that, in
healthy eyes, the reaction of the pupils in the right and
left eyes are linked  consensual light reflex.
• light reflex pathway has two parts :
1. The afferent part of the pathway (red) refers to the
nerve impulse/message sent from the pupil to the brain
along the optic nerve when a light is shone in that eye.
2. The efferent part of the pathway (blue) is the
impulse/message that is sent from the mid-brain back to
both pupils via the ciliary ganglion and the third cranial
nerve (the oculomotor nerve), causing both pupils to
constrict, even though only one eye is being stimulated
by the light
Broadway DC. Relative Afferent Pupillary Defect. Community Eye Health Journal | VolUME 25 ISSUES 79 & 80 | 2012
 • Common causes of unilateral • A RAPD is an extremely important
optic nerve disorders that can be localising clinical sign that can be
associated with a RAPD include : detected by a simple, quick, non-
– Maculopathy (retinal detachment, invasive clinical test, provided
major retinal vascular occlusion, that the test is performed
extensive retinal damage) carefully and correctly
– ischaemic optic neuropathy, • The ‘swinging light test’ is used to
– optic neuritis, detect a relative afferent pupil
– optic nerve compression (orbital defect (RAPD)
tumours or dysthyroid eye
disease), • A positive RAPD means there are
– trauma, and differences between the two eyes
– asymmetric glaucoma. in the afferent pathway due to
retinal or optic nerve disease.
• Less common causes include
– infective, infiltrative,
carcinomatous, or radiation optic
neuropathy.

Broadway D.C.How to test for a relative afferent pupillary defect. Community eye health journal: 25(79). 2012
 Swinging light test
• The swinging light test :
– Used to detect a RAPD; detecting differences between the
two eyes in how they respond to a light shone in one eye
at the time
• The test can be very useful for detecting unilateral or
asymmetrical disesase of the retina or optic nerve (but
only optic nerve disease that occurs in front of the
optic chiasm)
• Interpretation:
– Swinging light test Normal
– Swinging light test positif RAPD
– Swinging light test negatif  non reactive pupil
 The swinging light test
Swinging light test Normal Swinging light test + Swinging light test -
 51. UVEITIS
•Uveitis :
–inflamasi di uvea
yaitu iris, badan siliar
dan koroid yang
dapat menimbulkan
kebutaan.
–Di negara maju,
10% kebutaan pada
populasi usia
produktif adalah
akibat uveitis
 Klasifikasi
• The International Uveitis Study Group (IUSG) dan The
Standardization of Uveitis Nomenclatur (SUN) membagi uveitis
berdasarkan anatomi, etiologi, dan perjalanan penyakit
• Anatomi :
– uveitis anterior, uveitis intermediet, uveitis posterior, dan panuveitis
• Etiologi:
– infeksi (bakteri, virus, jamur, dan parasit), non-infeksi, dan idiopatik.
• Perjalanan penyakit
– Akut (onset mendadak dan durasi kurang dari empat minggu),
– Rekuren (episode uveitis berulang),
– Kronik (uveitis persisten atau kambuh sebelum tiga bulan setelah
pengobatan dihentikan), dan
– Remisi (tidak ada gejala uveitis selama tiga bulan atau lebih)

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Uveitis anterior
• Inflamasi di iris (iritis) dan badan siliar (siklitis).
Bila inflamasi meliputi iris dan badan siliar maka
disebut iridosiklitis
• Etiologi :
– kelainan sistemik seperti spondiloartropati, artritis
idiopatik juvenil, sindrom uveitis fuchs, kolitis ulseratif,
penyakit chron, penyakit whipple, tubulointerstitial
nephritis and uveitis
– Infeksi yang sering menyebabkan uveitis anterior
adalah virus herpes simpleks (VHS), virus varisela
zoster (VVZ), tuberkulosis, dan sifilis.

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 Diagnosis Uveitis Anterior
• Gejala Klinis : • Tanda
– mata merah – injeksi siliar akibat
– visus turun akibat kekeruhan vasodilatasi arteri siliaris
cairan akuos dan edema posterior longus dan arteri
kornea walaupun uveitis tidak siliaris anterior yang
selalu menyebabkan edema memperdarahi iris serta
kornea badan siliar.
– Nyeri tumpul berdenyut, dan – Bilik mata depan : pelepasan
fotofobia akibat spasme otot sel radang, pengeluaran
siliar dan sfingter pupil protein (cells and flare) dan
– Jika disertai nyeri hebat, endapan sel radang di endotel
perlu dicurigai peningkatan kornea (presipitat keratik).
tekanan bola mata. – Presipitat keratik halus 
– Spasme sfingter pupil inflamasi nongranulomatosa;
mengakibatkan miosis dan – Presipitat keratik kasar 
memicu sinekia posterior. inflamasi granulomatosa

Sitompul R. Diagnosis dan Penatalaksanaan Uveitis dalam Upaya Mencegah Kebutaan. Jurnal universitas Indonesia. Vol. 4, No. 1, April 2016
 No. Jenis Keterangan
Pemeriksaan
Penunjang pada
Uveitis
1 Slit lamp menilai segmen anterior injeksi siliar dan episklera, skleritis,
edema kornea, presipitat keratik, bentuk dan jumlah sel di bilik
mata, hipopion serta kekeruhan lensa
2 Oftalmoskop menilai kelainan di segmen posterior seperti vitritis, retinitis, perdarahan
retina, koroiditis dan kelainan papil nervus optik

3 Pemeriksaan
laboratorium
4 Optical coherence
tomography (OCT)
5 USG B –scan
bermanfaat pada kelainan sistemik misalnya darah perifer lengkap, laju
endap darah, serologi, urinalisis, dan antinuclear antibody
merupakan pemeriksaan non-invasif yang dapat memperlihatkan edema
makula, membran epiretina, dan sindrom traksi vitreomakula
sangat membantu memeriksa segmen posterior mata pada keadaan
media keruh misalnya pada katarak dan vitritis

6 Fundus fluoresen
angiografi (FFA)
fotografi fundus yang dilakukan berurutan dengan cepat setelah injeksi
zat warna natrium fluoresen (FNa) intravena.
FFA memberikan informasi mengenai sirkulasi pembuluh darah retina dan
koroid, detail epitel pigmen retina dan sirkulasi retina serta menilai
integritas pembuluh darah saat fluoresen bersirkulasi di koroid dan retina.
 52. KELAINAN REFRAKSI -MIOPIA
• Miopia secara klinis :
– Simpleks: kelainan fundus ringan, < -6D
– Patologis: Disebut juga sebagai miopia degeneratif, miopia maligna atau
miopia progresif, adanya progresifitas kelainan fundus yang khas pada
pemeriksaan oftalmoskopik, > -6D
• Miopia berdasarkan ukuran dioptri lensa :
– Ringan : lensa koreksinya 0,25 s/d 3,00 Dioptri
– Sedang : lensa koreksinya 3,25 s/d 6,00 Dioptri.
– Berat : lensa koreksinya > 6,00 Dioptri.
• Miopia berdasarkan umur :
– Kongenital : sejak lahir dan menetap pada masa anak-anak.
– Miopia onset anak-anak : di bawah umur 20 tahun.
– Miopia onset awal dewasa : di antara umur 20 sampai 40 thn.
– Miopia onset dewasa : di atas umur 40 tahun (> 40 tahun).
 52. Degenerative/ Progressive/
Pathological Myopia
• Progressive retinal and choroidal degeneration in myopic eyes of at least - 6.00
Diopter refractive errors with an axial length of more than 26 mm.
• Progressive chorioretinal stretching results in characteristic fundus findings:
– Optic disc crescent, area of depigmentation due to dragging of the choroids and RPE
from the optic nerve
– Ruptures of Bruch's membrane (lacquer crack)
– Focal areas of chorioretinal atrophy
– Localized ectasia involving the sclera, the pigment epithelium and the choroid
(posterior staphyloma)
– Oval with vertical axis and slightly tilted optic disc
– Localized areas of pigment epithelial proliferation (Foerster-Fuchs spots)
– Lattice degeneration in the pre-equatorial area may be found
– Thinning of the RPE and the choriocapillaris give a 'tigroid' or 'tesselated' fundus
appearance
 As the eye enlarges, the retinal pigment epithelium thins, resulting in a tessellated
(checkered) appearance of the fundus and increased visibility of the choroidal vasculature.
POSTERIOR STAPHYLOMA: Staphylomas are localized ectasia (“enlargement”)
of the sclera, choroid, and RPE. It can be easily seen on a B-scan or CT Scan.
Staphylomas can eventually lead to atrophy and loss of vision.
Lacquer cracks are spontaneous ruptures of the elastic lamina of Bruch’s
membrane that appear yellowish-white and are usually located in the posterior
pole. They generally have linear or stellate patterns. IVFA will show
hyperfluorescence as the fluorescein leaks through Bruch’s membrane,
highlighting these cracks. These can lead to CNV in the 4th-6th decade of life.
 FUCHS SPOTS: Fuchs spots are dark spots due to RPE hyperplasia. They can involve
subretinal neovascular membrane with an overlying retinal pigment epithelial
hyperplasia. The CNV can eventually cause disciform scars on the macula in the 4th-
6th decade of life.
Myopic
Crescent

