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Dr. Masitha Dewi Sari,SpM
Anatomi segmen anterior
CONJUNCTIVITIS
• Definisi:
peradangan conjunctiva ditandai dengan discharge (sekret) dapat berair, mucoid, mucopurulent atau berair, mucoid, mucopurulent atau purulent
KLASIFIKASI BERDASARKAN ETIOLOGI
1. Infective conjunctivitis : bacterial, chlamydial, viral, fungi, spirochaetal, protozoal, paracitic,etc,
2. Allergic conjunctivitis
3. Irritative conjunctivitis3. 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
Hebat
nodule sering jarang Sering pd inclusion
Tidak ada
Scraping,pewarnaan
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 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 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 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-(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 • 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 – 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 – 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 – 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• 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• 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”
Infections
– “Pseudodentrite”
• Mucous corneal plaque with
epithelial erosion
– Treatment:
• Acyclovir
• Topical antivirals
• Warm compresses
• Oral analgesics or cycloplegics
for pain relief
– Ophthalmology consult mandatory
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 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 berbentuki segitigapuncaknya dekat ke kornea/mencapai ke kornea
•Klinis :
- Pembuluh darah membesar
- visus menurun oleh karena astigmatisma
irruguler pembiasan tidak pada satutempat
- stroma proliferasi
- sering pada bagian nasal, dalampertumbuhannya 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(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 (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(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 expgenous olehorganismeorganisme
pyogenik
- penyebab ulcus cornea tanpa lesi epithel :
* gonorrhea
* diphterioe
Bakteri lain harus ada lesi epithel ulcuscornea stophylococcus menyebabkansuperficial punctate erotion
• PENYEBAB1. Bakteri
a. Pneumococcusb. Staphylococcus aureus, Staphylococcus epidermidisc. Alpha Haemolyticus Streptococcus d. Nocardiae. Mycobacteriumf. Streptococcus viridansg. Klebsiella pneumonia
2. Virusa. Herpes simplexb. varicella zosterb. varicella zosterc. Variolad. Adenovirus
3. Fungala. Aspergillusb. Candidac. Cephalosoriumd. Fusariume. Penicillium
4. Autoimmune5. Amuba
PATOLOGI
• Terjadi nekrose setempat pada lapangan pandang cornea (sampai stroma) sequestrum lepas danjatuh 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.karena adanya inhibisi cairan sekret ulcus.
• Batas antara ulcus dengan jaringan sehat, sama seperti bagian tubuh yang lain, yaitu ada dinding PMN leukosit membentuk lapisan kedua pertahanan sehingga lekosit berfungsi sebagai :
- digestive : mencerna
- macerating : menghancurkan
- dissolving : melarutkan jaringan nekrose
Jaringan terlepas ulkus tambah lebar dan kekeruhan berkurang
• Dasar dan pinggiran transparan Perbaikan mulaiterjadi, terbentuk pembuluh darah halus dari limbusdekat ulcus untuk mensuplai bahan-bahan yang rusak
• Antibodi untuk mengatasi infeksi (pannus)• Meresap ke cornea di COA) merangsang
pembuluh darah iris dan corpus ciliare sehinggaterjadi hiperemi iris tanpa ciliary infection
• Iritasi/peradangan bisa terlalu hebat sehingga• Iritasi/peradangan bisa terlalu hebat sehinggaleukosit dan PMN keluar dari pembuluh darah masukke COA dan mengendap di bagian COA disebuthypopion
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 infection• Iridocyclitis keratitis precipitate (bentuk segitiga
di epitel cornea), hypopion• Pannus (pembuluh darah yang masuk ke cornea)• Pannus (pembuluh darah yang masuk ke cornea)
DD MATA MERAH1. conjunctivitis akut2. Glaukoma akut3. Keratitis4. Uveitis
PENYEMBUHAN ULCUS
• Pannus (+) ada cicatrix pada bekas ulcus
• Serabut yang baru terbentuk tidak tersusunteratur sebagaimana normalnya bias cahaya tidak teratur
• Parut luas pembuluh darah besar/menetap/menetap
• Membran bowman tidak tumbuh lagi
• Cornal focet’s cicatrix tidak keruh / transparan dan permukaannya datar (mataserangga)
• 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 telanjangdapat 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 bekasulcus menonjol/bulging disebut : ECTATIC CICATRIX = KERAECTASIS
• DescematoceleUlcus dalam seluruh stroma dikenai kecuali descementmembrane menonjol oleh karena tekanan intra oculisehingga terlihat gelembung yang transparant
• Hypopionsebelum perforasi : steril (Ag-Ab reaction)
