Red Eye

Kel. 11
Conjunctivitis
10100119056 – Andita Noveralioni
 Conjunctivitis
Inflamasi konjungtiva (konjungtivitis) secara klasik didefinisikan sebagai hiperemia konjungtiva yang
berhubungan dengan sekret yang mungkin encer, mukoid, mukopurulen atau purulen.

Type of conjunctivitis
A. Infective conjunctivitis
1. Bacterial conjunctivitis
Acute bacterial conjunctivitis • Enterovirus conjunctivitis
Hyperacute bacterial conjunctivitis • Molluscum contagiosum conjunctivitis
Chronic bacterial conjunctivitis • Herpes simplex conjunctivitis
Angular bacterial conjunctivitis 4. Ophthalmia neonatorum (A separate entity)
2. Chlamydial conjunctivitis 5. Granulomatous conjunctivitis
Trachoma • Parinaud oculoglandular syndrome
Adult inclusion conjunctivitis
Neonatal chlamydial conjunctivitis
3. Viral conjunctivitis
• Adenovirus conjunctivitis
– Epidemic keratoconjunctivitis
– Pharyngoconjunctival fever
B. Allergic Conjunctivitis
1. Simplex allergic conjunctivitis
Hay fever conjunctivitis (rhino conjunctivitis)
Seasonal allergic conjunctivitis (SAC)
Perennial allergic conjunctivitis (PAC)
2. Vernal keratoconjunctivitis (VKC)
3. Atopic keratoconjunctivitis
4. Giant papillary conjunctivitis (GPC)
5. Phlyctenular conjunctivitis (PKC)
6. Contact dermoconjunctivitis (drop conjunctivitis)
C. Cicatricial conjunctivitis
• Ocularmucousmembranepemphigoid(OMMP),
• Stevens Johnson syndrome (SJS),
• Toxic epidermal necrolysis (TeN), and
• Secondary cicatricial conjunctivitis.
D. Toxic conjunctivitis
 1
Infective
Conjunctivitis
 Infective conjunctivitis

Konjungtivitis infektif, yaitu peradangan pada konjungtiva yang

disebabkan oleh mikroorganisme (jenis yang paling umum).
Natural protective mechanism :
• Suhu rendah karena terpapar udara,
• Perlindungan fisik by lids,
• Tindakan pembilasan air mata,
• Aktivitas antibakteri lisozim, dan
• Perlindungan humoral oleh immunoglobulin air mata
 Bacterial
conjunctivitis
 Telah terjadi penurunan relatif dalam kejadian konjungtivitis bakteri pada umumnya dan
yang disebabkan oleh Gonococcus dan Corynebacterium Diphtheriae pada khususnya.
Namun, di negara berkembang masih terus menjadi jenis konjungtivitis yang paling
umum. Ini dapat terjadi sebagai kasus sporadis dan epidemi. Wabah konjungtivitis bakteri,
epidemi cukup sering terjadi selama musim hujan.
 Etiologi
F. Predisposisi
1 Lalat, hyegine buruk, iklim panas,
sanitasi buruk, kebiasaan kotor
Organisme
2 Staphylococcus aureus,
Staphylococcus epidermidis,
Streptococcus pneumoniae
 Cara Penularan

Eksogen Penyebaran lokal Endogen

Kontak dekat (infeksi melalui Berasal dari struktur
udara dan air), penularan vector disebelahnya ex. Infeksi Melalui darah misalnya infeksi
(lalat), pemindahan material kantung lacrimal, kelopak mata, gonococcal dan meningococcus
(yang terinfeksi) nasofaring
 Pathology

1. Respons vascular
Ciri : kongesti dan peningkatan permeabilitas konjungtiva pembuluh darah yang terkait dengan proliferasi kapiler
2. Respon seluler
Hal ini dalam bentuk eksudasi sel polimorfonuklear dan sel inflamasi lainnya ke dalam substansia propria konjungtiva
sebagai juga pada kantung konjungtiva
3. Respon konjungtiva
Konjungtiva edema, sel epitel basal konjungtiva dan peningkatan jumlah sel goblet yang mensekresi musin
4. Debit konjungtiva
Terdiri dari lendir, sel inflamasi, sel epitel deskuamasi, fibrin dan bakteri. Jika peradangan parah : diapedesis sel darah
merah dan keluarnya cairan

Tingkat keparahan perubahan patologis bervariasi bergantung tingkat keparahan peradangan dan organisme penyebab.
Jenis klinis konjungtivitis bakteri

Konjungtivitis Konjungtivitis
Bakteri akut bacterial
hiperakut

Konjungtivitis Konjungtivitis
bakteri kronis angular
Acute bacterial
conjunctivitis
Epidemiologi

• Konjungtivitis akut dari semua penyebab

diperkirakan terjadi pada 6 juta orang setiap tahun
di Amerika Serikat. Masalah mata merah
merupakan satu - empat persen dari kunjungan
dokter umum di negara maju dengan konjungtivitis
bakteri akut yang paling sering didiagnosis.
• Konjungtivitis etiologi bakteri adalah penyebab
infeksi kedua yang paling sering terjadi dan
mempengaruhi anak-anak dengan frekuensi yang
meningkat.
 ACUTE BACTERIAL
Penyebab umum :
Staphylococcus aureus,
Konjungtiviitis bacterial akut ditandai Koch-Weeks Bacillus,
dengan hiperemia konjungtiva dan secret Pneumococcus dan
mukopurulen dari mata. Secara klinis disebut Streptococcus
konjungtivitis mukopurulen akut
 Manifestasi Klinis
Symptom
Ketidaknyamanan, benda asing, berpasir, kabur, dan kemerahan muncul
secara tiba-tiba (karena pembengkakan pembuluh darah)
Fotofobia ringan
Mukopurulen
Sticking together of lid margins with discharge during sleep
Coloured halos

Sign
Serpihan mucous terlihat di forniks, canthi dan margin kelopak
Kongesti konjungtiva (lebih terlihat di konjungtiva palpebra, forniks, dan
bagian perifer konjungtiva bulbi) menggambarkan mata merah menyala
Kemosis (pembengkakan konjungtiva)
Papila halus
Perdarahan petekie (penyebabnya pneumococcus)
Silia kusut dan ada kuning kerak
Kelopak mata sedikit edema
Patogenesis Patofisiologi
 Perjalanan klinis

Konjungtiva mukopurulen biasanya bilateral, meskipun satu

mata dapat terkena 1-2 hari sebelu yang satunya. Penyakit
ini biasanya mencapai puncak dalam 3 -4 hari. Jika tidak
diobati, dalam kasus infeksi ringan dapat diatasi dan kondisi
sembuh dalam 10-15 hari atau bisa jadi konjungtivitis
katarak kronis
 Diagnosis
1. Anamnesis dan Pemeriksaan fisik
- Riwayat penyakit dan Riwayat infeksi mata
- Pemeriksaan mata dan menilai tanda dan gejala