Lacquer cracks
TO 6
 53. Konjungtivitis Alergi
• Allergic conjunctivitis may be divided into 5
major subcategories.
• Seasonal allergic conjunctivitis (SAC) and
perennial allergic conjunctivitis (PAC) are
commonly grouped together.
• Vernal keratoconjunctivitis (VKC), atopic
keratoconjunctivitis (AKC), and giant papillary
conjunctivitis (GPC) constitute the remaining
subtypes of allergic conjunctivitis.
 Konjungtivitis Atopi
• Biasanya ada riwayat atopi • Terapi topikal jangka
• Gejala + Tanda: sensasi panjang: cell mast stabilizer
terbakar, sekret mukoid • Antihistamin oral
mata merah, fotofobia • Steroid topikal jangka
• Terdapat papila-papila halus pendek dapat meredakan
yang terutama ada di tarsus gejala
inferior
• Jarang ditemukan papila
raksasa
• Karena eksaserbasi datang
berulanga kali 
neovaskularisasi kornea,
sikatriks
 Konjungtivitis Atopik

Papila halus pada konjungtiva

tarsal superior dan inferior

Keratokonjungtivitis atopik disertai

vaskularisasi  tindakan:
transplantasi kornea
 Etiologi Diagnosis Karakteristik
Viral Konjungtivitis folikuler Merah, berair mata, sekret minimal, folikel sangat
akut mencolok di kedua konjungtiva tarsal
Klamidia Trachoma Seringnya pd anak, folikel dan papil pd konjungtiva
tarsal superior disertai parut, perluasan pembuluh
darah ke limbus atas
Konjungtivitis inklusi Mata merah, sekret mukopurulen (pagi hari), papil
dan folikel pada kedua konjungtiva tarsal (terutama
inferior)
Alergi/hiper- Konjungtivitis vernalis Sangat gatal, sekret berserat-serat, cobblestone pd
sensitivitas konjungtiva tarsal superior, horner-trantas dots
(limbus)
Konjungtivitis atopik Sensasi terbakar, sekret berlendir, konjungtiva
putih spt susu, papil halus pada konjungtiva tarsal
inferior
Konjungtivitis Reaksi hipersensitif tersering akibat protein TB,
fliktenularis nodul keabuan di limbus atau konjungtiva bulbi,
mata merah dan berair mata
Autoimun Keratokonjungtivitis sicca Akibat kurangnya film air mata, tes shcirmer
abnormal, konjungtiva bulbi hiperemia, sekret
mukoid, semakin sakit menjelang malam dan
berkurang pagi
 Tatalaksana Konjungtivitis Alergi
• Self-limiting • Jangka panjang & prevensi
• Akut: sekunder:
• Antihistamin topikal
• Steroid topikal (+sistemik • Stabilisator sel mast Sodium
kromolin 4%: sebagai
bila perlu), jangka pengganti steroid bila gejala
pendek  mengurangi sudah dapat dikontrol
gatal (waspada efek • Tidur di ruangan yang sejuk
dengan AC
samping: glaukoma, • Siklosporin 2% topikal (kasus
katarak, dll.) berat & tidak responsif)

• Vasokonstriktor topikal • Desensitisasi thdp antigen

(belum menunjukkan hasil
• Kompres dingin & ice baik)
pack

Vaughan & Asbury General Ophtalmology 17th ed.

Allergic Conjunctivitis
 54. Congenital Nasolacrimal Duct
Obstruction (CNDO)
• Embriology
– This condition affects nearly 20 % of all newborns
– The development of the lacrimal drainage system begins at
approximately 6 weeks of gestation
– Communication between the lacrimal drainage system and
the nose occurs at the end of the sixth month.
– Tears are normally produced a few weeks after birth;
hence nasolacrimal duct (NLD) obstruction may not be
recognised until several weeks after birth.

• Etiology :
– Most commonly, this is due to the presence of a
membrane at the level of the valve of Hasner, which is
present at the nasal opening of the nasolacrimal duct
Murthy R. Congenital Nasolacrimal Duct Obstruction (CNLDO). Kerala Journal of Ophthalmology. 2007.9:2
Congenital nasolacrimal duct obstruction

Epiphora and matting Infrequently acute dacryocystitis

 Treatment
• one third: bilateral
• Role out congenital glaucoma 
fotophobia
• Conservative management by
massage can be done safely upto 1
year of age;
• the reason being most of the cases
(96 %) will resolve within the first
year of life
• Massage of nasolacrimal duct: 10
strokes 4 times a day
• antibiotic drops 4 times daily for
mucopurulent discharge
• If no improvement - probe at 12
months
• Results - 90% cure by first probing,
6% by repeated probing
 DAKRIOSISTITIS
• Partial or complete obstruction of the nasolacrimal duct
with inflammation due to infection (Staphylococcus aureus
or Streptococcus B-hemolyticus), tumor, foreign bodies,
after trauma or due to granulomatous diseases.
• Clinical features : epiphora, acute, unilateral, painful
inflammation of lacrimal sac, pus from lacrimal punctum,
fever, general malaise, pain radiates to forehead and teeth
• Diagnosis : Anel test(+) :not dacryocystitis, probably skin
abcess; (-) or regurgitation (+) : dacryocystitis. Swab and
culture
• Treatment : Systemic and topical antibiotic, irrigation of
lacrimal sac, Dacryocystorhinotomy
 55. KELAINAN REFRAKSI: HIPERMETROPIA
ANAMNESIS

MATA MERAH MATA MERAH MATA TENANG

MATA TENANG VISUS
VISUS NORMAL VISUS TURUN VISUS TURUN
TURUN MENDADAK
• struktur yang PERLAHAN
mengenai media
bervaskuler 
refraksi (kornea, • uveitis posterior • Katarak
sklera konjungtiva •
uvea, atau perdarahan vitreous • Glaukoma
• tidak • Ablasio retina • retinopati
seluruh mata)
menghalangi • oklusi arteri atau vena penyakit sistemik
media refraksi retinal • retinitis
• neuritis optik pigmentosa
• Keratitis
• Konjungtivitis murni • neuropati optik akut • kelainan refraksi
• Keratokonjungtivitis
• Trakoma karena obat (misalnya
• Ulkus Kornea
• mata kering, etambutol), migrain,
• Uveitis
tumor otak
xeroftalmia • glaukoma akut
• Pterigium • Endoftalmitis
• Pinguekula • panoftalmitis
• Episkleritis
• skleritis
 HIPERMETROPIA
• Gangguan kekuatan pembiasan mata dimana sinar
sejajar jauh tidak cukup dibiaskan sehingga titik
fokusnya terletak di belakang retina (di belakang
makula lutea)
• Etiologi :
– sumbu mata pendek (hipermetropia aksial),
– kelengkungan kornea atau lensa kurang (hipermetropia
kurvatur),
– indeks bias kurang pada sistem optik mata (hipermetropia
refraktif)
• Gejala : penglihatan jauh dan dekat kabur, sakit kepala,
silau, rasa juling atau diplopia