• Perforation• Perforation• Synechia Anterior
Kalau perforasi kecil, iris akan menutupnya sehingga adaperlengketan iris ke kornea atau organisasi
• Leucoma Adherentpada bagian cornea yang perforasi terbentuk parut tebal
dimana iris tetap melekat dibawahnya.• Intra Oculer Haemorrhage
Perforasi tiba-tiba dilatasi tiba-tiba pada pembuluh darahintra ocular ruptur pembuluh darah
KOMPLIKASI• Cicatrix
Penyembuhan cicatrix yang tidak sempurna, cornea di bekas ulcus menonjol/bulging disebut : ECTATIC CICATRIX = KERAECTASIS
• DescematoceleUlcus dalam seluruh stroma dikenai kecuali descement membrane menonjol oleh karena tekanan intra oculi sehingga terlihat gelembung yang transparant
• Hypopionsebelum perforasi : steril (Ag-Ab reaction)
• Perforation• Synechia Anterior• Synechia Anterior
Kalau perforasi kecil, iris akan menutupnya sehingga ada perlengketan iris ke kornea atau organisasi
• Leucoma Adherentpada 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
2. Midriaticum
Sulfasatropin 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 hango
Fungsi :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 Umum6. Benda asing (corpus alineum)
- diangkat / ekstersi
7. Scrapping dan CautherizationScrapping mengatasi meluasnya ulcus, dinding dan dasar ulcus
Cautherization- panas : electrocautery
actual cautery
- Chemical : yodium tinctur- Chemical : yodium tincturpuroliqueel carbonic acid 2 sampai 3 kali interval 1-2 hari
8. Tarsorrhapy
Menjahit kelopak mata atas dan bawah (agar obat dapat mencapai ulcusmelalui conjunctiva)
9. Conjunctival Flap
Ulcus ditutup dengan conjunctiva bulbi brigde ataupun total
10. ParasintesisTujuan
- mencegah erosi- menghilangkan rasa sakit- Nutrisi pada cornea yang sakit- penambahan 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 • 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• 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.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 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 Pneumococciand 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 fashioncornea 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 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 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 KeratitisFungal 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. like cornea and sclera.
Risk Factors
1. Trauma outdoor/ or the one which involves plant matter (including contact lenses)
2. Topical medications: 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, 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: 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, BlastomycesCoccidiodes, Blastomyces
Clinical FeaturesClinical Features
Symptoms
• Onset is slow
• Symptoms are less compared to signssigns
• Diminution of vision, pain, foreign body sensation
Signs
• Diminution of vision, depending on location of ulcer
• Conjunctival and ciliary congestion
• Epithelial defect• 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)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 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 • 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 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 1/3rd cases of fungal approximately 1/3 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 • 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)• 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• 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 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 endings
Viral genome Cell body in transport along
enters nucleus trigeminal ganglionnerve axon
at neuron
(Persists indefinitely
in a latent state)
www.emedicine.com
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 • 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.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 blepharoconjunctivitis occasionally with corneal involvement
• Usually occurs in young children
• Topical antiviral therapy may be used as prophylaxis and as therapy
Vaughan & Asbury’s General Ophthalmology 16th Edition, 136
CLINICAL FINDINGS
• Recurrent type herpetic keratitis
Attacks triggered by
• Fever
• Overexposure to UV light• 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 & Asbury’s General Ophthalmology 16th Edition, 136
SYMPTOMS
• Irritation
• Photophobia
• Tearing
• Reduction in vision (when central • 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.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• 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 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.• Edema is most prominent sign.
• Keratic precipitates may lie directly under
disciform lesion but may also involve the
endothelial lesion.
