Dr.

Masitha Dewi Sari,SpM

Anatomi segmen anterior
CONJUNCTIVITIS
Definisi:
peradangan conjunctiva ditandai
dengan discharge (sekret) dapat
berair, mucoid, mucopurulent atau
purulent

KLASIFIKASI BERDASARKAN ETIOLOGI
1. Infective conjunctivitis : bacterial,
chlamydial, viral, fungi, spirochaetal,
protozoal, paracitic,etc,
2. Allergic conjunctivitis
3. Irritative conjunctivitis
4. Keratocinjunctivitis associated with
diseases of skin and mucous membrane
5. Traumatic conjunctivitis
6. Keratoconjunctivitis of unknown
etiology
Viral Bacteri Chlamydial Allergic
gatal minimal minimal minimal hebat
hyperemia Menye
luruh
Menye
luruh
Menye
luruh
Menyeluruh
(merah muda)
lakrimasi hebat sedang sedang Sedang
sekret minimal Paling
Hebat
hebat Hebat
nodule sering jarang Sering pd
inclusion
Tidak ada
Scraping,
pewarnaa
n
monosit Bacteri
PMN
PMN <
plasma sel
Eosinofil
demam kadang kadang Tidak ada Tidak ada
Gejala-gejala umum Conjunctivitis
1. Merasa seperti ada benda asing
2. Merasa panas (burning/scratching
sensation)
3. Perasaan mata bengkak (fullness
around the eye)
4. Gatal
5. Fotofobia (jika terkena kornea)
Tanda-tanda umum Conjunctivitis
1. Hyperemi
2. Banyak air mata
3. Chemosis (oedem conjunctiva bulbi )
4. Exudation/discharge ( kotoran mata )
5. Pseudoptosis
6. Hypertrophy papil
7. Folicle
8. Pseudomembran
9. Granuloma
10. Preauriculer adenopathy (pembesaran
kelenjar preauriculer)
Bacterial conjunctivitis
Viral conjunctivitis
Allergic conjunctivitis
Chlamydial conjunctivitis
PENANGANAN
Tergantung kausa
Hindari faktor iritasi atau alergen
Antibiotik tetes / salep tergantung
jenis konjungtivitis 3-4x/hari selama
5- 7 hari
Bacterial Conjunctivitis
Infections
Conjunctivitis
Bacterial
If severe purulent discharge and hyperacute onset
(12-24 hours), need prompt ophtho eval for work-
up of Gonococcal conjunctivitis

Gonococcal Conjunctivitis
Infections
Conjunctivitis
Viral
Monocular/Binocular watery discharge, chemosis,
conjunctival inflammation
Associated with
Viral respiratory symptoms
Palpable preauricular node
Fluorescein stain may reveal superficial keratitis
Treatment:
Cool compresses
Naphazoline/pheniramine for conjunctival congestion
Ophthalmology follow up in 7-14 days
Infections
Conjunctivitis
Allergic
Monocular/binocular pruritis, watery discharge, chemosis
History of allergies
No lesions seen with fluorescein staining, no preauricular
nodes, Conjunctival papillae
Treatment:
Eliminate inciting agent
Cool compresses
Artificial tears
Naphazoline/pheniramine
Infections
Conjunctivitis
Allergic
Monocular/binocular pruritis, watery discharge, chemosis
History of allergies
No lesions seen with fluorescein staining, no preauricular
nodes, Conjunctival papillae
Treatment:
Eliminate inciting agent
Cool compresses
Artificial tears
Naphazoline/pheniramine
Infections
Herpes Simplex Virus
Classic: Dendritic epithelial defect
ED care depends on the site of infection
Eyelid and conjunctiva
Topical antivirals (trifluorothymidine drops/vidarabine
ointment) 5 times/day
Topical erythromycin ointment
Warm soaks
Cornea
Topical antivirals 9 times/day
Anterior chamber
Cycloplegic agent may be used
First 3 days of infection: Acyclovir/famcyclovir
Infections
Herpes Zoster Ophthalmicus
Shingles with trigeminal distribution, ocular
involvement, concurrent iritis
Pseudodentrite
Mucous corneal plaque with epithelial erosion
Treatment:
Acyclovir
Topical antivirals
Warm compresses
Oral analgesics or cycloplegics for pain relief
Ophthalmology consult mandatory
Infections
Herpes Zoster Ophthalmicus
Shingles with trigeminal distribution, ocular
involvement, concurrent iritis
Pseudodentrite
Mucous corneal plaque with epithelial erosion
Treatment:
Acyclovir
Topical antivirals
Warm compresses
Oral analgesics or cycloplegics for pain relief
Ophthalmology consult mandatory
Herpes Zoster Ophthalmicus
Shingles with trigeminal
distribution, ocular involvement,
concurrent iritis
Pseudodentrite
Mucous corneal plaque with
epithelial erosion
Treatment:
Acyclovir
Topical antivirals
Warm compresses
Oral analgesics or cycloplegics
for pain relief
Ophthalmology consult
mandatory
Infections
Traumatic Eye Injuries
Conjunctival Foreign Bodies
Lid eversion
Remove with a moistened sterile swab
PENGUICULA

