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Dr. Masitha Dewi Sari,SpM
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Anatomi segmen anterior
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CONJUNCTIVITIS
Definisi:
peradangan conjunctiva ditandai
dengan discharge (sekret) dapatberair, mucoid, mucopurulent atau
purulent
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KLASIFIKASI BERDASARKAN ETIOLOGI
1. Infective conjunctivitis : bacterial,chlamydial, viral, fungi, spirochaetal,protozoal, paracitic,etc,
2. Allergic conjunctivitis3. Irritative conjunctivitis
4. Keratocinjunctivitisassociated withdiseases of skin and mucous membrane
5. Traumatic conjunctivitis
6. Keratoconjunctivitis of unknownetiology
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Viral Bacteri Chlamydial Allergic
gatal minimal minimal minimal hebat
hyperemia Menyeluruh
Menyeluruh
Menyeluruh
Menyeluruh(merah muda)
lakrimasi hebat sedang sedang Sedang
sekret minimal PalingHebat
hebat Hebat
nodule sering jarang Sering pd
inclusion
Tidak ada
Scraping,
pewarnaa
n
monosit Bacteri
PMN
PMN 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, kantungamnion atau conjunctiva lain
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Patologi :
- epitel kornea
- membrana bowmen hilang/rusak- stroma prokiferasi seperti jaringan
granulasi
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INFLAMASI PADA KORNEA
Peradangan pada kornea (keratitis)
dengan karakteristik oedem kornea,
infiltrasi seluler, dan kongesti siliar
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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
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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 impendingperforat ion
(d) ulkus kornea perforasi
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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
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GEJALA
Mata merah
Nyeri
Fotofobia Pandangan kabur
berair
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Pemeriksaan
Tajam penglihatan menurun
tes fluorescein (+) defek
Pada infeksi berat hypopion
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KERATITIS SUPERFICIAL PURULENTA
(ULCUS CORNEAL)
Defenisi- infeksi cornea dengan adanya infiltrasi dan
hilangnya substansi cornea
- hampir slamanya exogenous olehorganisme pyogenik
- penyebab ulcus cornea tanpa lesi epithel :
* gonorrhea
* diphterioeBakteri lain harus ada lesi epithel ulcuscornea
Staphylococcus menyebabkan superficial
punctate erotion
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PENYEBAB
1. Bakteri
a. Pneumococcusb. Staphylococcus aureus, Staphylococcus epidermidis
c. Alpha Haemolyticus Streptococcus
d. Nocardia
e. Mycobacterium
f. Streptococcus viridansg. Klebsiella pneumonia
2. Virus
a. Herpes simplex
b. varicella zosterc. Variola
d. Adenovirus
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3. Fungal
a. Aspergillus
b. Candida
c. Cephalosorium
d. Fusarium
e. Penicillium
4. Autoimmune
5. Amuba
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PATOLOGI
Terjadi nekrose setempat pada lapisan cornea (sampai
stroma) Sequestrum lepas dan jatuh pada saccus conjunctiva
(sel mati dan mikroorganisme, sel-sel radang). Sebagiansequestrum 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 padapinggir bahkan diatas infiltrat. Dasar ulcus menonjol
karena adanya inhibisi cairan sekret ulcus.