Ilmu Penyakit Mata, Sidharta Ilyas ; dasar – teknik Pemeriksaan dalam Ilmu Penyakit Mata, sidarta Ilyas
 HIPERMETROPIA
• Pengobatan : Pemberian lensa sferis
positif akan meningkatkan kekuatan
refraksi mata sehingga bayangan
akan jatuh di retina
• koreksi dimana tanpa siklopegia
didapatkan ukuran lensa positif
maksimal yang memberikan tajam
penglihatan normal (6/6), hal ini
untuk memberikan istirahat pada
mata.
• Jika diberikan dioptri yg lebih kecil,
berkas cahaya berkonvergen namun
tidak cukup kuat sehingga bayangan
msh jatuh dibelakang retina,
akibatnya lensa mata harus
berakomodasi agar bayangan jatuh
tepat di retina.
• Contoh bila pasien dengan +3.0 atau
dengan +3.25 memberikan tajam
penglihatan 6/6, maka diberikan
kacamata +3.25
Ilmu Penyakit Mata, Sidharta Ilyas
 BENTUK HIPERMETROPIA
• Hipermetropia total = laten + manifest
– Hipermetropia yang ukurannya didapatkan sesudah diberikan siklopegia
• Hipermetropia manifes = absolut + fakultatif
– Yang dapat dikoreksi dengan kacamata positif maksimal dengan hasil visus 6/6
– Terdiri atas hipermetropia absolut + hipermetropia fakultatif
– Hipermetropia ini didapatkan tanpa siklopegik
• Hipermetropia absolut :
– “Sisa”/ residual dari kelainan hipermetropia yang tidak dapat diimbangi
dengan akomodasi
– Hipermetropia absolut dapat diukur, sama dengan lensa konveks terlemah
yang memberikan visus 6/6

Ilmu Penyakit Mata, Sidharta Ilyas

 BENTUK HIPERMETROPIA

• Hipermetropia fakultatif :
– Dimana kelainan hipermetropia dapat diimbangi sepenuhnya dengan
akomodasi
– Bisa juga dikoreksi oleh lensa
– Dapat dihitung dengan mengurangi nilai hipermetrop manifes – hipermetrop
absolut
• Hipermetropia laten:
– Hipermetropia yang hanya dapat diukur bila diberikan siklopegia
– bisa sepenuhnya dikoreksi oleh tonus otot siliaris
– Umumnya lebih sering ditemukan pada anak-anak dibandingkan dewasa.
– Makin muda makin besar komponen hipermetropia laten, makin tua akan
terjadi kelemahan akomodasi sehingga hipermetropia laten menjadi fakultatif
dan kemudia menjadi absolut

Ilmu Penyakit Mata, Sidharta Ilyas & Manual of ocular diagnosis and therapy
• Contoh pasien hipermetropia, 25 tahun, tajam penglihatan
OD 6/20
– Dikoreksi dengan sferis +2.00  tajam penglihatan OD 6/6
– Dikoreksi dengan sferis +2.50  tajam penglihatan OD 6/6
– Diberi siklopegik, dikoreksi dengan sferis +5.00  tajam penglihatan
OD 6/6
ARTINYA pasien memiliki:
– Hipermetropia absolut sferis +2.00 (masih berakomodasi)
– Hipermetropia manifes Sferis +2.500 (tidak berakomodasi)
– Hipermetropia fakultatif sferis +2.500 – (+2.00)= +0.50
– Hipermetropia laten sferis +5.00 – (+2.50) = +2.50
 56. Trauma Mekanik Bola Mata
• Cedera langsung berupa ruda
paksa yang mengenai jaringan
mata.
• Beratnya kerusakan jaringan
bergantung dari jenis trauma
serta jaringan yang terkena
• Gejala : penurunan tajam
penglihatan; tanda-tanda
trauma pada bola mata
• Komplikasi :
 Endoftalmitis
 Uveitis
 Perdarahan vitreous
 Hifema
 Retinal detachment
 Glaukoma
 Oftalmia simpatetik
Panduan Tatalaksana Klinik RSCM Kirana, 2012
• Pemeriksaan Rutin :
 Visus : dgn kartu Snellen/chart
projector + pinhole
 TIO : dgn tonometer
aplanasi/schiotz/palpasi
 Slit lamp : utk melihat segmen
anterior
 USG : utk melihat segmen
posterior (jika memungkinkan)
 Ro orbita : jika curiga fraktur
dinding orbita/benda asing
• Tatalaksana :
 Bergantung pada berat trauma,
mulai dari hanya pemberian
antibiotik sistemik dan atau
topikal, perban tekan, hingga
operasi repair
 Ocular Foreign body
• An ocular foreign body :
– common condition, in which a small particle (such as a
piece of grit or small rust particle) becomes stuck on eye.
• Corneal foreign body  CA stuck on the eye ;
• sub-tarsal foreign body  the object is stuck under your lid
scratches to the surface of your cornea.
– Symptoms
• painful, red, watery and light sensitive and ↓ vision
• Subconjunctival hemorrhage
• Corneal laceration and abrasion  heal within 48 hours after
removal
• if CA is metal, a small ring of rust may form around it  a dark
spot on the white of eye and can cause a scar that may affect
vision
 Management
• First aid
– Wash the eye with water or saline. Do not try to
remove a foreign body yourself.  Go straight to
doctor
• Emergency departement
1. Local anaesthetic eye drops to numb the eye  pain
may return after the anaesthetic drops wear off, 20
to 60 minutes.
2. Remove the foreign body with a cotton bud or a
small sterile needle
3. Painkiller  PCT or ibuprofen
4. Antibiotic drops or oinment to prevent infection

www.moorfields.nhs.uk
 Benda Asing di Konjungtiva
•
• Gejala :
– nyeri, mata merah dan berair,
sensasi benda asing, dan
fotofobia.
• Faktor Risiko
– Pekerja di bidang industri yang
tidak memakai kacamata
pelindung, seperti: pekerja
gerinda, pekerja las,
pemotong keramik, pekerja
yang terkait dengan bahan-
bahan kimia (asam-basa), dll.
• Pemeriksaan Fisik
– Biasanya visus normal;
– Ditemukan injeksi
konjungtiva tarsal dan/atau
bulbi
– Pada konjungtiva tarsal
Penatalaksanaan (menurut buku panduan layanan
primer IDI & emedicine)
– Berikan tetes mata pantokain 2% sebanyak 1-2
tetes pada mata yang terkena benda asing.
– Gunakan kaca pembesar (lup) dalam
pengangkatan benda asing.
– Periksa lokasi benda asing dengan meminta
pasien melihat ke atas, ke bawah, kiri, dan kanan
– Periksa inferior conjunctival cul-de-sac dengan
meminta pasien melihat ke atas ketika pemeriksa
membuka kelopak mata bawah
– Untuk memeriksa superior conjunctival cul-de-
sac, lakukan eversi kelopak mata atas dengan
kapas lidi atau paper clip (seperti gambar)
– Angkat benda asing dengan menggunakan lidi
kapas yang lembab atau jarum suntik ukuran
23G.
– Arah pengambilan benda asing dilakukan dari
tengah ke tepi.
– Oleskan lidi kapas yang dibubuhkan betadin pada
tempat bekas benda asing.
– Kemudian, berikan antibiotik topikal (salep atau
tetes mata) seperti kloramfenikol tetes mata, 1
gtt setiap 2 jam selama 2 hari.
 Corneal Foreign Body
• If a corneal foreign body is discovered, it must be
removed to prevent permanent scarring and
vision loss. Saline irrigation is often successful.
• If irrigation is unsuccessful, a topical anesthetic
should be administered and a cotton swab gently
swept over the cornea.
• If the foreign body is superficial, irrigate the eye
to moisten the cornea and attempt to remove the
foreign body by using a gentle rolling motion with
a wetted cotton-tipped applicator.
– Take care not to apply pressure, which may push
the foreign body deeper into the cornea, or scrape,
which may create a large corneal abrasion.
• If swabbing is unsuccessful, foreign body removal
using an eye spud or 25-gauge needle should be
done by a trained, experienced physician.