Definisi
Penebalan conjunctiva mata berbentuk
segitiga yang puncaknya menghadap kornea
yang terdapat di conjunctiva bulbi pada celah
mata. Bisa terjadi pada nasal dan temporal sit
Patologinya sama dengan pterygeum
Etiologi :
Iritasi
Matahari
Debu
Angin
Klinis :
Penonjolan warna kuning seperti lemak
PA : hyalin (+) dan suatu elastic degeneration
dari lapisan submucosa
Penimbunan kalsium pada penguicula tsb

Pengobatan :
Tidak perlu
Bila terjadi inflamasi beri steroid topical
Artificial tears
PTERYGEUM
Definisi : Penebalan conjunctiva berbentuk
segitiga puncaknya dekat ke kornea/mencapai
ke kornea

Klinis :
- Pembuluh darah membesar
- visus menurun oleh karena astigmatisma
irreguler pembiasan tidak pada satu tempat
- stroma proliferasi
- sering pada bagian nasal, dalam
pertumbuhannya bisa sampai pada pupil
Gejala :
- panas
- merasa seperti ada benda asing
Pengobatan :
tidak spesifik, bila ada tanda-tanda inflamasi
beri steroid topikal

Indikasi Operasi
- pertumbuhannya progressif > 2 cm
- Gangguan visus
- gangguan gerakan bola mata
- iritasi berulang merah
- keluhan kosmetik
- apabila recidif, beri sinar beta atau extirpasi,
lakukan transplantasi dari mukosa mulut, kantung
amnion atau conjunctiva lain

Patologi :
- epitel kornea
- membrana bowmen hilang/rusak
- stroma prokiferasi seperti jaringan
granulasi

INFLAMASI PADA KORNEA
Peradangan pada kornea (keratitis)
dengan karakteristik oedem kornea,
infiltrasi seluler, dan kongesti siliar
Klasifikasi topographical
(morphological)
A. Ulcerative keratitis (corneal ulcer)
1. Berdasarkan lokasi
(a) ulkus kornea sentral
(b) ulkus kornea perifer
2. Berdasarkan purulen
(a) ulkus kornea purulenta / suppurative
(b) ulkus kornea non purulen
3. Berdasarkan hypopion
(a) ulkus kornea simple (tanpa hypopion)
(b) ulkus kornea hypopion

4. Berdasarkan kedalaman ulkus
(a) superfisial
(b) deep
(c) ulkus kornea dengan impending
perforation
(d) ulkus kornea perforasi
B. Non ulcerative Keratitis
1. Superficial keratitis
(a) diffuse superficial keratitis
(b) superficial punctate keratitis
2. Deep keratitis
(a) non suppurative
(b) suppurative deep keratitis
GEJALA
Mata merah
Nyeri
Fotofobia
Pandangan kabur
berair
Pemeriksaan
Tajam penglihatan menurun
tes fluorescein (+) defek
Pada infeksi berat hypopion
KERATITIS SUPERFICIAL PURULENTA
(ULCUS CORNEAL)
Defenisi
- infeksi cornea dengan adanya infiltrasi dan
hilangnya substansi cornea
- hampir slamanya exogenous oleh
organisme pyogenik
- penyebab ulcus cornea tanpa lesi epithel :
* gonorrhea
* diphterioe
Bakteri lain harus ada lesi epithel ulcus
cornea
Staphylococcus menyebabkan superficial
punctate erotion
PENYEBAB
1. Bakteri
a. Pneumococcus
b. Staphylococcus aureus, Staphylococcus epidermidis
c. Alpha Haemolyticus Streptococcus
d. Nocardia
e. Mycobacterium
f. Streptococcus viridans
g. Klebsiella pneumonia