Dalam kebanyakan kasus tidak diperlukan pemeriksaan lab untuk melakukan diagnosis,
namun bila kasusnya parah atau tidak ada respon terhadap pengobatan, pasien akan
dilakukan swab kelopak mata dan mengujinya untuk mengidentifikasi penyebab infeksi
dan untuk pengobatan yang tepat

2. Penunjang
- Pewarnaan Gram berguna untuk mengidentifikasi karakteristik bakteri, termasuk titer
bakteri kasar, perkiraan kasar jumlah sel darah putih (WBC), dan adanya rantai, cluster,
atau inklusi intracytoplasmic
- Pewarnaan Giemsa berguna untuk identifikasi chlamydia

respon seluler pada konjungtivitis sesuai penyebabnya :

• Infeksi bakteri: Neutrofil mendominasi
• Infeksi virus: Limfosit mendominasi
• Reaksi alergi: Eosinofil mendominasi
Differential Diagnosis
 Treatment
1. Antibiotik topical (utama)
Untuk mengendalikan infeksi disesuaikan dengan penyebab bakteri hasil dari tes kultur
dan sensitivitas
Co : Kloramfenikol, gentamisin, tobramycin, framycetin
Tetes mata setiap 3-4 jam di siang hari dan salep untuk malam hari (untuk mengurangi
lengket)

Jika tidak ada respon, berikan tetes antibiotic kuinolon : ciprofloxacin, ofloxacin,
gatifloxacin, moksifloksasin

2. Irigasi conjunctiva sac

Menggunakan sterile warm saline 1x/2x sehari untuk membantu menghilangkan material.
Pencucian mata tidak disarankan karena merupakan kontraindikasi dan dapat
membersihkan lisozim dan protein pelindung lain yang ada di dalam air mata
 Treatment

3. Kacamata gelap
Harus digunakan untuk mencegah fotofobia
4. Perban tidak boleh digunakan (untuk konjungtivitis mukopurulen). Paparan udara
menjaga suhu cul-de-sac konjungtiva rendah yang menghambat pertumbuhan bakteri,
penggunaan perban juga dapat memperluas infeksi dalam waktu 24 jam dan mencegah
cairan keluar
5. Tidak perlu steroid
6. anti-inflammatory and analgesic drug
Co : ibuprofen dan paracetamol diberikan oral selama 2-3 hari untuk meredakan nyeri
ringan
 Komplikasi
Epiteliopati punctata superficial
Ulserasi kornea marginal
Keratitis superficial
Blepharitis
dakriosistitis
 Prognosis
konjungtivitis bakterial tanpa komplikasi : baik dengan
resolusi lengkap dan efek samping yang jarang dengan
pengobatan antibiotic dan management yang baik
 Prevention
Sering mencuci tangan
Menghindari berbagi handuk, sapu tangan dan bantal
dengan orang lain
 Hyperacute
bacterial
conjunctivitis
 Hyperacute bacterial

Konjungtivitis bakteri hiperakut juga dikenal

sebagai konjungtivitis purulent akut atau blenorea
akut ditandai dengan respon inflamasi yang hebat.
Terjadi dalam dua bentuk :
1. Konjungtivitis purulent dewasa
2. Oftalmia neonatorum pada bayi baru lahir
Hyperacute bacterial conjunctivitis of adult (Gonococcal conjunctivitis)

Etiologi Manifestasi klinis

Menyerang orang dewasa Onset : hiperakut (12-24 jam)
terutama laki-laki yang Gejala : nyeri sedang-berat,
menyebar langsung dari alat cairan purulent, edema kelopak
kelamin ke mata mata
 Sign

Discharge thick
Kelopak mata tegang
Tenderness purulent, copius menetes
dan bengkak
ke bawah pipi

Konjungtiva kemosis, Biasanya berhubungan

Lymph node
kongesti dan papilla,
preauricular membesar, dengan urethritis dan
penampilan beludru merah
ceran. Kadang ada dan nyeri tekan artritis
pseudomembran
 Symptom

10% 20% 30%

Nyeri sedang - berat Swelling of eyelid

Purulent discharge
 Komplikasi

1. Corneal involvement
2. Iridocyclitis
3. Systemic complications : gonorrhea
arthritis, endocarditis dan septicaemia
 Treatment
1. Systemic therapy
• Third generation cephalosporin such as cefoxitim 1.0 gm or cefotaxime 500 mg IV qid or ceftriaxone 1.0 gm IM qid,
all for 5 days; should be preferred treatment.
• Quinolones such as norfloxacin 1.2 gm orally qid for 5 days, or
• Spectinomycin 2.0 gm IM for 3 days, may be used alternatively.

Semua aturan di atas kemudian harus diikuti satu minggu baik doksisiklin 100 mg dua kali sehari atau eritromisin 250-
500 mg per oral tiga kali sehari.
2. Terapi antibiotik topikal, yang saat ini direkomendasikan meliputi tetes mata ofloxacin, ciprofloxacin atau tobramycin
atau bacitracin atau salep mata eritromisin setiap 2 jam selama 2-3 hari pertama dan kemudian 5 kali sehari selama 7
hari.
3. Irigasi mata sering dengan saline steril sangat terapeutik dalam membasuh kotoran yang terinfeksi.
4. Tindakan umum lainnya serupa dengan konjungtivitis mukopurulen akut.
5. Tetes mata atropin 1% topikal harus diberikan sekali atau dua kali sehari jika melibatkan kornea.

Pasangan seksual juga harus diobati dengan antibiotik sistemik. Selanjutnya, pasien dan pasangan seksual harus dirujuk
untuk evaluasi penyakit menular seksual lainnya.
Chronic Bacterial
Conjunctivitis
 Chronic Bacterial

Konjungtivitis bakteri kronis juga dikenal

‘konjungtivitis catarrhal kronis’ atau ‘simple
chronic conjunctivitis’ ditandai dengan
peradangan catarrhal ringan pada konjungtiva
 Etiologi

A. Faktor predisposisi
1. Paparan kronis terhadap debu, asap dan bahan kimia iritasi
2. Penyebab iritasi local seperti trikiasis, beton, benda asing dan seborrhoeic scales
3. Ketegangan mata karena Kelaina refraksi, phorias atau ketidakcukupan konvergensi
4. Penyalahgunaan alcohol, insomnia dan gangguan metabolism

B. Organisme penyebab
5. Staphylococcus aureus (tersering)
6. Batang gram negative co : Proteus mirabilis, klebsiella pneumoniae, E.coli dan Moraxella lacunata

