Corneal ulcers occur due to loss of corneal epithelium and inflammation. Bacteria are a common cause and can penetrate breaks in the epithelium. Symptoms include reduced vision, pain, watering and photophobia. Examination reveals the size, depth and borders of the ulcer. Treatment involves topical antibiotics based on smear or culture results along with cycloplegics. Systemic antibiotics may be needed for severe cases. Surgery with tissue adhesives or grafting is used for perforations. Prognosis depends on severity, depth and cause of the ulcer.

1. Dr. Bhushan Patil.

2. DEFINATION

A loss of epithelium with inflammation in the
sorrounding cornea is called as corneal ulcer.

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. NORMAL DEFENCE MECHANISM

Corneal epithelium- mechanical barrier

Conjunctiva- cellular & chemical components

Tear film- biological protective system
Major components of ocular defence system

4. BARRIERS OF MICROBIAL INFECTION
Anatomical
• Bony orbital rim,eyelids,
• Intact corneal & conjunctival
epithelium
Mechanical
• Tear film-mucus layer
• Lacrimal system
Antimicrobial
• Tear film constitutes-IgA,
complement components, and
enzymes lysozyme, lactoferrin,
betalysins have antibacterial effect
• CALT

5. PREDISPOSING FACTORS
OCULAR

1. Trauma-breach in corneal epithelium
-inoculation of organism

2.Eyelid & adnexal diseases- blepharitis, ectropion, entropion, trichiasis, lagophthalmos,
chronic dacryocystitis
Disturbed Tear film
Recurrent epithelial erosions

6. 3. Ocular surface disorder- Dry eye, Steven-Johnson syndrome, ocular burn,
bullous keratopathy.


4. Contact lens use-Increased risk of bacterial keratitis with use of Extended
soft contact lens
corneal hypoxia & decompensation.
- Contamination of CL solution.

5. Local immune suppression due to topical corticosteroids.

6.Ocular surgery- cataract , LASIK.

7. SYSTEMIC FACTORS
1.Malnutrition
2.Diabetes
3.Immunosupression-Systemic steroids, AIDS
4.Chronic alcoholism

8. AETIOLOGY OF BACTERIAL ULCER

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

9. AETIOLOGY OF BACTERIAL ULCER

Most of the bacteria are capable of producing corneal
ulcer only when the epithelium is damaged

N Gonorrhoeae, C Diphtheriae, Hemophilus , Shigella
and Listeria Monocytogenes – can penetrate intact
corneal epithelium.

10. ORGANISM
SPECIES
BACTERIOLOGY
Staphylococcus S.Aureus
Gram positive cocci
S.Epidermidis
1.Most common organism
2.Eyelid diseases
3.Dry eye, bullous
keratopathy, atopic disease.
Streptococcus
S.Pneumoniae Gram positive cocci
S. Viridans
chronic Dacryocystitis.
Corneal grafts .
Pseudomonas
P. Aeruginosa Gram negative
bacilli
1.Contact Lens users
2.Comatose pt.
3.Pt on mechanical ventillator
4.HIV
Moraxella
M.Lacunata
Malnourished, alcoholics ,
diabetes
Nocardia,Actin
omycets
Atypical
Mycobacteria
Gram negative
diplobacilli
Gram positive bacilli Ocular trauma contaminated
by soil
M. Chelonae
Acid fast bacilli
Following LASIK

11. PATHOGENESIS
Corneal abrasion Microbes adhere to epithelium, 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

12. STAGE OF PROGRESSIVE INFILTRATION

Entry and adherance of organism to breached
epithelium  enters into stroma.

PMNs and lymphocytes infiltrate into stroma and
epithelium.

Infective organism multiplies  release toxins and
enzymes.

13. STAGE OF ACTIVE ULCERATION

Necrosis occurs due to toxins and enzymes released by
infective organism.

Sloughing of epithelium and stroma  ulcer.

Ulcer Borders thickening due to infiltrates and edema.

It is associated with iritis due to diffusion of toxins of
infecting bacteria into AC.

14. 
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
AC to form hypopyon (sterile).

15. STAGE OF REGRESSION
Natural host defence & antimicrobial treatment
 Line of demarcation forms around ulcer which contains
leucocytes which phagocytose the organism & necrotic debris
 Necrotic material fall off- ulcer becomes larger -> infiltration and
swelling reduce and disappears -> margin & floor becomes
smooth.
 Vascularization develops from limbus to corneal ulcer to restore
lost tissue and to supply antibodies.


