2. Introduction
• Bacterial keratitis usually develops when ocular defens
have been compromised.
•Host cellular and immunologic responses to offending agent which
may be bacterial, viral, fungal or protozoal organisms leads to
formation of ulcer.
•Sight threatening condition and should be considered as ocular
emergency.
3. Barriers Of Microbial Infection
• Bony orbital rim,eyelids,
• Intact corneal & conjunctival
epithelium
Anatomical
• Tear film-mucus layer
• Lacrimal systemMechanical
• Tear film constitutes-IgA, complement
components, and enzymes lysozyme,
lactoferrin, betalysins
• CALT
Antimicrobial
4. Risk Factors
• 1. TRAUMA
-breach in corneal epithelium
-refractive surgery
-agricultural injury
-inoculation of organism
• 2. OCULAR SURFACE DISEASES
- blepharitis, ectropion, entropion, trichiasis, lagophthalmos,
chronic dacryocystitis
• 3.CONTACT LENS WEAR
• 4. LOCAL IMMUNE SUPPRESSION DUE TO TOPICAL
CORTICOSTEROIDS
6. Aetiology
• Caused by organisms which produce toxins causing tissue
death i.e. necrosis characterized by pus formation.
• Such purulent keratitis is usually exogenous due to infection
by pyogenic bacteria such as
-Pseudomonas,
-Staphylococcus,
-Streptococcus,
-N. gonorrhoeae and
-C. diphtheriae
7. Aetiology
• Most of the bacteria are capable of producing corneal ulcer
only when the epithelium is damaged.
• N. gonorrhoeae, C. diphtheriae, Haemophilus , N. meningitidis
can penetrate intact corneal epithelium.
8. Pathogenesis
Corneal abrasion Microbes adhere to epithelium, cloning ,invasion to stromal
lamellae,release toxins & lytic enzymes
Host response
PMNs at the site of ulcer from tears & limbal vessels release of cytokines &
interleukins progressive invasion of cornea & increase in size of ulcer
Phagocytosis
Release of free radicals, proteolytic enymes Necrosis & sloughing of epithelium,
Bowman’s membrane & stroma
A saucer shaped defect with projecting walls above the normal surface due to
swelling of tissue resulting from fluid imbibition by corneal stroma with grey zone
of infiltration
9. Presentation
1. Diminution of vision, depending on location of
corneal ulcer
2. Watering due to reflex lacrimation
3. Photophobia
4. Pain due to exposed nerve endings
5. Mucopurulent / purulent discharge
11. 4. Cornea
-Location of the ulcer- central, paracentral peripheral,total.
-Size , shape, depth, margins & floor- depends on stage of
ulcer.
-Density and extent of stromal infiltration.
5. Anterior chamber
- Cells/flare, mobile Hypopyon.
14. Special Features
1.Staphylococcal
• Central,oval, opaque
• Distinct margins.
• Mild oedema of remaining
cornea.
• Stromal abscess in longstanding
cases.
• Mild to moderate AC reaction.
• Affects compromised corneas
e.g. Bullous keratopathy , dry
eyes , atopic diseases.
15. 2.Pneumococcal
• Ulcer serpens is greyish
white or yellowish disc
shaped ulcer occuring near
center of cornea.
• starts at periphery &
spreads towards centre
• Tendency to creep over the
cornea in serpiginous
fashion- Ulcus Serpen.
• Violent iridocyclitis is often
associated with it.
• Hypopyon – always
present
• It has great tendency for
PERFORATION.
16. 3. Pseudomonas
• Rapidly spreading.
• Extends periphery & deep
within 24 hrs.
• Stromal necrosis with shaggy
surface
• Spreads concentrically and
symmetrically to involve
whole depth of cornea-Ring
ulcer.
• Greenish-yellow discharge.
• Hypopyon is present.
• Untreated corneal
melting.
17. 4. Streptococcus viridans
• Infectious crystalline
keratopathytype of
stromal keratitis.
• Crystalline arborifoem
(needle like) white
opacities in stroma , not
associated with
infiltration & ocular
inflammation
• Due to proliferation of
bacteria between the
stromal lamellae.