Emedicine & AAFP

 57. Eyelid trauma
• Eyelid is specialized tissue • Eyelid margin has slightly
characterized by skin on rounded anterior edge and
anterior surface and mucous sharp posterior edge.
membrane – tarsal conjunctiva – Mucocutaneous junction
on its posterior. – Meibomian gland orifices
• Eyelid skin is thinnest in the – Gray line
body. – Eyelash follicles
• It has loose attachment and
absence of fat in corium.
• Lid contains muscle, glands,
blood vessels and nerves.
• The firmness to the lid is
provided with tarsus which is
dense fibrous tissue and not a
cartilage

Vichare N. Management of Eyelid Lacerations. DOS Times - Vol. 20, No. 8 February, 2015
 Eyelid laceration
• Eyelid lacerations are an important subtype of facial trauma
• Ocular injury (eg, open globe, traumatic hyphema, corneal abrasion) may
accompany eyelid laceration in up to two-thirds of cases.
 Eyelid Laceration
• Assume penetrating injury until proven
otherwise
• History: mechanism of trauma, symptoms: pain, altered
vision, etc
• Examination:
– visual acuity
– assess superficial structures: use a slit lamp/magnifying glass.
– rule out serious eye injury before wound closure — this may
require detailed funduscopic examination
– explore the wound fully to assess depth and rule out foreign
bodies — lid lacerations may appear deceptively superficial.
– Suspect damage to the nasolacrimal drainage system if a
laceration is present nasal to the upper or lower eyelid
punctumAnel test may be required.
 Repair of eyelid trauma
• Repairing of eyelid injuries
requires knowledge and
meticulous approach.
• Gentle tissue handling and proper
alignment should be done.
• Aim should be to achieve best
possible functional and cosmetic
outcome
• Timing of repair
– Every effort must be made to
reconstruct the injured
tissues as soon as possible.
– Primary repair can be done
even after 24 -48 hrs after the
patient is stabilized.
• Preoperative evaluation
– Detailed history is obtained to determine
time, course and circumstances of injury.
– Management of ocular injury starts after
traumatized patient is stabilized and life
threatening injuries are addressed
– Detailed ocular examination includes visual
acuity, ocular movements, intra ocular
pressure, pupillary reactions and posterior
segment examination.
– Eyelid trauma can be associated with
hyphema, angle recession or retinal
detachment.
– Globe injuries should be attended before lid
injuries.
– Systemic antibiotics should be started. 
Intravenous antibiotics are preferable for
severely contaminated wounds.
– Wounds are irrigated thoroughly to remove
all debris.
– Tetanus toxoid must be given to non-
immunized patients.
Refer to ophthalmologist if any of the following are present:
• laceration involving the lid margin
• possible damage to the nasolacrimal duct system (i.e.
punctum, canaliculus, common duct, or lacrimal sac) — a
laceration that is nasal to either the upper or lower eyelid
punctum.
• full thickness lid laceration
• extensive tissue loss or distortion of anatomy
• medial canthal tendon avulsion (suspect when there is
displacement, excessive rounding, or abnormal laxity of the
medial canthus)
• involvement of the levator aponeurosis of the upper eyelid
(producing ptosis) or the superior rectus muscle
• visible orbital fat in an eyelid laceration, indicating
penetration of the orbital septum. Such patients require CT
imaging and careful assessment of levator and extraocular
muscle function.
• associated ocular trauma requiring surgery (e.g. ruptured
globe, intraorbital foreign body)
 http://sdhawan.com/ophthalmology/lens&cataract.pdf E-mail: sdhawan@sdhawan.com

58. Cataract
• Any opacity of the lens or loss of transparency of the lens that causes
diminution or impairment of vision
• Classification : based on etiological, morphological, stage of maturity
• Etiological classification :
 Senile
 Traumatic (penetrating, concussion, infrared irradiation, electrocution)
 Metabolic (diabetes, hypoglicemia, galactosemia, galactokinase deficiency,
hypocalcemia)
 Toxic (corticosteroids, chlorpromazine, miotics, gold, amiodarone)
 Complicated (anterior uveitis, hereditary retinal and vitreoretinal disorder, high myopia,
intraocular neoplasia
 Maternal infections (rubella, toxoplasmosis, CMV)
 Maternal drug ingestion (thalidomide, corticosteroids)
 Presenile cataract (myotonic dystrophy, atopic dermatitis)
 Syndromes with cataract (down’s syndrome, werner’s syndrome, lowe’s syndrome)
 Hereditary
 Secondary cataract
• Morphological classification : • Sign & symptoms:
 Capsular – Near-sightedness (myopia
 Subcapsular shift) Early in the
 Nuclear development of age-related
cataract, the power of the
 Cortical lens may be increased
 Lamellar – Reduce the perception of
 Sutural blue colorsgradual
• Chronological classification: yellowing and opacification of
 Congenital (since birth) the lens
 Infantile ( first year of life) – Gradual vision loss
 Juvenile (1-13years) – Almost always one eye is
 Presenile (13-35 years) affected earlier than the
other
 Senile
– Shadow test +
Klasifikasi morfologi katarak