Vaughan & Asbury’s General Ophthalmology 16th Edition, 136
Peripheral lesions of the cornea
• Caused by HSV
• Usually linear lesions, show loss of epithelium
• Testing for corneal sensation is • 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.inflammatory response.
Vaughan & Asbury’s General Ophthalmology 16th Edition, 136-137
Treatment
• DEBRIDEMENT
• Epithelial debridement is an effective way to treat dendritic keratitis
• Infected epithelium is easy to • Infected epithelium is easy to remove with tightly wound cotton tip applicator.
• Adjunctive therapy with topical antiviral accelerates epithelial healing.
Vaughan & Asbury’s General Ophthalmology 16th Edition, 136-137
Treatment Antiviral medicines used in treatment of Herpes Simplex Virus
Ocular Disease
Inhibits viral DNA 5 times daily3% TopicalVidarabine
Inhibits viral thymidine
kinase, thymidylate
kinase and DNA
polymerase
Hourly while
awake
0.1%
solution
TopicalIdoxuridine
ActionFrequencyFormRouteAntiviral
TREATMENT : DRUGS
Ophthalmology 2004, (2), 475-482
Activated by viral
thymidine kinase to
inhibit DNA polymerase
5 times daily
400 mg 5
times daily
3%
ointment
200/400/
800 DT
Topical
Oral
Acyclovir
Inhibits viral
thymidylate synthetase
Every 2
hours while
awake
1%
solution
TopicalTrifluridine
Inhibits viral DNA
polymerase
5 times daily3%
ointment
TopicalVidarabine
Ophthalmology 2004, 2; 475-482
Treatment
• Trifluridine and acyclovir are much more effective in stromal disease than others.
• Idoxuridine and trifluridine are • 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 & Asbury’s General Ophthalmology 16th 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 • 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 & Asbury’s General Ophthalmology 16th 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 • 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 & Asbury’s General Ophthalmology 16th 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 & Asbury’s General Ophthalmology 16th Edition, 136-137
Varicella zoster viral keratitis
(VZV)
Ocular manifestations
• Usual eye lesions are pocks on lids and lid margins.
• Keratitis occurs rarely.• 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 • 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 & Asbury’s General Ophthalmology 16th 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
Elevated, painted-on
appearance
surrounded by
edematous epithelial
cells
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 • 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 & Asbury’s General Ophthalmology 16th 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
• POSTERIOR
• Viruses
• Bacteria
• Fungi• Malignancy
• Others• Autoimmune
• Malignancy
• Unknown
UVEITIS
• Inflammation of the uveal tract
• Symptoms
• blurred vision
• Photophobia
• Pain
UVEITIS
• Inflammation of the uveal tract
• Signs
• Injection• 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– Ulcerative colitis
– Crohn’s disease
– Reiter’s syndrome
– Lens induced
UVEITIS
• Infections
– Syphilis
– Tuberculosis
– Herpes zoster– Herpes zoster
– Herpes simplex
– Adenovirus
UVEITIS
• Malignancy
– Retinoblastoma
– Leukemia
– Lymphoma– Lymphoma
– Malignant melanoma
UVEITIS
• Others
– Idiopathic
– Traumatic
– RD– RD
– Fuch’s iridocyclitis
– Gout
UVEITIS
• Posterior
– CMV
– Toxoplasmosis
– Aids– Aids
– Herpes simplex
– Herpes zoster
– Candida
UVEITIS
• Autoimmune
– Behcet’s syndrome
– VKH syndrome
– Polyarteritis nodosa– Polyarteritis nodosa
– Sympathetic ophthalmia
UVEITIS
• Malignancy
– Malignant melanoma
– Leukemia
– Metastatic lesions – Metastatic lesions
– Unknown
– Sarcoidosis
UVEITIS
• TREATMENT
– Steroids
• topical
• local• 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 posteriorcamera 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• 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 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• 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• Chemosis konjungtiva
• Kornea keruh
• COA ���� berisi pus seluruhnya
• Tajam penglihatan hilang (NLP)
• TIO menigkat
• perforasi
panophthalmitis
Penanganan
• Anti-inflamasi dan analgetik
• Antibiotika spektrum luas
• eviscerasi
eviscerasi