2. Virus
a. Herpes simplex
b. varicella zoster
c. Variola
d. Adenovirus

3. Fungal
a. Aspergillus
b. Candida
c. Cephalosorium
d. Fusarium
e. Penicillium
4. Autoimmune
5. Amuba

PATOLOGI

Terjadi nekrose setempat pada lapisan cornea (sampai
stroma)
Sequestrum lepas dan jatuh pada saccus conjunctiva
(sel mati dan mikroorganisme, sel-sel radang). Sebagian
sequestrum menempel pada permukaan ulcus,
epitel yang rusak lebih luas dari ulcusnya sendiri,
begitu juga pada lapisan bowman

Epitel dengan cepat tumbuh ke arah ulcus, tumbuh pada
pinggir bahkan diatas infiltrat. Dasar ulcus menonjol
karena adanya inhibisi cairan sekret ulcus.
Batas antara ulcus dan jaringan sehat, sama
seperti bagian tubuh yang lain, yaitu ada dinding
PMN leukosit, lekosit membentuk lapisan kedua
pertahanan, sedang lekosit berfungsi sebagai :
- digestive : mencerna
- macerating : menghancurkan
- dissolving : melarutkan jaringan nekrose

Jaringan mati terlepas ulkus tambah lebar
dan kekeruhan berkurang

Dasar dan pinggiran ulkus transparan
perbaikan mulai terjadi
Terbentuk pembuluh darah halus dari limbus dekat
ulcus untuk mensuplai antibody dan menyerap
bahan-bahan yang rusak untuk mengatasi infeksi
beberapa bakteri mengeluarkan toksin meresap ke
cornea sampai COA merangsang pembuluh
darah iris dan corpus ciliare sehingga terjadi
hiperemi iris

Iritasi/peradangan bisa terlalu hebat sehingga
leukosit dan PMN keluar dari pembuluh darah masuk
ke COA dan mengendap di bagian COA disebut
hypopion


SIMPTOM
Ulcus cornea pada stadium akut/progresive ulcus
- blepharospasme
- lacrimation
- fotophobia dan pain

SIGN
Visus menurun ulcus central
Infiltrat dengan lesi epitel di atasnya
Ciliary injection
Iridocyclitis keratitis precipitate , hypopion
Pannus (pembuluh darah yang masuk ke cornea)


DD MATA MERAH
Conjunctivitis akut
Glaukoma akut
Keratitis
Uveitis

PENYEMBUHAN ULCUS
Pannus (+) ada cicatrix pada bekas
ulcus
Serabut yang baru terbentuk tidak tersusun
teratur sebagaimana normalnya bias
cahaya tidak teratur
Parut luas pembuluh darah besar
/menetap
Membran bowman tidak tumbuh lagi
Cornal focets cicatrix tidak keruh /
transparan dan permukaannya datar (mata
serangga)
Nb : tidak terbentuk jaringan ikat, tapi cornea
masuk ke dalam.

BERDASARKAN KETEBALAN
CICATRIX DIBAGI :
1. Nebula : kekeruhan ringan, dapat
dilihat dengan lup
2. Macula : kekeruhan lebih jelas
dapat dilihat dengan mata telanjang
3. Leucoma : kekeruhan jelas sekali
jika kekeruhan sangat menebal
(leukoma adherent) pelengketan ke
depan ke belakang cornea
dengan permukaan iris
KOMPLIKASI
Cicatrix
Penyembuhan cicatrix yang tidak sempurna, cornea di bekas
ulcus menonjol/bulging disebut : ECTATIC CICATRIX =
KERAECTASIS
Descematocele
Ulcus dalam seluruh stroma dikenai kecuali descement
membrane menonjol oleh karena tekanan intra oculi
sehingga terlihat gelembung yang transparant
Hypopion
sebelum perforasi : steril (Ag-Ab reaction)
Perforation
Synechia Anterior
Kalau perforasi kecil, iris akan menutupnya sehingga ada
perlengketan iris ke kornea atau organisasi
Leucoma Adherent
pada bagian cornea yang perforasi terbentuk parut tebal
dimana iris tetap melekat dibawahnya.
Intra Oculer Haemorrhage
Perforasi tiba-tiba dilatasi tiba-tiba pada pembuluh darah
intra ocular ruptur pembuluh darah

