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
NORMAL DEFENCE MECHANISM
Corneal epithelium- mechanical barrier
Conjunctiva- cellular & chemical components
Tear film- biological protective system
Major components of ocular defence system
BARRIERS OF MICROBIAL INFECTION
• Bony orbital rim,eyelids,
• Intact corneal & conjunctival
• Tear film-mucus layer
• Lacrimal system
• Tear film constitutes-IgA,
complement components, and
enzymes lysozyme, lactoferrin,
betalysins have antibacterial effect
3. Ocular surface disorder- Dry eye, Steven-Johnson syndrome, ocular burn,
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.
3.Immunosupression-Systemic steroids, AIDS
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.
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
Gram positive cocci
1.Most common organism
3.Dry eye, bullous
keratopathy, atopic disease.
S.Pneumoniae Gram positive cocci
Corneal grafts .
P. Aeruginosa Gram negative
1.Contact Lens users
3.Pt on mechanical ventillator
Malnourished, alcoholics ,
Gram positive bacilli Ocular trauma contaminated
Acid fast bacilli
Corneal abrasion Microbes adhere to epithelium, release toxins & lytic
PMNs at the site of ulcer from tears & limbal vessels release of
cytokines & interleukins progressive invasion of cornea & increase in
size of ulcer
Release of free radicals,proteolytic enymesNecrosis & 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
STAGE OF PROGRESSIVE INFILTRATION
Entry and adherance of organism to breached
epithelium enters into stroma.
PMNs and lymphocytes infiltrate into stroma and
Infective organism multiplies release toxins and
STAGE OF ACTIVE ULCERATION
Necrosis occurs due to toxins and enzymes released by
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.
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).
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
Vascularization develops from limbus to corneal ulcer to restore
lost tissue and to supply antibodies.
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
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
1. Diminution of vision, depending on location of
2. Watering due to reflex lacrimation
4. Pain due to exposed nerve endings
5. Mucopurulent / purulent discharge
Evaluation of predisposing and aggravating Factors
1. A detailed history.
Prior ocular history
Review of related medical problems, current ocular
medications and history of systemic steroids.
Grading of corneal ulcer
Harrison SM. Grading corneal ulcers. Ann Ophthalmol 1975;7:537-9, 541-2.
Mild oedema of
Stromal abscess in
Mild to moderate AC
corneas e.g. Bullous
keratopathy , dry eyes ,
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
Extends periphery & deep
within 24 hrs.
Stromal necrosis with shaggy
Spreads concentrically and
symmetrically to involve
whole depth of cornea-Ring
Hypopyon is present.
Untreated corneal melting.
4. Streptococcus viridans
keratopathytype of stromal
(needle like) white opacities
in stroma , not associated
with infiltration & ocular
Due to proliferation of
bacteria between the stromal
Seen in following corneal
grafts , prolonged use of
COMPLICATIONS OF CORNEAL ULCER
Spread of ulcer horizontally and depth-wise, leading to
thinning of cornea
2. Descemetocele –
This appears as transparent vesicle surrounded by grayish zone
It represents condition of impending perforation of cornea
3. Perforation of ulcer –
sudden exertion such as coughing, sneezing, straining at stool or
firm closure of eyes increase in intra-ocular pressure (IOP)
a) Peripheral perforation iris prolapse through opening.
Exudation takes place on
prolapsed tissue ->
an adherent leucoma .
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 /
Routine – Hemogram
Specific – Corneal scraping
Gram stain, Culture &
Culture of contact lens & solution
TREATMENT OF UNCOMPLICATED ULCER
Treat the underlying cause/predisposing factor
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
Combination therapy with fortified broad spectrum antibiotics
1.Cephalosporin – gram positive cocci & some gram negative
Cefazolin 50mg/ml OR Ceftazidime 50mg/ml
2.Aminoglycoside - gram negative bacilli
Fluoroquinolone – broad spectrum-gram negative + gram
Topically every 30-60 min initially
In severe cases- every 5 min for 30 min as a loading dose.
Vancomycin- reserved for very severe or recalcitrant infections
Amikacin (10-20mg/ml) for AF-bacilli
Fluoroquinolone monotherapy – 4th generation
< 3mm in diameter, peripheral & not associated with thinning
Frank perforation with risk of intraocular spread
Infection in children
1.Cycloplegic : Atropine 1% or cyclopentolate 1% or
Homatropine 2%- prevents ciliary spasm, relieves pain, breaks
adhesions and prevent synechia formation.
3. Oral vitamin C
4. Acetazolamide Tab - impending perforation or perforated
corneal ulcer and in cases where there is raised intra-ocular
TREATMENT OF IMPENDING
Straining should be avoided.
Lowering of IOP
Tissue adhesive glue (cynoacrylate)
Soft contact lens Bandage
TREATMENT OF NON HEALING ULCER
Removal of any known cause.
Mechanical debridement of ulcer.
Cauterisation of ulcer.
Bandage soft contact lens.
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
Signs of healing :
-resolution of lid edema, congestion
-decreased density of stromal infiltrate
-reduction of corneal oedema
-reduction in AC reaction/hypopyon
Antibiotic frequency-tapered to 4hrly after 72 hrs
Signs of non-response
- Increase in infiltration, epithelial defect, height of hypopyon,
Corneal thinning, perforation
Non-infectious causes or
Modification of anti-microbial therapy according to antimicrobial
Scraping of ulcer floor followed by cauterization with pure
(100%) carbolic acid or 10-20% trichloracetic acid.
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