C. Sumber dan cara penularannya

7. Lanjytan dari konjungtivitis mukopurulen akut bila tidak diobati atau diobati sebagian
8. Infeksi kronis dari dakriosistitis kronis terkait rhinitis kronis atau radang selaput lendir hidung bagian atas kronis
9. Infeksi eksogen ringan yang diakibatkan oleh kontak langsung penularan meulalu udara atau material
 Manifestasi klinis

• Rasa terbakar dan berpasir di mata, terutama malam hari

• Kemerahan kronis ringan di mata. Perasaan panas dan kekeringan pada tepi kelopak mata
• Kesulitan menjaga mata tetap terbuka
• Sekret mucoid ringan terutama di canthi
• Perasaan mengantuk dan Lelah pada mata

Tanda :
• Kongesti pembuluh darah konjungtiva posterior
• Hipertrofi papiler ringan pada palpebra
• Tampak permukaan konjungtiva lengket
• Margin tersumbat
 Treatment

1. Hilangkan factor predisposisi

2. Antibiotik topical seperti kloramfenikol, tobramisin, atau gentamisin harus diberikan 3-4 kali sehari selama sekitar
2 minggu untuk menghilangkan gejala ringan dan infeksi kronis
3. Tetes mata astringen seperti seng-boricaciddrops memberikan pengungrangan gejala
Angular Bacterial
Connjunctivitis
 Angular Bacterial Etiologi

1. Faktor preedisposisi
2. Organisme penyebab : Moraxella
Adalah jenis kongjungtivitis kronis yang ditandai Axenfield (MA)
dengan peradangan ringan yang terbatas pada 3. Sumber infeksi dari rongga hidung
konjungtiva dan tepi kelopak mata di dekat sudut 4. Cara infeksi : ditularkan dari rongga
yang terkait dengan maserasi kulit di sekitarnya hidung ke mata melalui jari yang
terkontaminasi atau sapu tangan
 Pathology
Organisme penyebab yaitu bacillus MA menghasilkan enzim proteolitik yang
bekerja dengan maserasi epitel. Enzim proteolitik ini berkumpul di sudut-
sudutoleh aksi air mata dan dengan demikian merusak epitel konjungtiva, tepi
kelopak mata dan kulit, sudut-sudut sekitar mata. Maserasi diikuti oleh respon
vaskuler dan berupa inflamasi kronik derajar ringan
 Manifestasi Klinis
Gejala :
• Iritasi, sensasi terbakar dan perasaan ketidaknyamanan pada mata
• Riwayat pengumpulan keputihan berbusa putih kotor di sudut-sudut
• Kemerahan di sudut mata

Tanda :
• Hiperemia konjungtiva bulbi di dekat canthi
• Hiperemia tepi kelopal mata dekat sudut
• Eksoriasi kulit di sekitar sudut
• Debit mukopurulen berbusa di sudut
 Treatment

A. Profilaksis termasuk pengobatan infeksi hidung terkait dan kebersihan pribadi yang baik
B. Pengobatan kuratif terdiri dari :
1. Oxytetracycline (1%) 2-3 kali sehari selama 9-14 hari akan membasmi infeksi
2. 2. Lotion seng yan ditanam di siang hari dan salep seng oksida pada waktu tidur menghambat fermentasi proteolitik
dan membantu mengurangi kelelahan
 Chlamydial
conjunctivitis
 Chlamydial conjunctivitis
Siklus hidup Chlamydia. Partikel infektif
menyerang sitoplasma sel epitel, di mana ia
membengkak dan membentuk ‘initial body'.
Badan-badan awal dengan cepat membelah
menjadi 'badan-badan dasar' yang tertanam dalam
matriks glikogen yang dibebaskan ketika sel-sel
meledak. Kemudian ‘elementary bodies'
menginfeksi sel lain di mana seluruh siklus
diulang.
 Trachoma

Trachoma (sebelumnya dikenal sebagai Egypt ophthalmia) adalah keratokonjungtivitis kronis, terutama mempengaruhi
epitel superfisial konjungtiva dan kornea secara bersamaan. Hal ini ditandai dengan respon folikular dan papiler
campuran dari jaringan konjungtiva. Merupakan penyebab utama kebutaan yang dapat dicegah di dunia. Kata 'trachoma'
berasal dari kata Yunani untuk 'kasar' yang menggambarkan penampilan permukaan konjungtiva pada trachoma kronis.

Etiologi
 Trachoma

B. Faktor Predisposisi
1. Usia. Infeksi biasanya pada bayi dan anak usia dini.
2. Jenis kelamin pada perempuan
3. Ras. Tidak ada ras yang kebal terhadap trachoma, tetapi penyakit ini sangat umum pada orang Yahudi dan relative
kurang umum di kalangan orang Negro.
4. Iklim. Trachomais lebih umum dengan cuaca kering dan berdebu.
5. Status sosial ekonomi. Penyakitnya lebih umum di kelas miskin karena kondisi hidup yang tidak higienis, kepadatan
penduduk, kondisi tidak bersih, populasi lalat melimpah, kekurangan air, kurangnya bahan seperti handuk dan sapu
tangan terpisah, dan kurangnya pendidikan dan pemahaman tentang penyebaran penyakit menular.
6. Faktor lingkungan seperti paparan debu, asap, iritan, sinar matahari, dll meningkatkan risiko tertular penyakit. Oleh
karena itu, pekerja di luar ruangan lebih terpengaruh dibandingkan dengan pekerja kantoran.

C. Sumber infeksi. Di zona endemik trakoma, sumber utama infeksi adalah sekret konjungtiva dari orang yang terkena.
 Trachoma

D. Cara Infeksi.
Infeksi dapat menyebar dari mata ke mata melalui :
1. Penyebaran infeksi secara langsung dengan mode airborne atau waterborne.
2. Penularan vektor trachoma sering terjadi melalui lalat.
3. Transfer material memainkan peran penting dalam penyebaran trakoma. Pemindahan material dapat terjadi melalui
jari-jari dokter, perawat, dan tonometer yang terkontaminasi. Sumber lain dari transfer material infeksi adalah
penggunaan handuk biasa, saputangan, tempat tidur dan surma-rods.
 Manifestasi klinis

Gambaran klinis trachoma dapat digambarkan menjadi dua fase:

I. Fase trachoma aktif
Fase trachoma aktif biasanya terjadi pada masa kanak-kanak akibat infeksi klamidia aktif.
• Masa inkubasi trakoma aktif bervariasi dari: 5 sampai 22 hari.
• Onset penyakit biasanya berbahaya (subakut), namun, jarang dapat muncul dalam bentuk akut.