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Batas antara ulcus dan jaringan sehat, samaseperti bagian tubuh yang lain, yaitu ada dindingPMN leukosit, lekosit membentuk lapisan keduapertahanan, sedang lekosit berfungsi sebagai :
- digestive : mencerna- macerating : menghancurkan
- dissolving : melarutkan jaringan nekrose
Jaringan mati terlepas ulkus tambah lebardan kekeruhan berkurang
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Dasar dan pinggiran ulkus transparan perbaikan mulai terjadi
Terbentuk pembuluh darah halus dari limbus dekatulcus untuk mensuplai antibody dan menyerapbahan-bahan yang rusak untuk mengatasi infeksibeberapa bakteri mengeluarkan toksin meresap kecornea sampai COA merangsang pembuluhdarah iris dan corpus ciliare sehingga terjadi
hiperemi iris
Iritasi/peradangan bisa terlalu hebat sehinggaleukosit dan PMN keluar dari pembuluh darah masukke COA dan mengendap di bagian COA disebuthypopion
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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)
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DD MATA MERAH
Conjunctivitis akut
Glaukoma akut
Keratitis
Uveitis
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BERDASARKAN KETEBALAN
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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
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KOMPLIKASI
Cicatrix
Penyembuhan cicatrix yang tidak sempurna, cornea di bekasulcus menonjol/bulging disebut : ECTATIC CICATRIX =KERAECTASIS
Descematocele
Ulcus dalam seluruh stroma dikenai kecuali descementmembrane menonjol oleh karena tekanan intra oculisehingga terlihat gelembung yang transparant
Hypopion
sebelum perforasi : steril (Ag-Ab reaction) Perforation
Synechia Anterior
Kalau perforasi kecil, iris akan menutupnya sehingga adaperlengketan iris ke kornea atau organisasi
Leucoma Adherent
pada bagian cornea yang perforasi terbentuk parut tebaldimana iris tetap melekat dibawahnya.
Intra Oculer Haemorrhage
Perforasi tiba-tiba dilatasi tiba-tiba pada pembuluh darahintra ocular ruptur pembuluh darah
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Treatment :
1. Mengatasi infeksi:
Antibiotika tetes & salepbroadspectrum k/p sensitivity test
Ada tak menganjurkan salepdasar
salep memperlambat epithelisasi Skrg dipakai fortified anti biotic drops
k/p antibiotica sub-conjunctival
AB systemic oral & injectionobat yg
dpt melalui blood aquouse barrier
2 Midriaticum
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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 lebihdengan 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)
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4. Pemanasan (Heat)
Moist heat kompres hangat dengan acidumboricum hangat beri 3 kali atau lebih
Dry heat penyembuhan lebih cepat
5. Perbaiki Keadaan Umum6. Benda asing (corpus alineum)
- diangkat / ekstersi
7. Scrapping dan Cautherization
Scrapping mengatasi meluasnya ulcus, dinding dandasar ulcus
Cautherization
- panas : electrocautery
actual cautery
- Chemical: yodium tincturpuroliqueel carbonic acid 2 sampai 3 kali
interval 1-2 hari
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8. Tarsorrhapy
Menjahit kelopak mata atas dan bawah (agar obatdapat 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
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Superficial punctate keratitis
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Ulkus kornea
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Ulkus kornea dgn hypopion
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penangananan
Antibiotika tetes / salep dapat diberi setiap30 menit1 jam, tergantung keparahaninfeksinya
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),penetrasike kornea baik
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Injeksi subconjunctiva
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Complicated Corneal Ulcer
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Perforated Corneal Ulcer
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Healed Keratocele
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Hypopyon Ulcer
Types
Corneal Ulcer (Superficial Purulent
Keratitis) with Hypopyon
Ulcer Serpen
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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 vesselsand these cells gravitate to bottom of
the anterior chamber to form hypopyon
(pus in anterior chamber)
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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
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Etiology
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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
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Organisms
Pyogenic organisms like
Staphylococci, Streptococci,
Gonococci, Moraxella, Pseudomonas
and Pneumococci
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Ulcus Serpen
Ulcus Serpen is hypopyon ulcer
caused by Pneumococciin adults
and has tendency to creep over the
cornea in serpiginous fashion
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Symptoms
Sever pain, photophobia, marked
diminution of vision, watering,
foreign body sensation (grittiness)
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Signs
Grayish white or yellowish disc likelesion near centre of cornea. Opacity ismarked at edges than at the centre and
more marked in one direction (where itis progressive). In the direction ofprogression there is cloudiness (greycoloured) and fine line ahead of disc
Cornea may be lusterless. There issevere iritis and aqueous is hazy orthere may be rank hypopyon amountwhich varies
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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 interveninglamellae, due to which there is tendency
for perforation of cornea. Intra-ocular
tension is usually raised in these cases.