Oxford American Handbook of Ophthalmology 2011

Oxford American Handbook of Ophthalmology 2011
Oxford American Handbook of Ophthalmology 2011
Oxford American Handbook of Ophthalmology 2011
Klasifikasi Katarak Senilis Berdasarkan
Lokasi
Katarak nuklear
• kekeruhan terutama pada nukleus
dibagian sentral lensa.
• Terjadi akibat sklerosis nuklear;
nukleus cenderung menjadi gelap
dan keras (sklerosis), berubah dari
jernih menjadi kuning sampai
coklat.
• Biasanya mulai timbul sekitar usia
60-70 tahun dan progresivitasnya
lambat.
• Pengerasan yang progresif dari
nukleus lensa peningkatan
indeks refraksi lensa terjadi
perpindahan miopik (myopic shift),
dikenal sbg miopia lentikularis.
• Akibat myiopic shift,individu
dengan presbiopia dapat
membaca tanpa kacamata
(disebut penglihatan
kedua/second sight).
• Menyebabkan gangguan yang
lebih besar pada penglihatan jauh
daripada penglihatan dekat
• Bisa terjadi pada pasien diabetes
melitus dan miopia tinggi
• Bisa timbul diplopia monokular
(akbibat perubahan mendadak
indeks refraksi antara korteks dan
nuklear) dan gangguan
diskriminasi warna (terutama biru
dan ungu, akibat kuningnya lensa)
Klasifikasi Katarak Senilis Berdasarkan
Lokasi
Katarak kortikal
• Kekeruhan pada korteks lensa ( bisa di • Gejala katarak kortikal adalah
daerah anterior, posterior dan
equatorial korteks) fotofobia dari sumber cahaya
• Muncul pada usia 40-60 tahun dan fokal yang terus-menerus dan
progresivitasnya lambat. diplopia monokular
• Terdapat wedge-shape • Kekeruhan dimulai dari celah dan
opacities/cortical spokes atau
gambaran seperti ruji. vakoula antara serabut lensa oleh
• Efeknya terhadap fungsi penglihatan karena hidrasi oleh korteks.
bervariasi, tergantung dari jarak • Disebabkan oleh berkurangnya
kekeruhan terhadap aksial penglihatan
• Katarak kortikal umumnya tidak
protein total, asam amnio, dan
memberi gejala sampai tingkat kalium yang dihubungkan dengan
progresifitas lanjut ketika jari-jari peningkatan konsentrasi natrium
korteks membahayakan axis dan hidrasi lensa, diikuti oleh
penglihatan (penglihatan dirasakan
lebih baik pada cahaya terang ketika koagulasi protein.
pupil miosis.)
 Klasifikasi Katarak Senilis Berdasarkan
Lokasi
Katarak subkapsular posterior
(katarak cupuliformis)
• Terdapat pada korteks di dekat kapsul
posterior bagian sentral dan biasanya di • Kadang mengalami diplopia
aksial. monokular.
• Biasanya mulai timbul sekitar usia 40-60 • Sering terlihat pada pasien
tahun dan progresivitasnya cepat. yang lebih muda dibandingkan
• Sejak awal, menimbulkan gangguan dengan pasien katarak nuklear
penglihatan karena adanya keterlibatan / kortikal.
sumbu penglihatan.
• Gejala yang timbul adalah fotofobia dan
• Sering ditemukan pada pasien
penurunan visus dibawah kondisi cahaya DM, miopia tinggi dan retinitis
terang, akomodasi, atau miotikum. pigmentosa, akibat trauma,
• Penglihatan dirasakan lebih baik ketika penggunaan kortikosteroid
pupil midriasis pada malam hari dengan sistemik atau topikal,
cahaya yang suram (day blindness) inflamasi, dan paparan radiasi
• Ketajaman penglihatan dekat menjadi ion.
lebih berkurang daripada penglihatan
jauh.
 BEDAH KATARAK
Lensa diangkat dari mata (ekstraksi lensa) dengan prosedur intrakapsular atau
ekstrakapsular:
•Ekstraksi Katarak Intrakapsular (EKIK) :
 Mengeluarkan seluruh lensa bersama kapsulnya
 Tidak boleh dilakukan pada pasien usia <40thn, yang masih mempunyai
ligamen hialoidea kapsular
•Ekstraksi Katarak Ekstrakapsular (EKEK):
 Dilakukan pengeluaran isi lensa dengan memecah atau merobek kapsul lensa
anterior sehingga massa lensa dapat keluar melalui robekan tersebut
 Dilakukan pada pasien muda, dengan kelainan endotel, bersama-sama
keratoplasti, implantasi lensa intraokuler posterior, perencanaan implastasi
sekunder lensa intraokuler, kemungkinan akan dilakukan bedah glaukoma,
mata dengan predisposisi terjadinya prolaps badan kaca, sebelumnya pasien
mengalami ablasio retina, mata dengan makular edema, pasca bedah ablasi.
•Fakofragmentasi dan Fakoemulsifikasi : teknik ekstrakapsular menggunakan
getaran ultrasonik untuk mengangkat nukleus dan korteks melalui insisi
lumbus yang kecil

Sidarta Ilyas, Ilmu Penyakit Mata

 59. Defisiensi vitamin A
• Vitamin A meliputi retinol, retinil ester, retinal
dan asam retinoat. Provitamin A adalah semua
karotenoid yang memiliki aktivitas biologi β-
karoten
• Sumber vitamin A: hati, minyak ikan, susu &
produk derivat, kuning telur, margarin, sayuran
hijau, buah & sayuran kuning
• Fungsi: penglihatan, diferensiasi sel, keratinisasi,
kornifikasi, metabolisme tulang, perkembangan
plasenta, pertumbuhan, spermatogenesis,
pembentukan mukus

Kliegman RM. Nelson’s textbook of pediatrics, 19th ed. McGraw-Hill; 2011

• Konjungtiva normalnya memiliki sel goblet.
Hilangnya/ berkurangnya sel goblet secara
drastis bisa ditemukan pada xerosis
konjungtiva.
• Gejala defisiensi:
– Okular (xeroftalmia): rabun senja, xerosis
konjungtiva & kornea, keratomalasia, bercak Bitot,
hiperkeratosis folikular, fotofobia
– Retardasi mental, gangguan pertumbuhan,
anemia, hiperkeratosis folikular di kulit
 Xerophthalmia (Xo)
Stadium :
XN : night blindness (hemeralopia)
X1A : xerosis conjunctiva
X1B : xerosis conjunctiva (with bitot’s spot)
X2 : xerosis cornea
X3A : Ulcus cornea < 1/3
X3B : Ulcus cornea > 1/3, keratomalacea
XS : Corneal scar
XF : Xeroftalmia fundus
 Xeroftalmia
XN. NIGHT BLINDNESS
• Vitamin A deficiency can interfere with rhodopsin
production, impair rod function, and result in
night blindness.
• Night blindness is generally the earliest
manifestation of vitamin A deficiency.
• “chicken eyes” (chickens lack rods and are thus
night-blind)
• Night blindness responds rapidly, usually within
24—48 hours, to vitamin A therapy
 X1A, X1B. CONJUNCTIVAL XEROSIS
AND BITOT’S SPOT
• The epithelium of the • Conjunctival xerosis first
conjunctiva in vitamin A appears billateraly, in the
deficiency is transformed temporal quadrant, as an
from the normal columnar isolated oval or triangular
to the stratified squamous, patch adjacent to the
with loss of goblet cells, limbus in the interpalpebral
formation of a granular cell fissure.
layer, and keratinization of
the surface.
• Clinically, these changes are
expressed as marked
dryness or unwettability,
the affected area appears
roughened, with fine
droplets or bubbles on the
surface.
 X1A, X1B. CONJUNCTIVAL XEROSIS
AND BITOT’S SPOT
• In some individuals, keratin • Conjunctival xerosis and
and saprophytic bacilli Bitot’s spots begin to
accumulate on the xerotic resolve within 2—5 days,
surface, giving it a foamy or most will disappear within 2
cheesy appearance, known weeks.
as Bitot’s spots and they’re
easily wiped off)
• Generalized conjunctival
xerosis, involving the
inferior and/or superior
quadrants, suggests
advanced vitamin A
deficiency.
 X2 CORNEAL XEROSIS
• Corneal changes begin early in • Clinically, the cornea develops
vitamin A deficiency, long before classical xerosis, with a hazy,
they can be seen with the naked lustreless, dry appearance, first
eye which characteristic are observable near the inferior
superficial punctate lesions of the limbus
inferior—nasal aspects of the • Corneal xerosis responds within
cornea, which stain brightly with 2—5 days to vitamin A therapy,
fluorescein with the cornea regaining its
• Early in the disease the lesions normal appearance in 1—2 weeks
are visible only through a slit-
lamp biomicroscope
• With more severe disease the
punctate lesions become more
numerous, spreading upwards
over the central cornea, and the
corneal stroma becomes
oedematous
 X3A, X3B. Corneal
ulceration/keratomalacia
• Ulceration/keratomalacia • Superficial ulcers heal
indicates permanent with little scarring,
destruction of a part or all deeper ulcers, especially
of the corneal stroma, perforations, form dense
resulting in permanent peripheral adherent
structural alteration leukomas.
• Ulcers are classically • Localized keratomalacia is
round or oval “punched- a rapidly progressive
out” defects condition affecting the
• The ulceration may be full thickness of the
shallow, but is commonly cornea
deep
 XS. SCARS
• Healed sequelae of prior
corneal disease related to
vitamin A deficiency include
opacities or scars of varying
density (nebula, macula,
leukoma), weakening and
outpouching of the
remaining corneal layers
(staphyloma, and
descemetocele), and
phthisis bulbi.
XF. XEROPHTHALMIC FUNDUS
• The small white retinal
lesions described in some
cases of vitamin A
deficiency
• They may be accompanied
by constriction of the visual
fields and will largely
disappear within 2—4
months in response to
vitamin A therapy
• Gambaran funduskopi “
fenomena cendol”
 Pemeriksaan Penunjang
• A serum retinol study is a costly • The serum retinol level may be
but direct measure using high- low during infection because of a
performance liquid transient decrease in the RBP.
chromatography. • A zinc level is useful because zinc
– A value of less than 0.7 mg/L in deficiency interferes with RBP
children younger than 12 years is production.
considered low.
• A serum RBP study • An iron panel is useful because
iron deficiency can affect the
– easier to perform and less metabolism of vitamin A.
expensive than a serum retinol
study, because RBP is a protein and • Albumin levels are indirect
can be detected by an measures of vitamin A levels.
immunologic assay.
• Obtain a complete blood count
– RBP is also a more stable (CBC) with differential if anemia,
compound than retinol
– However, RBP levels are less
infection, or sepsis is a possibility.
accurate, because they are
affected by serum protein
concentrations and because types
of RBP cannot be differentiated.
 Therapy and Prevention
• For treatment of xerophthalmia, vitamin A is given in three doses at
the age-specific doses:
– Infants < 6 months of age: 50,000 international units orally
– Infants 6 to 12 months of age: 100,000 international units orally
– Children >12 months: 200,000 international units orally
– Adolescent and adults is 200,000 international units orally

• The first dose is given immediately on diagnosis, the second on the

following day, and the third dose at least two weeks later.