Gejala
ditentukan oleh tidak adanya atau adanya infeksi bakteri sekunder.
Dengan tidak adanya infeksi sekunder, trachoma murni ditandai dengan gejala berikut:
• Sensasi benda asing ringan,
• Lakrimasi sesekali,
• lids sedikit lengket, dan
• Sedikit sekret mukoid.
Catatan. Gejala di atas sangat ringan sehingga penyakit ini biasanya diabaikan.
Dengan adanya infeksi bakteri sekunder, timbul gejala khas konjungtivitis mukopurulen akut
 Sign

A. Tanda-tanda konjungtiva
1. Kongesti tarsal atas dan forniceal penghubung.
2. Folikel konjungtiva.
Folikel terlihat seperti sagu yang direbus dan biasanya terlihat
pada konjungtiva tarsal atas dan forniks; tetapi mungkin juga
terdapat pada forniks bawah, plica semilunaris, dan caruncle

3. Hiperplasia papiler. Papila berwarna kemerahan, bagian

atas datar yang menonjol yang memberikan tampilan merah
dan seperti beludru pada konjungtiva tarsal
B. Tanda-tanda kornea
1. Keratitis superfisial mungkin ada di bagian atas bagian.
2. Folikel Herbert mengacu pada folikel khas yang ada di daerah limbus
3. Pannus progresif yaitu infiltrasi kornea terkait dengan vaskularisasi terlihat di bagian atas.
4. Ulkus kornea
II. Fase trakoma sikatrik
Fase sikatrikal trachoma bermanifestasi pada usia paruh baya. Ini terjadi karena peradangan kronis tingkat ringan yang
berkelanjutan. Infact infeksi berulang memunculkan respon imun kronis yang terdiri dari reaksi hipersensitivitas tertunda
yang diperantarai sel (Tipe IV) terhadap kehadiran intermiten antigen klamidia, yang bertanggung jawab untuk fase
sikatrik trachoma. Tahap akhir trachoma sikatricial juga disebut sebagai gejala sisa trachoma. Fase ini ditandai dengan
fitur klinis :
- Conjunctival scarring
- Concretions
- Other conjunctival sequelae
 Referensi

• Comprehensive Ophthalmology
• https://ada.com/conditions/bacterial-conjunctivitis/#diagnosis
• https://emedicine.medscape.com/article/1191730-overview
• https://www.ncbi.nlm.nih.gov/books/NBK546683/
Keratitis
Kel. 11
 Definisi
Inflamasi kornea yang dikarakteristikan dengan corneal oedema, cellular
infiltration dan ciliary congestion.
 Klasifikasi

Keratitis

Topographical Etiological
 Tophographical
Ulcerative keratitis
(corneal ulcer)
1. Berdasarkan Lokasi : 4. Berdasarkan kedalaman
• Central corneal ulcer ulcer :
• Peripheral corneal ulcer • Superficial corneal ulcer
2. Berdasarkan Purulensi : • Deep corneal ulcer
• Purulent corneal ulcer • Corneal ulcer with
• Non-Purulent corneal Ulcer impending perforation
3. Berdasarkan Hypopyon : • Perforated corneal ulcer
• Simple corneal ulcer (without 5. Berdasarkan pembentukan
hypopyon) slough :
• Hypopyon corneal ulcer • Non-sloughing corneal
ulcer
• Sloughing corneal ulcer
 Tophographical
Non - Ulcerative keratitis
1. Superficial keratitis
• Diffuse superficial keratitis
• Superficial punctate keratitis
(SPK)
2. Deep keratitis
a. Non-suppurative
• Interstitial keratitis
• Disciform keratitis
• Keratitis profunda
• Sclerosing keratitis
b. Suppurative deep keratitis
• Central corneal abscess
• Posterior corneal abscess.
 Disciform Keratitis

Sclerosing Keratitis
Intestitial Keratitis
 Etiological
1. Infective keratitis
• Bacterial keratitis
• Viral keratitis
• Fungal keratitis
• Chlamydial keratitis
• Protozoal keratitis
• Spirochaetal keratitis
2. Allergic keratitis
• Phlyctenular keratitis
• Vernal keratitis
• Atopic keratitis
3. Trophic keratitis
• Exposure keratitis
• Neurotrophic keratopathy
• Keratomalacia
• Atheromatous ulcer
4. Keratitis associated with
diseases of skin and mucous
membrane.
5. Keratitis associatedwith
systemic collagenvascular
disorders.
6.Traumatic keratitis which
may be due to mechanical
trauma, chemical trauma,
thermal burns, radiations.
7. Idiopathic keratitis e.g.,
• Mooren’s corneal ulcer
• Superior limbic
keratoconjunctivitis
• Superficial punctate
keratitis of Thygeson
Pharmacolo
gical
Properties
Kel. 11
Ulcerative
Keratitis
10100119177 Adinda Riany
Definisi
Corneal ulcer dapat didefinisikan sebagai
diskontinuitas permukaan epitel normal
kornea yang berhubungan dengan
nekrosis jaringan kornea sekitarnya.
Secara patologis ditandai dengan edema
dan infiltrasi seluler.
Infective keratitis
-bacterial corneal ulcer
-mycotic corneal ulcer
-viral corneal ulcer
-protozoal corneal ulcer
 01
Bacterial corneal
ulcer
 Bacterial corneal ulcer
● infective corneal ulcer may develop when:
● • Either the local ocular defence mechanism is
jeopardised, or
● • There is some local ocular predisposing disease, or
● • Host’s immunity is compromised, or
● • The causative organism is very virulen
 Epidemiology

1. The incidence of ulcerative keratitis was 27.6 per 100 000 person-years
2. The incidence of corneal ulceration in contact lens wearers was 130.4 per
100 000 person-years
 Etiology
Common bacteria associated with corneal
ulceration include :
• Staphylococci
• Pseudomonas
• Streptococcus pneumonia
• Enterobacteriaceae
• Neisseria.
following three pathogens can invade the intact
corneal epithelium and produce ulceration:
• Neisseria gonorrhoeae, Corynebacterium
diphtheriae, Neisseria meningitidis
 There are two main factors in the production of purulent corneal ulcer:
●Damage to corneal epithelium; and It
may occur in following conditions:
• Corneal abrasion due to small foreign
body, misdirected cilia, concretions and
trivial trauma in contact lens wearers or
otherwise.
• Epithelial drying as in xerosis and
exposure keratitis.
• Necrosis of epithelium as in
keratomalacia.
• Desquamation of epithelial cells as a
result of corneal oedema as in bullous
keratopathy.
• Epithelial damage due to trophic
changes as in neuroparalytic keratitis.
Infection of the eroded area, Sources of
infection include:
• Exogenous infection : arises from
exogenous source like conjunctival sac,
lacrimal sac (dacryocystitis), infected
foreign bodies, infected vegetative
material and waterborne or airborne
infections
• From the oculartissue. Owing to direct
anatomical continuity, diseases of the
conjunctiva readily spread to corneal
epithelium, those of sclera to stroma,
and of the uveal tract to the
endothelium of cornea.
 Faktor resiko

● A major risk factor for developing a corneal ulcer

is contact lens wear. People who wear soft contact
lenses for an extended period (including overnight)
are more likely to develop a corneal ulcer.
 Patogenesis
patofisiology
●Broadly bacterial corneal ulcers may manifest as:
• Purulent corneal ulcer without hypopyon; or
• Hypopyon corneal ulcer.

