it 14_ant kornea dan keratitis
TRANSCRIPT
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Anang Tribowo
Ophthalmology Department
Medical Faculty of Sriwijaya University
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KORNEA
ANATOMI DAN FISIOLOGI KORNEA. Bersifat: transparan, avaskular.
Diameter horizontal 11,7 mm, vertikal 11 mm.
Ketebalan sentral 0,52 mm, perifer 0,7 mm
Daya refraksi 45 D. Terdiri atas 5 lapis :
Lapisan Epitelium.
Terdiri sel epitel skuamosa bertingkat
5-6 lapisan:
Superfisial 2 lapis sel gepeng.
Tengah 2-3 lapis sel poligonal.
Basal berbentuk sel kolumnar.
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Tear film(+)permukaan licin. Bagian perifer: histiosit, makrofage, limfosit, dan
melanosit.
Lapisan Membrana Bowmen.
Pemadatan jar.kolagen superfisial stroma.
Tebal 12 mikrometer.
Untuk pertahanan terhadap infeksi.
Regenerasi (-)
Lapisan Stroma.
Tebal 0,5 mm.
Terdiri fibroblast(keratosit), substansi dasar, lamela
kolagen.
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Peran susunan kolagen fibril pada matrik ekstrasel:
Membuat kornea transparan. Menurunkan pendaran sinar. Indeks bias epitel
1.401, stroma 1.380, posterior 1,373.
Transparansi kornea dipengaruhi juga oleh:
Kandungan air stroma 78%.
Fungsi pompa endotel.
Lapisan Membrana Descemet.
Lapisan homogen, tdr jar.kolagen dan glikoprotein. Sangat tahan thd bahan kimia, trauma, proses patologi.
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Dapat mempertahankan integritas bola mata.
Dapat beregenerasi. Tebal 10-12 mikrometer.
Lapisan Endotel.
Selapis sel poligonal (hexagonal).
Kepadatan sel 3000sel/mm.
Tidak bisa beregenerasi.
Peran proses transport aktif dan mempertahankan
deturgensi kornea.
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BACKGROUND
Corneal ulcer the loss of corneal surface due to the
death of corneal tissue suppurative infiltrate,
excavation of cornea and corneal discontinuity from
epithel to stroma
Etiology of the ulcer infection of bacteria, viral, fungi
or a deficiency of vitamin A, lagophtalmus and trauma
damage the epithelium
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Blindness of corneal ulcer caused by:
1. Perforation of the eyeball followed by phtisis bulbi
2. Formation of the new vessel cornea becomes cloudy
3. And scarring occurs ( corneal cicatrix)
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Microorganism invates cornea induces PMN
phagocyte microorganism by using intracytoplasmic
lysosom destroy microorganism
inflammatory reaction (cytokin pro
inflammatory : IL-6, IL-8, TGF-beta)
Enzyme corneal ulcer
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Target cell lymphocytes Direct damage/
autoimmune
lymphokine
Virus, bacteria,
another Protein
cytokine
macrophageneutrophyl
Protease
LTB4
Genetic & environment
Inflammatory cascade
Various factors involved in IBD
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Incidence estimated to 11.3 in 10,000 population
Aim of treatment prevent bacterial growth,
inflammation, the healing of epithelial defect,
overcome complication and improve the visual acuity
Treatment choice must be appropriate with the clinical
feature of :
- Degree of ulcer in initial examination
- Result of the gram-KOH staining- Result of culture-resistance test
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Prognosis of corneal ulcer depends on :
- Degree of corneal ulcer
- Time of treatment- Type of microorganism that caused ulcer
- Complication of corneal ulcer
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PATOGENESIS
Ag-Ab complexComplement
activation
Chemotaxis of
Leukosit
Enzyme release lisosom
collagen destruction &
proteoglikan
(stroma melting)
Chemical trauma
Burn trauma
Bacterial infection
Homograf reaction
Herpes stroma
Autoimmune Keratitis
Tissue Denaturation
Epithel & keratosis
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Keratitis
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Bacterial Ocular Pathogens:
Ulcerative Keratitis
0
10
20
30
40
50
Levey SB, et al. Cornea. 1997;16:383-386.