Treatment :
1. Mengatasi infeksi:
Antibiotika tetes & salep broad
spectrum k/p sensitivity test
Ada tak menganjurkan salep dasar
salep memperlambat epithelisasi
Skrg dipakai fortified anti biotic drops
k/p antibiotica sub-conjunctival
AB systemic oral & injection obat yg
dpt melalui blood aquouse barrier
2. Midriaticum
Sulfas atropin tetes mata 1% 3 guttae/hari untuk :
Mengistirahatkan iris dan corpus ciliare
Mencegah synechia
Mencegah iridocyclitis

3. Kebersihan Ulcus
Bersihkan saccus conjunctiva 3 kali atau lebih
dengan antiseptik lotion hangat
Fungsi :
Antiseptik
Menghilangkan sekret dan jaringan mati
Menghilangkan mikroorganisme
Antiseptik :
Acidum boricum 3% (2%)
Amonium totrat normal 10%
Mercuryl axicyanide 0.01%

4. Pemanasan (Heat)
Moist heat kompres hangat dengan acidum
boricum hangat beri 3 kali atau lebih
Dry heat penyembuhan lebih cepat
5. Perbaiki Keadaan Umum
6. Benda asing (corpus alineum)
- diangkat / ekstersi
7. Scrapping dan Cautherization
Scrapping mengatasi meluasnya ulcus, dinding dan
dasar ulcus
Cautherization
- panas : electrocautery
actual cautery
- Chemical: yodium tinctur
puroliqueel carbonic acid 2 sampai 3 kali
interval 1-2 hari
8. Tarsorrhapy
Menjahit kelopak mata atas dan bawah (agar obat
dapat mencapai ulcus melalui conjunctiva)
9. Conjunctival Flap
Ulcus ditutup dengan conjunctiva bulbi
brigde ataupun total
10. Parasintesis
Tujuan
- mencegah perforasi
- menghilangkan rasa sakit
- Nutrisi pada cornea yang sakit
- membawa antibodi yang baru

Superficial punctate keratitis
Ulkus kornea
Ulkus kornea dgn hypopion
penangananan
Antibiotika tetes / salep dapat diberi setiap
30 menit 1 jam, tergantung keparahan
infeksinya
Hindari pemakaian steroid
Antibiotika fortified pd kasus ulkus
kornea berat (dgn hypopion)
Cycloplegic (atropin tetes)
Injeksi antibiotika subconjunctiva
Antibiotika oral gol.fluoroquinolone
(mis. Ciprofloxacin 2 x 500mg),penetrasi
ke kornea baik
Injeksi subconjunctiva
Complicated Corneal Ulcer
Perforated Corneal Ulcer
Healed Keratocele
Hypopyon Ulcer
Types
Corneal Ulcer (Superficial Purulent
Keratitis) with Hypopyon
Ulcer Serpen
Hypopyon Ulcer
There is always an associated iritis in
all cases of Corneal Ulcer due to
diffusion of toxins of infecting bacteria
into the eye.
Sometimes iridocyclitis is so severe
that it is accompanied by outpouring of
leucocytes from uveal blood vessels
and these cells gravitate to bottom of
the anterior chamber to form hypopyon
(pus in anterior chamber)
Introduction
The hypopyon which forms in bacterial
keratitis is sterile as the leucocyte
secretion is due to irritation by toxins and
not by the bacteria
Hypopyon may develop in hours and it
may change in quantity and may also
rapidly disappear.
Hypopyon in bacterial keratitis is fluid and
changes its position with change in head
posture
Etiology
Predisposing Factors
1. High Virulence of infecting
organism
2. Resistance of the tissues, which is
low
3. Dacryocystitis
4. Ocular trauma
5. Old, debilitated or alcoholic
6. Measles or scarlet fever
Organisms
Pyogenic organisms like
Staphylococci, Streptococci,
Gonococci, Moraxella, Pseudomonas
and Pneumococci