●In general, following symptoms and signs may be present:

●Symptoms
• Pain and foreign body sensation
• Watering from the eye occurs
• Photophobia, i.e., intolerance to light resuls
• Blurred vision
• Redness of eyes

● Signs
• Swelling of lids
• Moderato to severe Blepharospasm
• conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion.
• Corneal ulcer usually starts as an epithelial defect associated with greyish-white circumscribed infiltrate (seen in
early stage). Soon the epithelial defect and infiltrate enlarges and stromal oedema develops
• Anterior chamber may or may not show pus (hypopyon).
• Iris may be slightly muddy in colour.
• Pupil may be small
• Intraocular pressure may sometimes be raised (inflammatory glaucoma).
Hypopyon corneal ulcer definite hypopyon
 Hypopyon increases in size very rapidly and often
Causative organisms results in secondary glaucoma.
• Pneumococcus and the term ‘corneal ulcer with  Ulcer spreads rapidly and has a great tendency for
hypopyon’ for the ulcers associated with hypopyon early perforation
due to other organisms such as Staphylococci,
Streptococci, Gonococci, Moraxella and
Pseudomonas pyocyanea.
• The characteristic hypopyon corneal ulcer caused
by Pneumococcusis called ulcusserpens.

Factors predisposing to development of hypopyon.

• virulence of the infecting organism
• resistance of the tissues.

Clinical feature
• Secara umum sama seperti bacterial ulcer
• Karakteristik ulcus sepens:
 greyish white or yellowish discshaped ulcer occurring
 tendency to creep over the cornea along which the
ulcer spreads, shows more infiltration.
 . Violent iridocyclitis is commonly associated with a
Diagnosis

Physical Examination
 Slit-lamp examination:
- Gram-positive cocci: localised round or oval ulceration with greyish white stromal
infiltrates having distinct borders and minimal surrounding stromal haze.
- gram-negative bacteria : rapid inflammatory destructive course characterised by dense
stromal suppuration and hazy surrounding cornea with a ground glass appearance. 
Laboratory examination
 Routine laboratory investigations such as haemoglobin, TLC, DLC, ESR, blood sugar,
Microbiological investigations.
Microbiology examination

- Gram and Giemsa stained smears for possible identification of infecting organisms.
- 10% potassium hydroxide (KOH wet preparation is simple and quick to perform and
often gives useful information for initial medical management.
- Calcofluor white (CFW) stain preparation is viewed under fluorescence microscope
for fungal filaments, the walls of which appear bright apple green.
- Culture on blood agar medium for aerobic organisms.
- Culture on Sabouraud’s dextrose agar medium for fungi.
 Differential diagnosis

● Corneal abrasion
● Nonulcerative keratitis
● Foreign body
● Iritis
● Acute-anglen closure glaucoma
● Chemical burn
● Episcleritis
● Scleritis
● Anterior uvuitis
Treatment
Treatment of uncomplicated corneal ulcer

Specific treatment
a. Topical antibiotics
• Fortified Cefazoline, 5% i.e., 50 mg/ml freshly prepared by adding sterile water to 500 mg
powder to make 10 ml solution, and
• Fortified tobramycin, 1.3%, i.e., 13.6 mg/ml prepared by adding 2 ml of tobramycin
injection (40 mg/ml in 5 ml bottle of commercially available 0.3% tobramycin drops). or
• Freshly prepared fortified vancomycin 5%, i.e., 50 mg/ml (prepared by adding sterile water
to 500 mg vancomycin powder to form 10 ml solution) and one of commercially available
fluoroquinolones eye drops (0.3% ciprofloxacin, or 0.3% ofloxacin or 0.3% gatifloxacin or
0.5% moxifloxacin).

a. Systemic antibiotics
usually not required. However, a cephalosporine and an aminoglycoside or oral ciprofloxacin
(750 mg twice daily) may be given in fulminating cases with perforation or when sclera is also
involved
Nonspecific treatment

a. Cycloplegic drugs.
• 1% atropine eye ointment or drops should be used:
• 2% homatropine eye drops.

b. Systemic analgesics and anti-inflammatory drugs (paracetamol and ibuprofen relieve the pain
and decrease oedema)

c. Vitamins (A, B-complex and C) help in early healing of ulcer.

d. Physical and general measures

• Hot fomentation. Local application of heat (preferably dry) gives comfort, reduces pain and
causes vasodilatation.
• Dark goggles may be used to prevent photophobia
• Rest, good diet and fresh air may have a soothing effect
Treatment of non-healing corneal ulcer

• Removal of any known cause of non-healing ulcer

Local causes : intraocular pressure, concretions, misdirected cilia, impacted foreign body, dacryocystitis,
inadequate therapy, wrong diagnosis, lagophthalmos and excessive vascularization of ulcer

Systemic causes:Diabetes mellitus, severe anaemia, malnutrition, chronic debilitating diseases and patients on
systemic steroids

• Mechanical debridement ulcer to remove necrosed material by scraping floor of the ulcer with a spatula
under local anaesthesia may hasten the healing.
• Cauterisation of the ulcer may also be considered in non-responding cases. Cauterisation may be
performed with pure carbolic acid or 10–20% trichloracetic acid
• Bandage soft contact lens may also help in healing
• Peritomy, i.e., severing of perilimbal conjunctival vessels may be performed when excessive corneal
vascularization is hindering healing.
● Treatment of impending perforation
• No strain. The patient should be advised to avoid sneezing, coughing and
straining during stool, etc. He should be advised strict bed rest.
• Pressure bandage should be applied to give some external support
• Lowering of intraocular pressure by simultaneous use of acetazolamide 250
mg QID orally, intravenous mannitol (20%) drip stat, oral glycerol twice a
day, 0.5% timolol eye drops twice a day, and even paracentesis with slow
evacuation of aqueous from the anterior chamber may be performed if
required.
• Tissue adhesive glue such as cyanoacrylate is helpful in preventing
perforation
• Bandage soft contact lens may also be used.
• Conjunctival flap. The cornea may be covered completely or partly by a
conjunctival flap to give support to the weak tissue.
• Amniotic membrane transplantation may also be considered as an option.
• Penetrating therapeutic keratoplasty (tectonic graft) may be undertaken in
suitable cases, when available.
● Treatment of perforated corneal

● If perrated cornea. Depending upon the size of perforation and availability,

measures like use of
• tissue adhesive glues
• covering with conjunctival flap
• use of bandage soft contact lens or therapeutic keratoplasty should be
undertaken.
• Best option is an urgent tectonic keratoplasty
● Treatment for hypopyon corneal ulcer

treatment is almost same as the treatment of a corneal ulcer.

