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KORNEA

Anang Tribowo

Ophthalmology Department
Medical Faculty of Sriwijaya University
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.
 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.
 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.
 Dapat mempertahankan integritas bola mata.
 Dapat beregenerasi.
 Tebal 10-12 mikrometer.

 Lapisan Endotel.
 Selapis sel poligonal (hexagonal).
 Kepadatan sel 3000sel/mm².
 Tidak bisa beregenerasi.
 Peran proses transport aktif dan mempertahankan
deturgensi kornea.
BACTERIAL CORNEAL ULCERS
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
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)


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


Various factors involved in IBD

Inflammatory cascade
Genetic & environment

Target cell lymphocytes Direct damage/


autoimmune

Protease
LTB4 cytokine lymphokine

macrophage Virus, bacteria,


neutrophyl another Protein
• 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
Prognosis of corneal ulcer depends on :

- Degree of corneal ulcer


- Time of treatment
- Type of microorganism that caused ulcer
- Complication of corneal ulcer
PATOGENESIS

Homograf reaction Chemical trauma


Herpes stroma Burn trauma
Autoimmune Keratitis Bacterial infection

Complement
Ag-Ab complex Tissue Denaturation
activation

Chemotaxis of
Leukosit

Epithel & keratosis


Enzyme release lisosom

collagen destruction &


proteoglikan
(stroma melting)
Bacterial Ocular Pathogens:
Ulcerative Keratitis
50 47.4%
Distribution of Organisms in
Monomicrobial Cases (%)

40

30

21.1%
20
13.2%

10 7.9%
5.3% 5.3%

0
Staphylococcus Pseudomona Staphylococcus Serratia Streptococcus Other
epidermidis s aureus pneumoniae
aeruginosa

Levey SB, et al. Cornea. 1997;16:383-386.


Mohammad Hoesin Hospital in 2008, 70 cases

Bacterial 45,71%
Fungi 21,43%
Virus 18,57%
Others 14,29%
France
Diplobacillus of morax (H. duplex)

Palestine
Koch-Weeks bacillus (H. influenzae)

US
Staphylococcus aureus
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


Bacterial Keratitis-complications

• Corneal leukoma

• Irregular astigmatism

• Corneal perforation

– the most feared complications  result in secondary


endophthalmitis and possible loss of the eye
Ulcerative keratitis (Corneal Ulcer)

Ulcer

Hypopion
(pus in the AC)
Corneal Ulcer – affected area
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
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
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)
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%)


DISCUSSION

Pathogenesis of progressive and non progressive

according to how many expressed cell IL-6, IL-8, MMP-8

and TGF-β

progresssive type (13 subjects), and non progressive (11

subjects)
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), chemokines  important in the
recruitment of neutrophils in the infected cornea.
- 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


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
Suggestion:

Heal and maintain the structural integrity of corneal tissue

with nutrients and medication can prevent the progression

of ulcer
• 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 +.
• 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 +.