47.4%
21.1%
13.2%
5.3% 5.3%
7.9%
Staphylococcus
epidermidis
Pseudomona
s
aeruginosa
Staphylococcus
aureus
Serratia Streptococcus
pneumoniae
Other
D
istributionofOrganismsin
MonomicrobialC
ases(%)
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Mohammad Hoesin Hospital in2008, 70
cases
Bacterial 45,71%
Fungi 21,43%
Virus 18,57%
Others 14,29%
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France
Diplobacillus of morax (H. duplex)
PalestineKoch-Weeks bacillus (H. influenzae)
US
Staphylococcus aureus
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Problem Magnitude
Microbial keratitis one of the most visually threatening
ocular infectious pathologies
The avascular corneal stroma susceptible of bacterial
infection
Poor outcome if appropriate treatment is not initiated
promptly
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Bacterial Keratitis-complications
Corneal leukoma
Irregular astigmatism
Corneal perforation
the most feared complications result in secondary
endophthalmitis and possible loss of the eye
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Ulcerative keratitis (Corneal Ulcer)
Ulcer
Hypopion
(pus in the AC)
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Corneal Ulcer affected area
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Pseudomonas Ulcer
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Criteria of Ideal Topical Antibiotic
Broad spectrum activity
Bactericidal
Quick Bacterial eradication
Bioavailability
Low risk of resistance
Non-toxic and comfort to use
Effective against resistant organism
Penetration to the intraocular tissue
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Strategies to prevent resistance
Appropriate use of antibiotics
Use of acute (not chronic)
Surgical prophylaxis with high dose and short term
Provision of appropiate
Avoid dose reduction
New generation of AB
Less likely to induced resistance strain
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Corneal Ulcers associated with location progressivity
Location Progressive Non Progressive Total
Central 13 (92,9%) 1 (7,1%) 14 (100,0%)
Paracentral 0 (0,0%) 10 (100,0%) 10 (100,0%)
Total 13 (54,2%) 11 (45,8%) 24 (100,0%)
C = 0,677 (p = 0,000)
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Table 1. Bacterial Distribution and Progressivity
Bacteri Progressive Non-progressive Total
Negatif 2 (50,0%) 2 (50%) 4 (100,0%)
P. Aeruginosa 5 (62,5%) 3 (37,5%) 8 (100,0%)
Acinobacter spp 2 (100,0%) 0 ( 0%) 2 (100,0%)
Staphylocoocus au 3 (37,5%) 5 (62,5%) 8 (100,0%)
Staphylocoocus epi 1 (50,0%) 1 (50,0%) 2 (100,0%)
Total 13 (54,2%) 11 (45,8%) 24 (100,0%)
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DISCUSSION
Pathogenesis of progressive and non progressive
according to how many expressed cell IL-6, IL-8, MMP-8
and TGF-
progresssive type (13 subjects), and non progressive (11
subjects)
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Cole, and Hume (2006)
- A pro-inflammatory mediator IL-6 extremely potent
- IL-6 as an alarm if the cornea infection & inflammation
- IL-6 role stimulating the release of macrophage
Inflamatory protein (MIP), chemokinesimportant in the
recruitment of neutrophils in the infected cornea.
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- Greenberg et al. (2000): MMPs play a role in regulating
cell migration of epithelial cells
- Biswas, 2005: MMPs ability of lysis collagen type I and II
greater than type III, VII and X
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Summary
- IL-6 shows significant differences between progressive
and non progressive whereas IL-8, MMP-8 & TGF-beta
no significant difference
- Corneal ulcer progression is not through this interleukin
mechanism
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Suggestion:
Heal and maintain the structural integrity of corneal tissue
with nutrients and medication can prevent the progression
of ulcer
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THANK YOU
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Staphilococcus Aureus identifikasi
melalui:
Morfologi mikroskopis grm + dan coccus +
bergerombol seperti anggur. Katalase +. Morfologi koloni, aktivitas hemolisis+.
Differensiasi Staphilococcus, warna koloni
emas, coagulase+, mannitol+, hemolisis+,
novobiocin sensitif.
Reaksi plasma okslat dan plasma sitrat +.
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Staphilococcus Epidemidis identifikasi
melalui:
Morfologi mikroskopis grm + dan coccus +
bergerombol seperti anggur. Katalase +. Morfologi koloni, aktivitas hemolisis+.
Differensiasi Staphilococcus, warna koloni
putih, coagulase -, mannitol -, hemolisis -,
novobiocin sensitif.
Reaksi plasma okslat dan plasma sitrat +.