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Complications
Untreated cases progresses to
increase in hypopyon which
becomes fibrinous leading to
perforation Iris prolapse throughlarge opening whole cornea may
slough leaving peripheral cornea
which is nourished by limbalvascular loops. Eventually
panophthalmitis develops which
destroys the eye
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Fungal Keratitis
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Fungal Keratitis
Fungal keratitis is challenging corneal
disease and presents as very difficult form
bacterial keratitis. Difficulty arise in
making correct clinical and laboratorydiagnosis. 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.
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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.
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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.
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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)
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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
le ros
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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
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Clinical Features
Symptoms
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Symptoms
Onset is slow
Symptoms are less compared tosigns
Diminution of vision, pain, foreign
body sensation
Signs
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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
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Fungal Keratitis with Hypopyon
Signs
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Signs
Satellite lesions
Brown pigmentation due to
dematiaceous fungus (Curvularia
lunata)
Intact epithelium with stromal
infiltrates
Anterior chamber reaction
Fungal Keratitis
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Fungal Keratitis
Fungal KeratitisPigmented Lesion
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Case of Fungal+ Bacterial Keratitis
Laboratory Diagnosis
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Laboratory Diagnosis
The Gram and Giemsa stains are used asinitial 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
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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 46 weeks
Treatment
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Treatment
Sub-conjunctival injection of
Miconazole 510 mgm of 10 mgm/ml
suspension (indicated in severe form
of keratitis, scleritis andendophthalmitis)
Systemic:
Fluconazole or Ketoconazole isindicated in severe form of keratitis,
scleritis and endophthalmitis
Surgical Treatment
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g
1. Daily debridement with spatula/blade every 2448 hours
2. Surgical treatment is required in
approximately 1/3rdcases of fungalkeratitis due to failure of medicaltreatment or perforation
3. Surgical treatment in the form of :
therapeutic keratoplasty,conjunctival flap or lamellarkeratoplasty
Surgical Treatment
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g
Surgery is usually indicated within 4
weeks due to failure of medical
treatment or recurrence of infection
Unfavorable outcome is due toscleritis, endophthalmitis and
recurrence
Cryotherapy with topical antifungaltreatment or corneoscleral graft in
cases of fungal scleritis and
keratoscleritis
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Introduction
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Viruses are obligate intracellular parasitesthat contain only one type of nucleic acidwithin he infectious unit and are unable toreplicate by binary fission.
Viruses that cause corneal disease are
Herpes simplex ( HSV) Varicella zoster ( VZV)
Epstein Barr ( EBV)
Adenovirus
Cytomegalovirus (CMV) can also causekeratitis and is more commonlyassociated with AIDS
Epidemiology and pathogenesis
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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
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Herpes simplex keratitis is a leading causeof corneal blindness in the developingworld.
Estimated prevalence is approx 150 per
100,000 population. Ocular HSV tends to be a unilateral
disease with only one eye affected byprimary disease in approx 80-90% of
cases. Atopy appears to be risk factor for
bilateral disease, & is associated withgastric cancer, lumbar zoster, malaria and
pulmonary tuberculosis
HERPES SIMPLEX KERATITIS
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HERPES SIMPLEX KERATITIS
Herpes Simplex Keratitis occurs in two
forms:
1. Primary
2. Recurrent
Primary HSV-1 (HSV type 1) infections
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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 transportalong
enters nucleus trigeminal ganglionnerve axon
at neuron
(Persists indefinitely
in a latent state)
PRIMARY HSV 1
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PRIMARY HSV-1
Primary infection of any of the 3 branches(ophthalmic, maxillary, mandibular) ofcranial nerve V leads to latent infection ofnerve cells in trigeminal ganglion.