• Women of reproductive age or who are pregnant and have night

blindness should be treated with frequent small doses of vitamin A,
rather than high doses used for other adults
 Therapy & Prevention
• Vitamin A deficiency is common among populations
in resource-limited countries.
• For populations in which vitamin A deficiency is
endemic the World Health Organization (WHO)
recommends the following replacement approaches
• Universal periodic distribution — Periodic
supplementation is recommended for populations
endemic for vitamin A deficiency, at the following
doses (where 1 microgram retinol = 3.3 international
units)
– Infants 6 to 12 months of age: 100,000 international units
orally (30 mg retinol equivalent) – One dose
– Children 12 to 59 months of age: 200,000 international units
orally (60 mg retinol equivalent) – Dose repeated every four
to six months
60. Komplikasi HIV pada Mata
 Uveitis
• Dibedakan dalam bentuk
granulomatosa akut-kronis dan
• Tanda :
non-granulomatosa akut- kronis – pupil kecil akibat rangsangan
proses radang pada otot
• Bersifat idiopatik, ataupun terkait sfingter pupil
penyakit autoimun, atau terkait
penyakit sistemik – edema iris
• Biasanya berjalan 6-8 minggu – Terdapat flare atau efek tindal
di dalam bilik mata depan
• Dapat kambuh dan atau menjadi
menahun – Bila sangat akut dapat terlihat
hifema atau hipopion
• Gejala akut:
– mata sakit
– Presipitat halus pada kornea
– Merah
– Fotofobia
– penglihatan turun ringan
– mata berair

Radang iris dan badan siliar menyebabkan rusaknya Blood Aqueous Barrier sehingga terjadi
peningkatan protein, fibrin, dan sel-sel radang dalam humor akuos. Pada pemeriksaan biomikroskop
(slit lamp) hal ini tampak sebagai flare, yaitu partikel-partikel kecil dengan gerak Brown (efek tyndall).

Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006

 HIV related anterior uveitis
• Direct manifestation of the human
immunodeficiency virus infection
• autoimmnune in origin
• drug induced ie: rifabutin, secondary to direct
toxic effect upon the non-pigmented epithelium
of the ciliary body
• Any of the different infections associated with
AIDS, ie: Herpes Zoster Virus, Herpes Simplex
Virus,Cytomegalovirus, Toxoplasma gondii,
Syphilis
 Retinal microvasculitis related to HIV
infection
• Retinal microvasculopathy occurs in more than half of the
patients with HIV
• It is seen as transient cotton wool spots (CWS), intra-
retinal haemorrhages and microaneurysm, which occurs in
50-70% of patients. It is usually asymptomaticusually
asymptomatic.
• It has an unclear pathogenesis, but it is thought to be HIV
infection of retinal vascular cells.
• In an otherwise healthy individual the presence of CWS,
should be differentiated from other forms of retinopathy,
such as diabeticor hypertensive retinopathy. Serological
test for HIV will confirm the diagnosis
• Treatment is based in delaying the progression of the
disease associated with HIV
 61. Diplopia
• Merupakan keluhan subjektif berupa melihat melihat
satu benda menjadi dua
• Diplopia terbagi menjadi 2, yaitu
Diplopia binokular
 Diplopia ini hanya terjadi kalau kedua mata
terbuka.
 Jika salah satu mata ditutup maka penglihatan
ganda akan hilang
Diplopia monokular
 Diplopia jenis ini tidak ada perbedaan jika salah
satu mata ditutup
 Etiologi
• Diplopia binokular terjadi karena kerusakan
dari sistem binokular untuk membuat fusi
(penyatuan) gambar dari kedua mata.
• Contoh salah satu kondisi yang menyebabkan
adalah strabismus
• Sedangkan monokular diplopia disebabkan
oleh gangguan transmisi cahaya ke retina
(distorsi kornea, scar, katarak, subluksasi
lensa, gangguan vitreous, dsb)
 Pemeriksaan
• Salah satu uji untuk mendeteksi kondisi ini adalah Worth 4 dots
 Worth 4 dots test
• Merupakan untuk menilai fusi dan supresi pada jarak
dekat dan jauh.
• Pemeriksaan ini terdiri dari empat buah titik yang
disusun sedemikian rupa, yang biasanya berupa titik
merah, putih dan dua titik hijau
• Pasien memakai kacamata red filter terletak didepan
satu mata dan green filter pada mata yang lain.
• Cahaya merah dapat dilihat oleh mata yang tertetak
dibelakang lensa merah, tetapi cahaya hijau tidak
tampak karena lensa merah menyerap panjang
gelombang cahaya hijau. Sebaliknya pada lensa hijau
dapat melihat cahaya hijau, tetapi tidak cahaya merah
• Pasien melihat pada sebuah target yang terdiri
dari empat titik cahaya, yaitu satu merah, dua
hijau, dan satu putih.
• Saat melihat target tersebut pada jarak jauh (6
meter), akan mensti-mulasi primary central
vision.
• Ketika pasien melihat keempat titik cahaya
tersebut pada jarak 33cm, peripheral fusion
yang akan terstimulasi
 62. Hifema
Darah di bilik mata anterior