18. Complications Of Corneal Ulcer
1. Spread of ulcer horizontally and depth-wise, leading to thinning
of cornea
2. Descemetocele
3. Perforation of ulcer –
sudden exertion such as coughing, sneezing, straining at stool or
firm closure of eyes increase in intra-ocular pressure (IOP)
perforation
a) Peripheral perforation -iris prolapse through opening.
Exudation takes place on prolapsed tissue an adherent
leucoma .
19. b) Central perforation anterior chamber collapse
lens comes in contact with corneal endothelial surface
anterior capsular cataract repeated healing and perforation
leading to corneal fistula formation
c) Sloughing of whole cornea: prolapse of iris pupillary block
and exudation on iris pseudocornea anterior synechiae
angle of anterior chamber is occluded leading to secondary
glaucoma anterior staphyloma .
d) Intra-ocular purulent infection: due to perforation bacteria
enter in the eye and causes endophthalmitis /
panophthalmitis
20. Investigations
Specific – Corneal scraping
Gram stain, Culture &
Antibiotic sensitivity
Culture of contact lens & solution
Conjunctival Swab
25. LOCAL TREATMENT
Control of infection with appropriate antibiotic(s)
a. based on clinical judgment
b. based on finding of smear examination
c. based on culture and sensitivity report
• Antibiotic Monotherapy
-fluroquinolone
-Ciprofloxacin or Ofloxacin
-New generation fluroquinolone
29. Systemic Antibiotics
Indications
• Severe keratitis
• Scleral involvement
• Hypopyon
• Impending perforation
• Frank perforation with risk of intraocular spread
• Infection in children
• P. aeruginosa infection
• N. meningitidis infection
• H. influenzae
• N. gonorrhoeae infection
30. Adjuvant Therapy
1.Cycloplegic : Atropine 1% or cyclopentolate 1% or Homatropine
2%- prevents ciliary spasm, relieves pain, breaks adhesions
and prevent synechia formation.
2.Analgesic anti-inflammatory
3. Oral vitamin C
4. Acetazolamide Tab - impending perforation or perforated
corneal ulcer and in cases where there is raised IOP
31. Treatment Of Impending Perforation
1. Straining should be avoided.
2. Pressure bandage
3. Lowering of IOP
4. Tissue adhesive glue (cynoacrylate)
5. Conjunctival flap
6. Soft contact lens Bandage
7. Penetrating keratoplasty
33. • Modification of initial antimicrobial therapy:
-Should be based on clinical response not on culture sensitivity
• If pt is responding no change in initial treatment
• If pt is not responding/ worsening drugs are changed
according to antimicrobial sensitivity
34. • SIGNS OF HEALING :
-resolution of lid edema, congestion
-decreased density of stromal infiltrate
-reduction of corneal oedema
-reduction in AC reaction/hypopyon
-re-epithelization
-corneal vascularization
• Antibiotic frequency-tapered to 4hrly after 72 hrs
35. • SIGNS OF NON-RESPONSE
- Increase in infiltration, epithelial defect, height of hypopyon,
Corneal thinning, perforation
Treatment
• Re-evaluate for
Drug toxicity,Non-infectious causes or Unusual organisms
• Modification of anti-microbial therapy according to
antimicrobial sensitivity
• Scraping of ulcer floor followed by cauterization with pure
(100%) carbolic acid or 10-20% trichloracetic acid.
• Therapeutic keratoplasty
36. Topical Corticosteroids
• Controversial in bacterial keratitis
• The rationale for using steroids - to decrease tissue destruction.
CRITERIA FOR TOPICAL STEROIDS IN ULCER --
1.Must not be used in presence of active infected corneal ulcer
2.If bacteria shows in-vitro sensitivity to the antibiotic being used
3.Patients compliance for follow-up
4. No other virulent organism is found
37. Surgical Treatment
• 1.Tissue adhesive-Cyanoacrylate glue- small perforations< 3mm
- descemetocele
• 2. Patch graft –perforation- 5mm in diameter
• 3 . Therapeutic keratoplasty
-large areas of perforation, necrosis
-Non-healing ulcer