16. STAGE OF HEALING

Vascularization is followed by cicatrization due to
regeneration of collagen and formation of fibrous tissue

Newly formed fibers are laid down irregularly, not
conforming to normal pattern of stromal fibers.
Therefore this fibrous tissue refracts light irregularly and
forms opacity.

17. CLINICAL FEATURES
Clinical signs and symptoms are variable depends on the
 virulence of the organism
 duration of infection,
 pre-existing corneal conditions
 immune status of host
 previous use of local steroids

18. 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

19. WORK-UP
Evaluation of predisposing and aggravating Factors
1. A detailed history.
2.
Prior ocular history
3.
Review of related medical problems, current ocular
medications and history of systemic steroids.

20. OCULAR EXAMINATION
1.Visual acuity-reduced
2.Slit lamp Biomicroscope
Lids - edema
Conjunctiva – Ciliary congestion

21. 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.

22. Iris- muddy
Toxin induced iritis
Pupil – miotic
Other:
-Sac syringing
-corneal sensation
-Fluorescein staining

23. Grading of corneal ulcer
Features
Mild
Size
<2mm
Depth of
ulcer
<20%
Stromal
infiltrate
1.Density
2.Extent
Scleral
involvement
Dense
Superficial
Moderate
2-5mm
Severe
>5mm
20-50%
>50%
Dense
Upto midstroma
Dense
Deep stromal
Harrison SM. Grading corneal ulcers. Ann Ophthalmol 1975;7:537-9, 541-2.
present

24. 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.

25. 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.

26. BACTERIAL ULCER WITH HYPOPYON
HYPOPYON.

27. 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.


28. 4. Streptococcus viridans
Infectious crystalline
keratopathytype 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.
 Seen in following corneal
grafts , prolonged use of
topical steroid.


29. COMPLICATIONS OF CORNEAL ULCER
1.
Spread of ulcer horizontally and depth-wise, leading to
thinning of cornea
2. Descemetocele –
This appears as transparent vesicle surrounded by grayish zone
of infiltration.
It represents condition of impending perforation of cornea

30. 
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 .

31. 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 .

32. d) Intra-ocular purulent infection: due to perforation
bacteria enter in the eye and causes endophthalmitis /
panophthalmitis

33. INVESTIGATIONS

Routine – Hemogram
BSL
HIV
Specific – Corneal scraping
Gram stain, Culture &
Antibiotic sensitivity
Culture of contact lens & solution

34. TREATMENT OF UNCOMPLICATED ULCER
Hospitalization
Treat the underlying cause/predisposing factor
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

35. Combination therapy with fortified broad spectrum antibiotics
1.Cephalosporin – gram positive cocci & some gram negative
rods
 Cefazolin 50mg/ml OR Ceftazidime 50mg/ml

2.Aminoglycoside - gram negative bacilli
 Tobramycin 14mg/ml
OR
Fluoroquinolone – broad spectrum-gram negative + gram
positive
 Moxiflox 5mg/ml
Topically every 30-60 min initially
 In severe cases- every 5 min for 30 min as a loading dose.


36. Vancomycin- reserved for very severe or recalcitrant infections
(50mg/ml)
 Amikacin (10-20mg/ml) for AF-bacilli

Fluoroquinolone monotherapy – 4th generation
< 3mm in diameter, peripheral & not associated with thinning

37. SYSTEMIC ANTIBIOTICS-FLUOROQUINOLONE
Indications
 Severe keratitis
 Scleral involvement
 hypopyon
 Impending perforation
 Frank perforation with risk of intraocular spread
 Infection in children
 P.aeruginosa infection

38. 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 intra-ocular
tension .

39. TREATMENT OF IMPENDING
PERFORATION
1.
2.
3.
4.
5.
6.
7.
Straining should be avoided.
Pressure bandage
Lowering of IOP
Tissue adhesive glue (cynoacrylate)
Conjunctival flap
Soft contact lens Bandage
Penetrating keratoplasty

40. TREATMENT OF NON HEALING ULCER
Removal of any known cause.
->LOCAL
->SYSTEMIC
 Mechanical debridement of ulcer.
 Cauterisation of ulcer.
 Bandage soft contact lens.


41. TREATMENT OF PERFORATED CORNEAL ULCER
Tissue adhesives
 Conjunctival flap
 Soft bandage
 Keratoplasty


42. 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

43. 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

44. 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

45. 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


Monitor pt at 24 & 48 hrs after initiation

46. SURGICAL TREATMENT
1.Tissue adhesives
Cyanoacrylate glue- small perforations< 3mm
-descemetocele


47. 2. Patch graft
-perforation –
5mm in diameter

3 . Therapeutic keratoplasty
-large areas of perforation, necrosis
-Non-healing ulcer