• overhanging edges of the ulcer are due to be excised, and the floor is to be
scraped with a spatula.
• Paracentesis to evacuate the pus if the hypopyon is massive.
• Secondary glaucoma is treated with antiglaucoma agent like Tab. acetazolamide
and timolol maleate (0.5%) eye drop.
• If there is any evidence of chronic dacryocystitis > Temporary punctal cautery
„dan Dacryocystectomy.
 Complications of Corneal Ulcer

• Toxic iridocyclitis
• Secondary glaucoma
• Descemetocele
• Perforation of corneal ulcer
Sequelae of corneal perforation include:
 Prolapse of iris
 Subluxation or anterior dislocation of lens
 Anterior capsular cataract
 Corneal fistula
 Purulent uveitis, endophthalmitis or even panophthalmitis
 Intraocular haemorrhage

• Corneal scarring
 prognosis

• If corneal ulcer is not identified and treated on time, then

it may lead to irreparable damage to the cornea leading to
permanent blindness. This is mainly because there is
significant scarring around the retina obstructing the
formation of an image in the eye.
• Corneal Ulcer is a treatable condition and majority of
people completely recover after treatment for this
condition. However, in some cases the eyesight of the
patient may become weak even after treatment of Corneal
Ulcer.
 Prevention

proper cleaning and hygiene guidelines for your contact lenses, such as:
• Wash your hands thoroughly before handling your contact lenses or touching your
eyes.
• Use commercial, not homemade, contact lens cleaning solutions.
• Clean and sterilize your contact lenses both before and after wearing them, and
store them in disinfecting solution.
• Never use tap water or saliva to moisten or store your lenses.
• Avoid wearing contact lenses for long periods of time, such as days or weeks.
• Avoid wearing contact lenses overnight.
 Prevention

Other ways yo preventing a corneal ulcer, including:

• Wash your face before you go to bed at night, especially if you wear eye makeup.
• Use protective eyewear when doing work or other activities that can cause eye
injury.
• Use artificial tears to keep your eyes lubricated if you have dry eyes and
lubricating ointment at bedtime if your eyelids do not close completely.
• If you have an eye injury or any symptoms of an eye infection, see your physician
immediately for treatment.
 02
Mycotic corneal
ulcer
●
Definisi
Corneal ulcer yang disebabkan oleh fungi has increased in the recent years due
to injudicious use of antibiotics and steroids.

● Etiology
1. Fungi
●Fungi commonly responsible for mycotic corneal ulcers are Aspergillus (most
common), Candida and Fusarium.

● 2. Modes of infection
● Injury by vegetative material , Injury by animal tail, Secondary fungal ulcers a

● 3. Role of antibiotics and steroids.

● Antibiotics disturb the symbiosis between bacteria and fungi; and the steroids
make the fungi facultative pathogens which are otherwise symbiotic
saprophytes. Therefore, excessive use of these drugs predisposes the patients
to fungal infections.
Clinical feature
• Corneal ulcer is dry-looking, greyish white, with elevated rolled
out margins
• Pigmented ulcer (brownish)
• Delicate feathery finger-like extensions are present into the
surrounding stroma under the intact epithelium.
• sterile immune ring (yellow line of demarcation)
• Multiple, small satellite lesions
• Usually a big hypopyon is present even if the ulcer is very
small, can penetrate into the anterior chamber without
perforation.
• Endothelial plaque, composed of fibrin and leucocytes, may be
located under the stromal lesion.
• Perforation
 Diagnosis
• history of injury by vegetative material are highly
suspicious of a mycotic corneal ulcer.
• Chronic ulcer worsening inspite of most efficient
treatment should arouse suspicion of mycotic
involvement.
• Laboratoryinvestigationsrequired for confirmation,
include examination of wet KOH, Calcofluor
white, Gram’s and Giemsa-stained films for fungal
hyphae and culture on Sabouraud’s agar medium.
• Confocal microscopic examination of cornea is
reported to identify actual fungi.
• Polymerase chain reaction (PCR) is also being
recommended for its rapid results.
Treatment
Specific treatment (antifunfal drugs)
1. Topical antifungal eyedrops should be used for a long period (6 to 8 weeks).
These include:
• Natamycin (5%), Amphotericin B (0.1 to 0.3%), and either Fluconalzole (0.2%), or miconazole (10
mg/ ml) or voriconazole (10%) eyedrops to be instilled initially one hourly around the clock, then
taper slowly over 6 to 8 weeks. These are effective against Aspergillus and Fusarium.
• Nystatin (3.5%) eye ointment, five times a day is effective against Candida. (For details see page
448)

2. Intracameral and intracorneal/intrastromal administration of voriconazole may be considered in cases

with intraocular extension or anterior chamber involvement.

3. Systemic antifungal drugs may be required for severe cases of deeper fungal keratitis. Tablet
fluconazole or ketoconazole or voriconazole may be given for 2–3 weeks.

Non-specific treatment
Non-specific treatment and general measures are similar to that of bacterial corneal ulcer (see page 104).
Therapeutic penetrating keratoplasty
may be required for nonresponsive cases
 03

Viral corneal ulcer

Common viral infections include herpes
simplex keratitis, herpes zoster ophthalmicus
and adenovirus keratitis
Herpes Simplex Keratitis

● Ocular infections with herpes simplex virus (HSV) are extremely common and
constitute herpetic keratoconjunctivitis and iritis

● Etiology
● Herpes simplex virus (HSV)
● HSV is of two types:
• HSV type I typically causes infection above the waist
• HSV type II below the waist (herpes genitalis). HSV-II has also been reported to
cause ocular lesions.
ocular lesions of herpes simplex
Ocular involvement by HSV occurs in two forms, primary and recurrent; with following lesions:

Primary herpes
Primary infection (first attack) involves a nonimmune person. It typically occurs in children of 6 months
till 5 years of age and in teenagers. Initial infection occurs by direct contact of mucous membranes with
infected secretions
• Systemic features
mild fever, malaise and non-suppurative lymphadenopathy. Rarely, severe morbidity can result from
multi-system failure. Disease may be fatal when encephalitis develops.
• Skin lesions
Vesicular lesions may occur involving skin of face, lips, lids, periorbital region and the lid margin
(vesicular blepharitis).
• Conjunctiva-acute follicular conjunctivitis
• Cornea
-Fine epithelial punctate keratitis
-Coarse epithelial punctate keratitis
-Dendritic ulcer
 Recurrent herpes
The reactivated virus in enveloped infectious form travels down along the trigeminal nerve to cause
recurrent infection

Active epithelial keratitis

-Symptoms : redness, pain, photophobia, tearing and decreased vision.
- sign : Punctate epithelial keratitis, Dendritic ulcer, Geographical ulcer
-treatment:
Stromal keratitis