• Komplikasi tersering dari trauma tumpul atau

penetrasi mata
– Anak  Tersering trauma tumpul (ex: bola)
– Remaja & Dewasa  Tersering karena
trauma dengan energi tinggi (ex: pukulan,
KLL)
• Pada sebagian besar kasus, visus kembali
normal.
• Penurunan visus permanen bila:
– Hifema luas
– Hemolgobinopati, ex: sickle cell disease
– Risiko perdarahan, ex:hemofilia, obat
antikoagulan
• Disertai ruptur bola mata  emergensi Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Hifema
Patofisiologi Hifema Traumatik
• Trauma tumpul  peningkatan TIO,
stretching bola mata & tekanan dari
posterior disalurkan ke sekitar iris
 “robekan” stuktur pada sudut
COA  perdarahan badan siliar
atau iris
• Trauma Penetrasi  kerusakan
langsung daerah iris
• Hifema spontan  bisa
perdarahan spontan atau trauma
minor pada pasien risiko
perdarahan, seperti:
• DM
• Melanoma iris,
retinoblastoma, tumor lainnya
• Gangguan pembekuan darah
• Obat yang mengganggu fungsi
platelet
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Hifema
Gejala&Tanda: • Kerusakan struktur sekitar:
• + darah COA dan peningkatan TIO  Abrasi kornea
• Penurunan visus  Anisokoria dan iridodialisis
• Nyeri mata dengan konstriksi pupil  Subluksasi lensa & gangguan
pada penyinaran cahaya langsung mobilitas lensa (fakodonesis)
dan konsensual  fotofobia  Gangguan sudut mata 
glaukoma sudut
• Tanda ruptur bola mata  terbuka/tertutup
emergency!!!  sinekia
– Penurunan visus signifikan
– Pupil eksentrik
– Penurunan/Peningkatan kedalaman
bilik mata depan signifikan
– Keluarnya vitreous
– Prolaps eksternal uvea atau struktur
internal lainnya
– Perdarahan subkonjungtiva luas
– Seidel’s sign  menilai kebocoran COA
dengan fluoresensi
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Hifema
• Diagnostik
– Inspeksi visual 
penlight dan slit lamp
– Cek Faktor predisposisi:
sickle cell
hemoglobinopathy,
gangguan pembekuan
darah, dll
– Imaging:
• CT orbital  curiga open
globe, benda asing,
fraktur orbita
• Ultrasound
biomicroscopy
© 2019 American Academy of Ophthalmology
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 Tata Laksana Hifema Traumatik
• Tangani
– life-threatening (pada kasus trauma)
– Vision-theatening:
• Orbital Compartment Syndrome  proptosis, penurunan visus
signifikan, perdarahan subkonjungtiva luas, kelopak mata tegang,
defek pupil aferen, kimosis, penurunan retropulsi  Canthotomy
• Ruptur bola mata  tutup bola mata, obat anti nyeri dan anti mual-
muntah untuk mencegah keluarnya isi okular  Operasi repair
• Tutup mata + lampu redup  cegah akomodasi berlebih
• Bedrest & Elevasi kepala 30 derajat
• Pemberian sikloplegia (bila tidak ada ruptur bola mata) 
mengurangi nyeri, mencegah sinekia serta disfungsi iris
• Cegah mual-muntah  menghindari peningkatan TIO
• Obat nyeri topikal (ex: proparacaine 0,5%), bila kurang
dapat ditambahkan antinyeri sistemik
• Tetes mata glukokortikoid  menurunkan risiko
perdarahan ulang  ex: prednisolone asetat 1% atau
dexamethasone sodium fosfat 0,1% Andreoli CM, Gardiner MF. Traumatic hyphema:
Management. Uptodate: 2018.
• Tata Laksana Lanjutan
– Monitor TIO harian  bila hipertensi, terapi menekan
aliran aquous humor, ex: beta adrenergik bloker
topikal (timolol) dan karbonik anhidrase inhibitor
topikal (dorzolamide) atau tambahkan oral
asetazolamide/methazolamide bila efek topikal tidak
adekuat
• Rujuk untuk intervensi dan pemberian manitol bila
hipertensi intraokular tidak terkontrol:
– > 50 mmHg selama 5 hari atau
– >35 mmHg selama 7 hari atau
– Pasien dengan hemoglobinopati
– >25 mmHg selama >24 jam
• Hipertensi intraokular, hifema Grade III dan IV lebih dari
10 hari, early corneal blood staining  evakuasi clot
dengan pembedahan
• Rujuk  pada sindrom kompartemen orbital, ruptur bola
mata, hifema grade III-IV, hifema pada pasien risiko
perdarahan, hifema dengan peningkatan TIO
Andreoli CM, Gardiner MF. Traumatic hyphema:
clinical feature and diagnosis. Uptodate: 2018.
 63. Blepharitis
• Inflammation of the eyelids Physical examination:
• Signs and symptoms: • Skin → erythema, papules,
– Redness/irritation pustules (rosacea)
– Burning/tearing • Eyelids → abnormal eyelid
– Itching position,hyperemia, ulceration,
– Crusting of eyelashes scaling, scarring
– Loss of eyelashes (madarosis_ • Eyelashes → malposition/
– Eyelid sticking misdirection, loss, pediculosis
– Blurring/fluctuating vision nits, cylindrical sleeves,
– Contact lens intolerance collarettes
– Photophobia • Tarsal conjunctiva →
– Increased frequency of blinking dilation/inflammation of
meibomian glands, capping of
meibomian orifices,
papillary/folicular reaction
• Bulbar conjunctiva → hyperemia,
phylctenules, follicles
• Cornea → epithelial defect,
edema, infiltrates

Clinical Ophthalmology. Kanski. 7th ed.

 Treatment
• Warm compresses to soften adherent scurf and scales, warm the
meibomian secretions → once or twice daily
• Eyelid cleansing, including eyelid massage in cases of MGD → once or
twice daily
• Antibiotics (topical and/or systemic)
– Topical bacitracin or erythromycin on eyelid margins
– Metronidazole gel if unresponsive to antibiotic treatment (off-label)
– Patients with MGD → oral + topical
– Doxycycline 100 mg or tetracycline 1000 mg in divided doses, tapered to
doxycycline 40-50 mg or tetracycline 250 mg after clinical improvement
– Alternative: erythromycin 250-500 mg daily or azithromycin 250-500 mg one
to three times a week
• Topical corticosteroid → for ocular surface inflammation eg severe
conjunctival infection, marginal keratitis, or phlyctenules. Applied several
times daily to the eyelids or ocular surface.
• Artificial tears

Clinical Ophthalmology. Kanski. 7th ed.

 Treatment
• Good lid hygiene is the mainstay of treatment for all forms of blepharitis.
• The goal is to alleviate symptoms and to develop a maintenance regimen
to prevent or minimize future exacerbations.
• Mild to moderate symptoms : can generally be managed with
symptomatic measures, including warm compresses, lid massage, lid
washing, and artificial tears.
• Severe or refractory symptoms : may require additional therapies such as
topical or oral antibiotics, topical glucocorticoids, or typical cyclosporine.
– Because of the potential for systemic side effects with oral drugs, topical
therapy is usually tried first.
– Antibiotic ointment (eg, bacitracin, erythromycin) is placed directly onto the
lid margin once daily at bedtime.
– Once symptoms improve (generally one to two weeks), treatment can be
stopped, but lid hygiene measures should be continued.
– Oral antibiotic therapy (eg, doxycycline, tetracycline, azithromycin) can be
given if the response to topical therapy is inadequate.
• All patients should be advised to eliminate or limit potential triggers or
exacerbating factors (eg, allergens, cigarette smoking, contact lenses).