Interneuronal spread of HSV withinganglion allows patients to develop oculardisease without ever having had primaryocular HSV infection.
www.emedic ine.com
RECURRENT HSV INFECTION
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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.emedic ine.com
CLINICAL FINDINGS
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CLINICAL FINDINGS
Primary Herpes Simplex Keratitis
Infrequently seen
Manifested as vesicular
blepharoconjunctivitis occasionally withcorneal involvement
Usually occurs in young children
Topical antiviral therapy may be used asprophylaxis and as therapy
Vaughan & Asburys General Ophthalmology 16thEdit io n, 136
CLINICAL FINDINGS
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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 atopicpatients. Vaughan & Asburys General Ophthalmology 16
thEdition, 136
SYMPTOMS
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SYMPTOMS
Irritation
Photophobia
Tearing
Reduction in vision (when centralcornea is affected)
Corneal anesthesia usually occurs
early in the course of infection andthus symptoms may be minimal.
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SYMPTOMS
Corneal ulceration can occasionallybe the only sign of recurrent herpetic
infections
Recurrent herpes simplex virus
dendritic ulcer with an adjacentstromal scar
LESIONS: Dendritic ulcer
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Most characteristic lesion, occurs in cornealepithelium
Typical branching, linear pattern with
feathery edges and terminal bulbs at ends. Visualized by fluorescein staining
HSV dendritic ulcer stained
with fluorescein
Dendritic keratitis
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This patient suffers from herpetic keratitis. Fluoresceinstaining reveals dendritic ulcer typical of herpes keratitis.
This is treated with topical 3% acyclovir
www.eyecasualty.co.uk/.../ cornealinfections.html
Geographic ulceration
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Form of chronic dendritic disease.
Delicate dendritic lesions take a
broader form.
Corneal sensation is diminished
HSV geographic ulcer
Other corneal lesions
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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
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Subepithelial lesions
Caused by HSV infection
Ghost like image,larger than original
epithelial defect seen in the area
immediately underlying epitheliallesion.
Does not persist for more than a year
Disciform keratitis
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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 16thEdition, 136
Peripheral lesions of the cornea
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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
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Treatment
Should be directed at eliminating
viral replication within the cornea,
while minimizing damaging effects of
inflammatory response.
Vaughan & Asburys General Ophthalmology 16thEdition, 136-137
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T t t
TREATMENT : DRUGS
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Treatment
Ophthalmology 2004, (2), 475-482
T t t
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Treatment
Trifluridine and acyclovir are muchmore effective in stromal disease than
others.
Idoxuridine and trifluridine arefrequently associated with toxic
reactions.
Oral acyclovir may be useful intreatment of severe herpetic eye
disease particularly in atopic
individuals.Vaughan & Asburys General Ophthalmology 16thEdition, 136-137
Treatment
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Oral acyclovir : DOSAGE:
For active treatment 400 mg five times daily innonimmunocompromised patients.
800 mg five times daily in compromised and atopicpatients.
Prophylactic dosage in recurrent disease is 400mg twice daily.
Famciclovir or valacyclovir may also be used. Topical corticosteroids accelerate corneal
thinning, increasing risk of corneal perforation.
Vaughan & Asburys General Ophthalmology 16thEdition, 136-137
Surgical treatment
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g
Penetrating keratoplasty indicated for visualrehabilitation 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 forseveral 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 16thEdition, 136-137
Varicella zoster viral keratitis
( )
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(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 16thEdition, 136-137
Varicella zoster viral keratitis
(VZV)
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(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 ofvarying duration has been reported.
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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 oftenoccur if there is skin eruption in areas supplied by
branches of the nasociliary nerve.Vaughan & Asburys General Ophthalmology 16thEdition, 136-137
Distinguishing features of dendrites
associated with HSV versus VZV
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associated with HSV versus VZV
Feature HSV VZVOverall Fine, lacy Thick ropy
Epithelium Linear defect with
bared stroma,
surrounded byedematous epithelial
cells
Elevated, painted-on
appearance
Staining Base stains with
fluorescein. Diseasedborder epithelial cells
stain with rose
bengal
Minimal fluoroescein
staining
Terminal bulbs Frequent None
Treatment
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Treatment Intravenous and oral acyclovir have been
used successfully for treatment of herpeszoster ophthalmicus, particularly in
immunocompromised patients.