Disciform keratitis
-Pathogenesis
It occurs due to delayed hypersensitivity reaction to the HSV antigen. Primarily,
there occurs endothelitis. Endothelial damage results in disciform corneal stromal
oedema due to imbibition of aqueous humour

- Symptoms : Photophobia, mild to moderate ocular discomfort, reduction in visual

acuity

-Sign
Disciform keratitis is characterized by (Figs. 6.9 G and H):
• Focaldisc-shapedpatchof stromal oedema without necrosis, usually with an
intact epithelium.
• Folds in Descemet’s membrane.
• Keratic precipitates under the round area of stromal edema.
• Ring of stromal infiltrate (Wessley immune ring) may be present surrounding
the stromal oedema. It signifies the junction between viral antigen and host
antibody
• Corneal sensations are diminished
• Intraocular pressure (IOP) may be raised despite only mild anterior uveitis due
to trabeculitis. In severe cases, anterior uveitis may be marked.
• Diffuse stromal necrotic keratitis
Diffuse stromal necrotic keratitis
type of interstitial keratitis (IK) caused by active
viral invasion and tissue destruction.
-Symptoms: Pain, photophobia , redness are
common symptoms.
- Signs are as below:
Corneal lesions include necrotic, blotchy, cheesy
white infiltrates that may lie under the
epithelial ulcer or may present independently
under the intact epithelium.
Mild iritis and keratic precipitates are usually
associated (herpetic keratouveitis).
Stromal vascularization
 Treatment for
disciform keratitis
• Diluted steroid eye drops instilled
4–5 times a day with an antiviral
cover (aciclovir 3%) twice a day.
Non-specific and supportive
treatment (see page 104)
• Sama kaya bacterial corneal ulcer
Treatment for
stromal nectoric
keratitis
is similar to disciform keratitis but frequently the results are
unsatisfactory.
 Systemic antiviral drugsfor 10 to 21 days are being
considered in recurrent cases and in those with
associated herpetic uveitis
 Keratoplasty should be deferred until the eye has been
quiet with little or no steroidal treatment for several
months; because viral interstitial keratitis is the form of
herpes which is most likely to recur in a new graft
Trophic keratitis (meta-herpetic)

Metaherpetic keratitis (epithelial sterile trophic ulceration) is not an active viral

disease, but is a mechanical healing problem due to persistent defects in the
basement membrane of corneal epithelium (similar to recurrent traumatic
erosions) which occurs at the site of a previous herpetic ulcer.

Clinical featurez
 indolent linear or ovoid epithelial detect
 Margin of the ulcer is grey and thickened due to heaped up epithelium.
Treatment is aimed to promote healing by use of lubricants (artificial tears),
bandage soft contact lens and lid closure (tarsorrhaphy).
Herpes Zoster Ophtalmicus
Herpes zoster ophthalmicus is an acute infection of Gasserian ganglion of the
fifth cranial nerve by the varicella-zoster virus (VZV).

Etiology
Varicella-zoster virus : It is a DNA virus and produces acidophilic intranuclear
inclusion bodies. It is neurotropic in nature

Clinical features

Acute phase lesion

1, General features: fever, malaise and severe neuralgic pain along the course of Asscociated neurological
the affected nerve
complication
2. Cutaneous lesions
3. Ocular lession -Motor nerve palsies.
Conjunctivitis -Optic neuritis occurs in
Zoster keratitis about 1% of cases
Episcleritis and scleritis -Encephalitis occurs rarely
Iridocyclitis with severe infection.
There may be associated hypopyon and hyphaema (acute haemorrhagic uveitis)
Acute retinal necrosis
Secondary glaucoma
Anterior segment necrosis and phthisis bulbi,
Chronic phase lesions
Chronic phase lesions are basically sequelae of acute phase, which may persist for up to 10 years.

1. Post-herpetic neuralgia
persistence of pain , intensity mild to moderate in intensity, worsens at night and is aggravated by
touch and heat
2, Lid lesions which occur as sequelae of scarring include ptosis, trichiasis, entropion and notching.
3, Conjunctival lesions
include chronic mucous secreting conjunctivitis
4, Corneal lesions are as below:
 neuroparalytic ulceration
 Exposure keratitis may supervene in some cases due to associated facial palsy.
 Mucous plaque keratitis develops in 5% of cases between 3rd and 5th months and is characterised by
sudden development of elevated mucous plaque which stain brilliantly with rose bengal
 Scleritis and Uveitis may persist in chronic form
Treatment
A. Systemic therapy for herpes zoster
1. Oral antiviral drugs.
Untuk decrease pain, curtail vesiculation, stop viral progression and reduce the incidence as well as severity
of keratitis and iritis
 Acyclovir in a dose of 800 mg 5 times a day for 10 days, or
 Valaciclovir in a dose of 500 mg TDS.
1. Analgesics. P
ain during the first 2 weeks of an attack is very severe and should be treated by analgesics such as
combination of mephenamic acid and paracetamol or pentazocin or even pethidine (when very severe)
2. Systemic steroids.
to inhibit development of postherpetic neuralgia when given in high doses. However, the risk of high doses
of steroids in elders should always be taken into consideration. Steroids are commonly recommended in
cases developing neurological complications such as third nerve palsy and optic neuritis.
3. Cimetidine
dose of 300 mg QID for 2–3 weeks starting within 48–72 hours of onset has also been shown to reduce pain
and pruritis in acute zoster— presumably by histamine blockade.
4. Amitriptyline should be used to relieve the accompanying depression in acute phase.
 04

Protozoal infection
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ACANTHAMOEBA KERATITIS

Etiology : Acanthamoeba castellani,

Mode of infection :
1. Contact lens wearers using home-made saline (from contaminated tap water and saline tablets) is the commonest
situation recognised for acanthamoeba infection in western countries.
2. contaminated vegetable matter, salt water diving, wind blown contaminant and hot tub use. Trauma with organic
matter and exposure to muddy water are the major (90% cases) predisposing factors in developing countries.
3. Opportunistic infection. Acanthamoeba keratitis can also occur as opportunistic infection in patients with herpetic
keratitis, bacterial keratitis, bullous keratopathy and neuroparalytic keratitis.

Clinical features
Symptoms
4. mild pain to severe pain (out of proportion to the degree of inflammation)
5. watering
6. photophobia
7. blepharospasm
8. blurred vision.
Sign
Epithelial lesions include:
● Epithelial roughening and irregularities,
● Epithelial ridges,i.e., raised epithelial lines
● Pseudodendrites formation, and
● Epithelial and subepithelial curvilinear opacities (usually fine)
Stromal lesions include:
● Radial keratoneuritis (Fig. 6.12A),
● Patchy and satellite stromal infiltrates.
● Ring infiltrates, central or paracentral,
● Ring abscess (Fig. 6.12C)
Limbal and scleral lesions include:
● Limbitis is reported in majority of cases in early stages of infection
● Scleritis, usually anterior diffuse or nodular, can be contiguous with
keratitis. Rarely posterior scleritis with optic neuritis is also reported
Allergic Keratitis

Phlyctenular keratitis, Vernal keratitis , 3.