Hypopyon Ulcer
Ulcus Serpen
Ulcus Serpen is hypopyon ulcer
caused by Pneumococci in adults
and has tendency to creep over the
cornea in serpiginous fashion
Symptoms
Sever pain, photophobia, marked
diminution of vision, watering,
foreign body sensation (grittiness)
Signs
Grayish white or yellowish disc like
lesion near centre of cornea. Opacity is
marked at edges than at the centre and
more marked in one direction (where it
is progressive). In the direction of
progression there is cloudiness (grey
coloured) and fine line ahead of disc
Cornea may be lusterless. There is
severe iritis and aqueous is hazy or
there may be rank hypopyon amount
which varies
Signs
Untreated ulcer increases in depth and
spread towards the side of dense
infiltration, while on the other side
simultaneously healing (cicatrization)
takes place.
There is infiltration just anterior to
Descemets membrane underneath the
floor of ulcer with normal intervening
lamellae, due to which there is tendency
for perforation of cornea. Intra-ocular
tension is usually raised in these cases.
Complications
Untreated cases progresses to
increase in hypopyon which
becomes fibrinous leading to
perforation Iris prolapse through
large opening whole cornea may
slough leaving peripheral cornea
which is nourished by limbal
vascular loops. Eventually
panophthalmitis develops which
destroys the eye
Treatment
Routine treatment of Corneal Ulcer
Tab Acetazolamide
Local Betablocker
Therapeutic keratoplasty
Control of infection results in
absorption of hypopyon


Fungal Keratitis
Fungal Keratitis
Fungal keratitis is challenging corneal
disease and presents as very difficult form
bacterial keratitis. Difficulty arise in
making correct clinical and laboratory
diagnosis. The treatment of fungal
keratitis is also difficult due to poor
availability of antifungal drugs and delay
in starting treatment.
Treatment is required on long term basis,
intensively and often cases require
therapeutic keratoplasty.
Fungal Keratitis
Fungi enter into corneal stroma through
epithelial defect, which may be due to
trauma, contact lens wear, bad ocular
surface or previous corneal surgery.
In stroma fungi multiply and causes tissue
necrosis and inflammatory reaction.
Organisms enter deep into the stroma and
through an intact Descemets membrane
into the anterior chamber and iris. They
can also involve Sclera.
Fungal Keratitis
The spread is due to the fact that the
blood borne growth inhibiting factors
may not reach the avascular tissue
like cornea and sclera.
Risk Factors
1. Trauma outdoor/ or the one which
involves plant matter (including
contact lenses)
2. Topical medications:
corticosteroids, anaesthetic drug
abuse and topical broad spectrum
antibiotics use for long time
(resulting in non-competitive
environment for growth)
Risk Factors
3. Systemic use of steroids
4. Corneal surgeries (Penetrating
keratoplasty, refractive surgery)
5. Chronic keratitis (herpes simplex,
herpes zoster, Vernal or allergic
keratoconjunctivitis, and
neurotrophic ulcer)
6. Diabetes , Chronically ill /
hospitalised patients, AIDS and
leprosy

Causative fungi
I. Yeast: Candida species (albicans),
Cryptococcus
II. Filamentous septated
A. Non-pigmented hyphae:
Fusarium species (solani),
Aspergillus species (fumigatus,
flavus, niger)
B. Pigmented hyphae
(dematiaceous): Alternaria,
Curularia , Cladosporium species
Causative fungi
III. Filamentous non-septated : Mucor
and Rhizopus species
IV. Diphasic forms: Histoplasma,
Coccidiodes, Blastomyces
Clinical Features
Symptoms

Onset is slow
Symptoms are less compared to
signs
Diminution of vision, pain, foreign
body sensation
Signs
Diminution of vision, depending on
location of ulcer
Conjunctival and ciliary congestion
Epithelial defect
Stromal infiltrates
Elevated areas, hypate (branching)
ulcers, irregular feathery margins
Dry and rough texture
Fungal Keratitis with Hypopyon
Signs
Satellite lesions
Brown pigmentation due to
dematiaceous fungus (Curvularia
lunata)
Intact epithelium with stromal
infiltrates
Anterior chamber reaction
Fungal Keratitis
Fungal Keratitis Pigmented Lesion
Case of Fungal+ Bacterial Keratitis
Laboratory Diagnosis
The Gram and Giemsa stains are used as
initial stains
Potassium Hydroxide (10-20 %) wet
mounts
Culture Media: Sheep blood agar,
Chocolate agar, Sabouraud dextrose
agar, Thioglycollate broth
Anterior chamber tap under aseptic
conditions to aspirate hypopyon and or
endothelial plaque
Treatment
Natamycin 5% suspension:
frequency will depend on severity of
condition
Candida species respond better to
Amphotericin B 0.15%
Fluconazole 2%
Miconazole 1%
Scrapping every 24 to 48 hours
Treatment is required for 4 6 weeks
Treatment
Sub-conjunctival injection of
Miconazole 5 10 mgm of 10 mgm/ml
suspension (indicated in severe form
of keratitis, scleritis and
endophthalmitis)
Systemic:
Fluconazole or Ketoconazole is
indicated in severe form of keratitis,
scleritis and endophthalmitis
Surgical Treatment
1. Daily debridement with spatula/
blade every 24 48 hours
2. Surgical treatment is required in
approximately 1/3
rd
cases of fungal
keratitis due to failure of medical
treatment or perforation
3. Surgical treatment in the form of :
therapeutic keratoplasty,
conjunctival flap or lamellar
keratoplasty
Surgical Treatment
Surgery is usually indicated within 4
weeks due to failure of medical
treatment or recurrence of infection
Unfavorable outcome is due to
scleritis, endophthalmitis and
recurrence
Cryotherapy with topical antifungal
treatment or corneoscleral graft in
cases of fungal scleritis and
keratoscleritis