Oral dosage is 800 mg five times daily for10-14 days.
Therapy needs to be started within 72
hours after appearance of the rash.Vaughan & Asburys General Ophthalmology 16thEdition, 136-137
Traumatic Eye Injuries
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Traumatic Eye Injuries
Corneal Foreign Bodies May be removed with fine needle tip, eye spud,
or eye burrafter 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 ringscan be removed with eye burr, but
not urgent
Optho follow up in 24 hours for residual rust or
deep stromal involvement
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UVEITIS
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UVEITIS
ANTERIOR
Autoimmune
Infections
Malignancy Others
POSTERIOR
Viruses
Bacteria
Fungi
Autoimmune
Malignancy
Unknown
UVEITIS
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UVEITIS
Inflammation of the uveal tract
Symptoms
blurred vision
Photophobia
Pain
UVEITIS
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UVEITIS
Inflammation of the uveal tract
Signs
Injection Flare
Keratic precipitates
Posterior synechias iris nodules
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UVEITIS
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UVEITIS
Complications
Anterior synechias
Posterior synechias
Cataract
Glaucoma
Macular edema
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UVEITIS
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UVEITIS
Autoimmune JRA
Ankylosing spondylitis
Ulcerative colitis
Crohns disease
Reiters syndrome
Lens induced
UVEITIS
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UVEITIS
Infections Syphilis
Tuberculosis
Herpes zoster
Herpes simplex
Adenovirus
UVEITIS
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UVEITIS
Malignancy Retinoblastoma
Leukemia
Lymphoma
Malignant melanoma
UVEITIS
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UVEITIS
Others Idiopathic
Traumatic
RD
Fuchs iridocyclitis
Gout
UVEITIS
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UVEITIS
Posterior CMV
Toxoplasmosis
Aids
Herpes simplex
Herpes zoster
Candida
UVEITIS
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UVEITIS
Autoimmune Behcets syndrome
VKH syndrome
Polyarteritis nodosa
Sympathetic ophthalmia
UVEITIS
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UVEITIS
Malignancy Malignant melanoma
Leukemia
Metastatic lesions
Unknown
Sarcoidosis
UVEITIS
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UVEITIS
TREATMENT Steroids
topical
local systemic
Cycloplegics
Antimetabolites
Analgesics
ENDOPHTHALMITIS
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ENDOPHTHALMITIS
Peradangan bola mata yg melibatkanuvea dan retina, disertai dgn eksudat
di vitreous, camera okuli anterior dan
camera okuli posterior
Gejala
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Geja a
Nyeri yg hebat
Pandangan kabur
Mata merah
Pemeriksaan
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Penurunan tajam penglihatan
Injeksi konjungtiva
Peradangan COA dan hypopion
Funduskopi: nervus opticus dan
retina tidak dapat dilihat dgn jelas
krn adanya inflamasi vitreous
endophthalmitis
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p
USG
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Penanganan
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g
Antibiotik fortified topikal tiap jam :cefazolin atau vancomycin,
gentamycin atau tobramycin
Antibiotika injeksi subconjunctiva Vitrectomy dan antibiotika injeksi
intravitreal
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Vitrectomydiindikasikan pada pasienyang tidak menunjukkan kemajuan
terapi dlm 4872 jam atau pd pasien
dgn infeksi berat dmn tajampenglihatan hanya persepsi cahaya.
Vitrectomy bermanfaat utk
mengeluarkan organisme,toksin danenzim pada vitreous
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PANOPHTHALMITIS
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Inflamasi purulenta pada seluruhstruktur bola mata termasuk kapsula
Tenon
Gejala
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j
Nyeri mata yg sgt berat dan nyeri kepala Hilangnya penglihatan
Sangat berair
Sekret purulen Mata sangat merah dan bengkak
Demam
malaise
Tanda
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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
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p p
Penanganan
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g
Anti-inflamasi dan analgetik
Antibiotika spektrum luas
eviscerasi
eviscerasi
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