k - 8 & k - 9 konjungtivitis (ilmu penyakit mata)

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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

    http://www.emedicine.com/http://www.emedicine.com/
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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

    http://www.emedicine.com/http://www.emedicine.com/
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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

    http://www.emedicine.com/cgi-bin/foxweb.exe/makezoom@/em/makezoom?picture=/websites/emedicine/oph/images/Large/822011.jpg&template=izoom2
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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

    http://www.eyecasualty.co.uk/maincontent1/cornealinfections.htmlhttp://www.eyecasualty.co.uk/maincontent1/cornealinfections.html
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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

    http://www.revoptom.com/handbook/IMAGES/oct02_sec3_fig4.jpg
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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

    http://images.google.co.in/imgres?imgurl=galery.eyenews.ru/corn/cor_06/cr-06-06.jpg&imgrefurl=http://galery.eyenews.ru/corn/cor_06.htm&h=340&w=510&sz=71&tbnid=ikOS1LwYOrkJ:&tbnh=85&tbnw=127&start=1&prev=/images%3Fq%3Ddisciform%2Bkeratitis,%2Bviral%26hl%3Den%26lr%3D%26ie%3DUTF-8
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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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