Atopic keratitis
 Throphic Corneal Keratitis
Trophic corneal ulcers develop due to disturbance in metabolic activity of epithelial cells.
This group includes: Neurotrophic keratopathy and Exposure keratopathy
Neurothropic Keratopathy
Neurotrophic keratopathy occurs due to decreased corneal sensations owing to damage of sensory nerve supply of the
cornea.

Causes
Congenital
1. Familial dysautonomia (Riley-Day syndrome)
2. Congenital insensitivity to pain
3. Anhidrotic ectodermal dysplasia
Acquired
4. Following alcohol-block or electrocoagulation of Gasserian ganglion or section of the sensory root of trigeminal
nerve for trigeminal neuralgia.
5. A neoplasm pressing on Gasserian ganglion.
6. Gasserian ganglion destruction due to acute infection in herpes zoster ophthalmicus.
7. Acute infection of Gasserian ganglion by herpes simplex virus.
8. Syphilitic (luetic) neuropathy.
9. Involvement of corneal nerves in leprosy, diabetes.
10. Injury to Gasserian ganglion.
Clinical features
Symptoms
1. red eye, swollen eyelids and defective vision are common
complaints
2. No pain, and no tearing are characteristic features
Signs
3. Ciliary congestion is marked
4. Corneal signs include:
5. Sensations are decreased
6. Sheen is lost (dull sheen)
7. Punctate epithelial erosions involving the interpalpebral
area are initial lesions, which soon converts into,
8. Frank epithelial defects due to exfoliation of corneal
epithelium, later followed by,
9. Corneal ulcer formation, which is typically horizontally
oval, located in the lower one-half of the cornea and have
grey heaped-up epithelial borders (Fig 6.13A)
Exposure Keratopathy
When eyes are covered insufficiently by the
lids and there is loss of protective
mechanism of blinking, the condition of
exposure keratopathy (keratitis
lagophthalmos) develops.
Causes
● Extreme proptosis due to any cause will
allow inadequate closure of lids.
● Bell’s palsy or any other cause of facial
palsy
● Ectropion of severe degree
● Symblepharon causing lagophthalmos
● Deep coma associated with inadequate
closure of lids
● Physiological lagophthalmos.
Occasionally, lagophthalmos during
sleep may occur in healthy individuals.
Symptoms ( worse in the morning ).
● ocular irritation
● burning
● foreign body sensation
● redness.
Signs
● Drying of cornea occurs to begin with
due to inadequate blinking or closure of
the lids.
● Punctate epithelial defects develop in
the lower third of cornea or as a
horizontal band in the region of
palpebral fissure (Fig. 6.13).
● Corneal ulceration may develop soon
due to necrosis followed by bacterial
superinfection. If neglected, corneal
ulcer may even perforate soon
Peripheral ulcerative keratopathies
Peripheral ulcerative keratopathies (PUKs), characterized by peripheral corneal thinning,
infiltrates and ulceration, includes various conditions with different etiologies.
● Peripheral Ulcerative Keratitis Associated With Connective Tissue
Diseases (Marginal Keratolysis)

● Causes
• Peripheral corneal ulceration and/or melting of corneal tissue is not of
infrequent occurrence in patients suffering from connective tissue diseases
such as:
• Rheumatoid arthritis
• Systemic lupus erythematosus (SLE)
• Polyarteritis nodosa, and
• Wegener’s granulomatosis.

● Clinical features
• Peripheral acute corneal ulceration with rapid progression, usually in one
sector, associated with inflammation at the limbus in one or both eyes.
• Peripheral corneal guttering or thinning may involve entire corneal periphery
(contact lens cornea).
• Peripheral corneal melting may result in descemetocele formation or even
perforation.
●Treatment
• Topical medication include, antibiotics, cycloplegics and frequent instillation
of lubricating drops. Topical steroids may be used with great caution, but not
in the presence of significant thinning.
• Systemic medication includes immunosuppressants (corticosteroids, or
methotrexate, cyclophosphamide), doxycycline and oral vitamin C (to promote
a healing stromal environment).
• Surgical measures needed include:
• Excision of adjacent inflamed conjunctiva
• Bandage contact lens or conjunctival flap for impending perforation
• tissue adhesive or peripheral tectonic keratoplasty for actual perforation
Mooren’s Ulcer
Mooren’s ulcer (chronic serpiginous or rodent ulcer) is a severe inflammatory peripheral
ulcerative keratitis.
Etiology
Most probably it is an autoimmune disease (antibodies against corneal epithelium have
been demonstrated in serum).
Clinical features
Symptoms
 pain
 photophobia
 lacrimation and defective vision.
Signs
 It is a superficial ulcer which starts at the corneal margin as patches of grey infiltrates
which coalesce to form a shallow furrow over the whole cornea.
 whitish overhanging edge.
 At the end-stage, the cornea is thinned and conjunctivalised.
 Ulcer rarely perforates and the sclera remains uninvolved
Rosacea Keratitis
Corneal ulceration is seen in about 10% cases of acne
rosacea, which is primarily a disease of the sebaceous glands
of the skin.
Clinical features
1. Facial eruptions presenting in butterfly configuration,
predominantly involving the malar and nasal area of
face typically occurs in elderly women.
2. Ocularlesions include chronic blepharoconjunctivitis
and keratitis.
Rosacea keratitis occurs as yellowish white marginal
infiltrates, and small ulcers that progressively advance
across the cornea and almost always become heavily
vascularised.
 Eye Drops

Obat tetes mata (gutta). Ini adalah yang paling sederhana dan paling
metode aplikasi topikal yang nyaman, terutama untuk penggunaan siang hari. Obat tetes mata bisa berbentuk
• Aqueous Solution (obat benar-benar larut) atau
• Aqueous Suspention (obat hadir sebagai kecil partikel tetap tersuspensi dalam media berair
• Oily Solution
 Flouroquinolone

Fluoroquinolones adalah agen sintetik kuat yang memiliki: spektrum aktivitas yang luas terhadap Gram-positif dan
organisme gram negatif.
MOA : . Fluoroquinolones bersifat bakterisidal yan akan menghambat sintesis DNA bakteri.
 Analgesic

NSAID dapat diberikan untuk meredakan nyerinya. NSAID yang dapat digunakan seperti Paracetamol.
MOA : Inhibisi COX sehingga nantinya PGE2 tidak terbentuk
Indikasi : Nyeri, Demam