VIRAL KERATITIS
Introduction
Viruses are obligate intracellular parasites
that contain only one type of nucleic acid
within he infectious unit and are unable to
replicate by binary fission.
Viruses that cause corneal disease are
Herpes simplex ( HSV)
Varicella zoster ( VZV)
Epstein Barr ( EBV)
Adenovirus
Cytomegalovirus (CMV) can also cause
keratitis and is more commonly
associated with AIDS
Epidemiology and pathogenesis
HSV, VZV, EBV, and CMV are all
members of the family Herpesviridae.
DNA viruses
There are two types of HSV
HSV-1 is more commonly associated
with labial and ocular infection.
HSV-2 is associated with genital
infection.
Ophthalmology 2004, (2), 475-481
Epidemiology and pathogenesis
Herpes simplex keratitis is a leading cause
of corneal blindness in the developing
world.
Estimated prevalence is approx 150 per
100,000 population.
Ocular HSV tends to be a unilateral
disease with only one eye affected by
primary disease in approx 80-90% of
cases.
Atopy appears to be risk factor for
bilateral disease, & is associated with
gastric cancer, lumbar zoster, malaria and
pulmonary tuberculosis
HERPES SIMPLEX KERATITIS
Herpes Simplex Keratitis occurs in two
forms:

1. Primary

2. Recurrent
Primary HSV-1 (HSV type 1) infections
Occurs most commonly in the mucocutaneous distribution of the
trigeminal nerve.
spread of
Primary virus Infected Nearby
Infection epithelial cells sensory nerve
endings

Viral genome Cell body in transport
along
enters nucleus trigeminal ganglion
nerve axon
at neuron

(Persists indefinitely
in a latent state)
PRIMARY HSV-1
Primary infection of any of the 3 branches
(ophthalmic, maxillary, mandibular) of
cranial nerve V leads to latent infection of
nerve cells in trigeminal ganglion.
Interneuronal spread of HSV within
ganglion allows patients to develop ocular
disease without ever having had primary
ocular HSV infection.

www.emedicine.com
RECURRENT HSV INFECTION
Has been thought of as reactivation of
virus in the sensory ganglion.
Virus migrates down nerve axon to
produce lytic infection in ocular disease.
Recent evidence suggests, virus may
subsist latently within corneal tissue,
serving as a potential source of recurrent
disease.
www.emedicine.com
CLINICAL FINDINGS
Primary Herpes Simplex Keratitis
Infrequently seen
Manifested as vesicular
blepharoconjunctivitis occasionally with
corneal involvement
Usually occurs in young children
Topical antiviral therapy may be used as
prophylaxis and as therapy

Vaughan & Asburys General Ophthalmology 16
th
Edition, 136
CLINICAL FINDINGS
Recurrent type herpetic keratitis
Attacks triggered by
Fever
Overexposure to UV light
Trauma
Onset of menstruation
Local/ systemic source of
immunosuppression
Bilateral lesions develop in 4-6% of
patients and seen mostly in atopic
patients.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136

SYMPTOMS
Irritation
Photophobia
Tearing
Reduction in vision (when central
cornea is affected)
Corneal anesthesia usually occurs
early in the course of infection and
thus symptoms may be minimal.
SYMPTOMS
Corneal ulceration can occasionally
be the only sign of recurrent herpetic
infections
Recurrent herpes simplex virus
dendritic ulcer with an adjacent
stromal scar

