keratitis iwan

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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