IT 14_ANT Kornea Dan Keratitis

8/11/2019 IT 14_ANT Kornea Dan Keratitis

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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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34

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 +.

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IT 14_ANT Kornea Dan Keratitis