Uptodate.com
 Blepharitis Complication
• Dry eye disease is a frequent complication of
blepharitis, occurring in 25 to 40 percent of
patients
• Keratitis
 Definisi
Blefaritis superfisial Infeksi kelopak superfisial yang
diakibatkan Staphylococcus
Hordeolum Peradangan supuratif kelenjar
kelopak mata
Blefaritis Blefaritis diseratai skuama atau
skuamosa/seboroik krusta pada pangkal bulu mata
yang bila dikupas tidak terjadi luka
pada kulit, berjalan bersamaan
dengan dermatitis sebore
Meibomianitis Infeksi pada kelenjar meibom
(blefaritis posterior)
Blefaritis Angularis Infeksi Staphyllococcus pada tepi
kelopak di sudut kelopak atau
kantus
Ilmu Penyakit Mata, Sidharta Ilyas
Gejala
Terdapat krusta dan bila
menahun disertai dengan
meibomianitis
Kelopak bengkak, sakit, rasa
mengganjal, merah, nyeri bila
ditekan
Etiologi: kelainan metabolik
atau jamur. Gejala: panas,
gatal, sisik halus dan
penebalan margo palpebra
disertai madarosis
Tanda peradangan lokal pada
kelenjar tersebut
Gangguan pada fungsi
pungtum lakrimal, rekuren,
dapat menyumbat duktus
lakrimal sehingga mengganggu
fungsi lakrimalis
Tatalaksana
Salep antibiotik
(sulfasetamid dan
sulfisoksazol), pengeluaran
pus
Kompres hangat, drainase
nanah, antibiotik topikal
Membersihkan tepi kelopak
dengan sampo bayi, salep
mata, dan topikal steroid
Kompres hangat, penekanan
dan pengeluaran pus,
antibiotik topikal
Dengan sulfa, tetrasiklin,
sengsulfat
 64. Presbiopia
• Merupakan keadaan berkurangnya daya akomodasi
pada usia lanjut
• Penyebab:
– Kelemahan otot akomodasi
– Lensa mata tdk kenyal / berkurang elastisitasnya akibat
sklerosis lensa
• Diperlukan kacamata baca atau adisi :
– + 1.0 D : 40 thn
– + 1.5 D : 45 thn
– + 2.0 D : 50 thn
– + 2.5 D : 55 thn
– + 3 .0 D : 60 thn
Sumber: Ilmu Penyakit Mata. Sidarta Ilyas. 2000.
 Presbiopia
Pemeriksaan dengan
kartu Jaeger untuk
melihat ketajaman
penglihatan jarak
dekat.
– The card is held 14
inches (356 mm) from
the persons's eye for
• Koreksi→ lensa positif untuk menambah
kekuatan lensa yang berkurang sesuai usia the test. A result of
• Kekuatan lensa yang biasa digunakan: 14/20 means that the
+ 1.0 D → usia 40 tahun person can read at 14
+ 1.5 D → usia 45 tahun inches what someone
+ 2.0 D → usia 50 tahun with normal vision can
+ 2.5 D → usia 55 tahun read at 20 inches.
+ 3.0 D → usia 60 tahun
http://www.ivo.gr/files/items/1/145/51044.jpg
 65. Dry Eye Syndrome
(Keratokonjungtivitis Sicca)
• International Dry Eye Workshop (DEWS) 2007
definition:
– Mata kering merupakan penyakit multifaktorial
pada produksi air mata dan permukaan mata yang
menyebakan rasa tidak nyaman, gangguan
penglihatan, dan instabilitas lapisan air mata yang
beresiko menyebabkan kerusakan permukaan
okular. Kondisi ini disertai pula dengan
peningkatan osmolaritas lapisan air mata dan
peradangan pada permukaan mata.
• Dry eye is a disorder of the
tear film due to tear
deficiency or excessive tear
evaporation which causes
damage to the
interpalpebral ocular
surface and is associated
with symptoms of ocular
discomfort
• Tear film  total thickness
7-10 µm, consist of:
– Mucus layer (0.02- 0.04 µm)
– Aqueous layer (6.5 µm)
– Lipid layer (0.1 µm)
 ELEMENTS OF OCULAR DEFENCE
Stable precorneal tear film

• Lipid • Meibomian gland

Compositional • Lacrimal gland

• Aqueous
factors
• Ocular surface
• Mucin epithelium

• Lid • Tear spread

Hydrodynamic blinking • Tear clearance
factor
• Lid • Prevents
closure evaporation
 VICIOUS CYCLE OF
DRY EYE

KCS Loss of goblet

cells

VICIOUS CYCLE

Tear film Absence of

destabilizes mucin
 CLASSIFICATION

• Tear-deficient dry eye:

– There is a disorder of lacrimal function or a
failure of transfer of lacrimal fluid into the
conjunctival sac
• Tear-sufficient dry eye:
– Lacrimal function is normal, the tear
abnormality is due to increased tear
evaporation
 TEAR - DEFICIENT

Sjogren syndrome Non- Sjogren tear deficient

Lacrimal Lacrimal
Primary Secondary Reflex
Disease obstruction

Rh arthritis Primary Contact

SLE Cong Secondary lens
Wegener’s Trachoma
alacrimia Sarcoid VII n
Granulomatosis Pemphigoid
Primary HIV Palsy
Systemic Burns
lacrimal Vit A def Neurop-
sclerosis disease keratitis
 EVAPORATIVE

Oil Ocular surface

Lid related Contact lens
deficient disorder

Blink,
Secondary Aperture Xerophthalmia
Primary
abnormal
Blepharitis
Absent
Meibomian Lid surface
glands
gland incongruity
Distichiasis
disease
 CLINICAL MANIFESTATION

• Burning or itching • Sore or tired eyes

• Fluctuating vision
• Foreign body sensation
• Grittiness or irritation
• History of Styes
• Ocular discharge
• Light sensitivity
• Contact lens discomfort
• Watering or excessive
tearing
 Dry Eye Severity Level
Variable 4 (must have signs
1 2 3
and symptoms)
Moderate,
Mild, episodic;
episodic or Severe, frequent or
Discomfort (severity occurs under Severe or disabling,
chronic; occurs constant; occurs
and frequency) environmental constant
with or without without stress
stress
stress
None or Annoying or Annoying, chronic
Constant and possibly
Visual symptoms episodic mild activity-limiting, or constant,
disabling
fatigue episodic activity-limiting
Conjunctival injection None to mild None to mild +/– +/++
Moderate to
Conjunctival staining None to mild Variable Marked
marked
Corneal staining
Severe punctate
(severity and None to mild Variable Marked central
erosions
location)
Filamentary
Filamentary keratitis,
Mild debris, keratitis, mucus
Corneal and tear mucus clumping,
None to mild decreased clumping,
signs increased tear debris,
meniscus increased tear
ulceration
debris
Trichiasis,
Lid and meibomian MGD variably MGD variably
MGD frequent keratinization,
glands present present
symblepharon
Tear breakup time Variable ≤ 10 s ≤5s Immediate

Schirmer score Variable ≤ 10 mm/5 min ≤ 5 mm/5 min ≤ 2 mm/5 min

MGD=meibomian gland dysfunction.

 DIAGNOSIS

• Slit lamp examination

• Demonstration of tear instability (Tear film break up time,
TBUT) with Tearscope/ Xeroscope
• Demonstration of ocular surface damage
– Schirmer’s test
– Fluorescein Staining
– Rose bengal stain
– Lissamine Green Staining
• Demonstration of tear hyperosmolarity
 SCHIRMER’S TEST

• Measurement of the aqueous layer quantity only

• 5x30 strips of Whatman filter paper
• The amount of moistening is of the exposed paper is
recorded at the end of 5minutes
 SCHIRMER’S TEST
Measures total reflex and basic tear secretion
Results:
 Normals will wet approximately 10 to 30mm at the
end of 5minutes.
 If wetting > 30 mm, reflex tearing is intact but not
controlled or tear drainage is insufficient
 A value of <5mm indicates hyposecretion
 Treatment
• Level 1 treatment consists of the
following: • If level 2 treatment is
– Education and environmental or dietary
modifications inadequate, level 3
– Elimination of offending systemic
medications measures are added,
– Preserved artificial tear substitutes, gels,
and ointments including the following:
– Eyelid therapy
• If level 1 treatment is inadequate, level – Autologous serum or
2 measures are added, including the umbilical cord serum
following:
– Nonpreserved artificial tear substitutes – Contact lenses
– Anti-inflammatory agents (topical – Permanent punctal occlusion
cyclosporine, topical steroids)
–
–
Tetracyclines (for meibomitis or rosacea)
Punctal plugs (after inflammation has been • If level 3 treatment is
controlled)
– Secretagogues inadequate, level 4
– Moisture chamber spectacles treatment, consisting of the
administration of systemic
anti-inflammatory agents, is
added.
 66. Keratokonjungtivitis toksik
• Definition :
– Corneal toxicity is caused by chemical trauma and by iatrogenic and
factitious disease, which are often overlooked

• Iatrogenic toxicity occurs in patients with acute or chronic ocular

surface disorders as a result of both the short-term and, more
often, the longtermuse of topical medications

• The commonest conjunctival reactions were toxic papillary, toxic

follicular, and delayed hypersensitivity

• The commonest associated drugs were :

– Idoxuridine (IDU), arabinoside A, aminoglycosides, pilocarpine,
chloramphenicol, and the preservatives benzalkonium chloride,
phenylmercuric nitrate (which is no longer used in the UK), thiomersal,
and EDTA

Dart J. Corneal toxicity : The epithelium and stroma in iatrogenic and factitious disease. Eye (2003) 17;886-92
• The clinical signs
– Both iatrogenic and factitious disease are usually
nonspecific and identical to those resulting from
other causes of corneal epithelial disease such as:
• punctate keratopathy,
• Coarse focal keratopathy,
• pseudodendrites,
• Filamentary keratopathy, and
• persistent epithelial defect