LESIONS: Dendritic ulcer
Most characteristic lesion, occurs in corneal
epithelium
Typical branching, linear pattern with
feathery edges and terminal bulbs at ends.
Visualized by fluorescein staining
HSV dendritic ulcer stained
with fluorescein
Dendritic keratitis

This patient suffers from herpetic keratitis. Fluorescein
staining reveals dendritic ulcer typical of herpes keratitis.
This is treated with topical 3% acyclovir
www.eyecasualty.co.uk/.../ cornealinfections.html

Geographic ulceration
Form of chronic dendritic disease.
Delicate dendritic lesions take a
broader form.
Corneal sensation is diminished
HSV geographic ulcer
Other corneal lesions
Other corneal epithelial lesions caused by
HSV are
Blotchy epithelial keratitis
Stellate epithelial keratitis
Filamentary keratitis
Usually transitory, often become typical
dendrites within a day or two.

Filamentary keratitis
Subepithelial lesions
Caused by HSV infection
Ghost like image, larger than original
epithelial defect seen in the area
immediately underlying epithelial
lesion.
Does not persist for more than a year
Disciform keratitis
Most common form of stromal disease in HSV
infection.
Edematous stroma without significant infiltration
and usually without vascularization.
Edema is most prominent sign.
Keratic precipitates may lie directly under
disciform lesion but may also involve the
endothelial lesion.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136
Peripheral lesions of the cornea
Caused by HSV
Usually linear lesions, show loss of
epithelium
Testing for corneal sensation is
unreliable.
Patient is far less photophobic than
patients with nonherpetic corneal
infiltrates.
Treatment
Should be directed at eliminating
viral replication within the cornea,
while minimizing damaging effects of
inflammatory response.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137
Treatment
DEBRIDEMENT
Epithelial debridement is an
effective way to treat dendritic
keratitis
Infected epithelium is easy to
remove with tightly wound cotton tip
applicator.
Adjunctive therapy with topical
antiviral accelerates epithelial
healing.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137

Treatment

Ophthalmology 2004, (2), 475-482
TREATMENT : DRUGS
Treatment
Trifluridine and acyclovir are much
more effective in stromal disease than
others.
Idoxuridine and trifluridine are
frequently associated with toxic
reactions.
Oral acyclovir may be useful in
treatment of severe herpetic eye
disease particularly in atopic
individuals.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137
Treatment
Oral acyclovir : DOSAGE:
For active treatment 400 mg five times daily in
nonimmunocompromised patients.
800 mg five times daily in compromised and atopic
patients.
Prophylactic dosage in recurrent disease is 400
mg twice daily.

Famciclovir or valacyclovir may also be used.
Topical corticosteroids accelerate corneal
thinning, increasing risk of corneal perforation.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137
Surgical treatment
Penetrating keratoplasty indicated for visual
rehabilitation in patients with sever corneal
scarring. Should not be undertaken until herpetic
disease has been inactive for many months.
Systemic antiviral agents should be used for
several months after keratoplasty to cover use of
topical steroids.

Lamellar keratoplasty has advantage over
penetrating keratoplasty of reduced potential for
corneal graft rejection.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137
Varicella zoster viral keratitis
(VZV)
Occurs in two forms:
Primary ( varicella)
Recurrent ( herpes zoster)

Ocular manifestations are
uncommon in varicella but common
in ophthalmic zoster.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137
Varicella zoster viral keratitis
(VZV)
Ocular manifestations
Usual eye lesions are pocks on lids
and lid margins.
Keratitis occurs rarely.
Epithelial keratitis with or without
pseudodendrites occurs more rarely.
Disciform keratitis with uveitis of
varying duration has been reported.
Ophthalmic herpes zoster
Is accompanied by keratouveitis that varies in
severity according to immune status of the
patient.
Children with zoster keratouveitis usually have
benign disease, aged have severe and sometimes
blinding disease.
Corneal complications in ophthalmic zoster often
occur if there is skin eruption in areas supplied by
branches of the nasociliary nerve.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137

Distinguishing features of dendrites
associated with HSV versus VZV
Feature HSV VZV
Overall Fine, lacy Thick ropy
Epithelium Linear defect with
bared stroma,
surrounded by
edematous epithelial
cells
Elevated, painted-on
appearance
Staining Base stains with
fluorescein. Diseased
border epithelial cells
stain with rose
bengal
Minimal fluoroescein
staining
Terminal bulbs Frequent None
Treatment
Intravenous and oral acyclovir have been
used successfully for treatment of herpes
zoster ophthalmicus, particularly in
immunocompromised patients.
Oral dosage is 800 mg five times daily for
10-14 days.
Therapy needs to be started within 72
hours after appearance of the rash.
Vaughan & Asburys General Ophthalmology 16
th
Edition, 136-137

Traumatic Eye Injuries
Corneal Foreign Bodies
May be removed with fine needle tip, eye spud,
or eye burr after topical anesthetic applied
Then treat as a corneal abrasion
Deep corneal stoma FB or those in central
visual axis require ophtho consult for removal
Rust rings can be removed with eye burr, but
not urgent
Optho follow up in 24 hours for residual rust or
deep stromal involvement
UVEITIS
ANTERIOR
Autoimmune
Infections
Malignancy
Others
POSTERIOR
Viruses
Bacteria
Fungi
Autoimmune
Malignancy
Unknown
UVEITIS
Inflammation of the uveal tract
Symptoms
blurred vision
Photophobia
Pain
UVEITIS
Inflammation of the uveal tract
Signs
Injection
Flare
Keratic precipitates
Posterior synechias
iris nodules
UVEITIS
Complications
Anterior synechias
Posterior synechias
Cataract
Glaucoma
Macular edema
UVEITIS
Autoimmune
JRA
Ankylosing spondylitis
Ulcerative colitis
Crohns disease
Reiters syndrome
Lens induced
UVEITIS
Infections
Syphilis
Tuberculosis
Herpes zoster
Herpes simplex
Adenovirus
UVEITIS
Malignancy
Retinoblastoma
Leukemia
Lymphoma
Malignant melanoma
UVEITIS
Others
Idiopathic
Traumatic
RD
Fuchs iridocyclitis
Gout
UVEITIS
Posterior
CMV
Toxoplasmosis
Aids
Herpes simplex
Herpes zoster
Candida
UVEITIS
Autoimmune
Behcets syndrome
VKH syndrome
Polyarteritis nodosa
Sympathetic ophthalmia
UVEITIS
Malignancy
Malignant melanoma
Leukemia
Metastatic lesions

Unknown
Sarcoidosis


UVEITIS
TREATMENT
Steroids
topical
local
systemic
Cycloplegics
Antimetabolites
Analgesics
ENDOPHTHALMITIS
Peradangan bola mata yg melibatkan
uvea dan retina, disertai dgn eksudat
di vitreous, camera okuli anterior dan
camera okuli posterior
Gejala
Nyeri yg hebat
Pandangan kabur
Mata merah

Pemeriksaan
Penurunan tajam penglihatan
Injeksi konjungtiva
Peradangan COA dan hypopion
Funduskopi : nervus opticus dan
retina tidak dapat dilihat dgn jelas
krn adanya inflamasi vitreous

endophthalmitis
USG
Penanganan
Antibiotik fortified topikal tiap jam :
cefazolin atau vancomycin,
gentamycin atau tobramycin
Antibiotika injeksi subconjunctiva
Vitrectomy dan antibiotika injeksi
intravitreal

Vitrectomy diindikasikan pada pasien
yang tidak menunjukkan kemajuan
terapi dlm 48 72 jam atau pd pasien
dgn infeksi berat dmn tajam
penglihatan hanya persepsi cahaya.
Vitrectomy bermanfaat utk
mengeluarkan organisme,toksin dan
enzim pada vitreous
PANOPHTHALMITIS
Inflamasi purulenta pada seluruh
struktur bola mata termasuk kapsula
Tenon
Gejala
Nyeri mata yg sgt berat dan nyeri kepala
Hilangnya penglihatan
Sangat berair
Sekret purulen
Mata sangat merah dan bengkak
Demam
malaise
Tanda
Kelopak mata oedem dan hiperemis
Bola mata sedikit proptosis, pergerakan
bola mata terbatas & nyeri
Chemosis konjungtiva
Kornea keruh
COA berisi pus seluruhnya
Tajam penglihatan hilang (NLP)
TIO meningkat
perforasi
panophthalmitis
Penanganan
Anti-inflamasi dan analgetik
Antibiotika spektrum luas
eviscerasi
eviscerasi