• Corneal ulcer may be defined as
discontinuation in normal epithelial
surface of cornea associated with
necrosis of the surrounding corneal
• Pathologically it is characterised by
oedema and cellular infiltration
• BACTERIAL CORNEAL ULCER
• the cornea is exposed to atmosphere and
hence prone to get infected easily
• Cornea is protected from the minor infections
by the normal defence mechanisms present in
tears lysozyme, betalysin, and other protective
• either the local ocular defence mechanism is
• there is some local ocular predisposing
• Host's immunity is compromised.
• The causative organism is very virulent.
• Damage to corneal epithelium.
• Infection of the eroded area.
• Neisseria gonorrhoeae,
• Neisseria meningitidis.
1. Corneal epithelial damage
• Corneal abrasion due to small foreign body,
misdirected cilia, concretions and trivial trauma in
contact lens wearers or otherwise.
• Epithelial drying as in xerosis and exposure
• Necrosis of epithelium as in keratomalacia.
• Desquamation of epithelial cells as a result of
corneal oedema as in bullous keratopathy.
• Epithelial damage due to trophic changes as in
• A corneal abrasion (scratched cornea or
scratched eye) is one of the most
common eye injuries. A scratched cornea often
causes significant discomfort, red eyes and
hypersensitivity to light. Corneal
abrasions result from a disruption or loss of
cells in the top layer of the cornea, called
the corneal epithelium.
From the ocular tissue.
• Anatomical continuity, diseases of
the conjunctiva readily spread to
corneal epithelium, those of sclera to
stroma, and of the uveal tract to the
endothelium of cornea.
• Avascular nature of the cornea,
endogenous infections are of rare
3. Causative organisms
• Common bacteria associated with corneal ulceration are:
• Staphylococcus aureus,
• Pseudomonas pyocyanea,
• E. coli,
• N. gonorrhoea,
• N. meningitidis
• C. diphtheriae.
• Once the damaged corneal epithelium is invaded by the
offending agents the sequence of pathological changes
which occur during development of corneal ulcer can
be described under four stages-
• active ulceration,
• regression and
• The terminal course of corneal ulcer depends upon the
virulence of infecting agent, host defence mechanism
and the treatment received
• In bacterial infections the outcome depends
upon the virulence of organism, its toxins and
enzymes, and the response of host tissue.
• Broadly bacterial corneal ulcers may manifest
• i. Purulent corneal ulcer without hypopyon; or
• ii. Hypopyon corneal ulcer.
1. Pain and foreign body sensation occurs due to
mechanical effects of lids and chemical effects of
toxins on the exposed nerve endings.
2. Watering from the eye occurs due to reflex
3. Photophobia, i.e., intolerance to light results from
stimulation of nerve endings.
4. Blurred vision results from corneal haze.
5. Redness of eyes occurs due to congestion of
1. Lids are swollen.
2. Marked blepharospasm
3. Conjunctiva is chemosed and shows conjunctival
hyperaemia and ciliary congestion.
4. Corneal ulcer
5. Anterior chamber may or may not show pus
6. Iris may be slightly muddy in colour
7. Pupil may be small due to associated toxin induced
8. Intraocular pressure may some times be raised
• Management of hypopyon corneal ulcer is
same as for other bacterial corneal ulcer.
Special points which need to be considered are
• Secondary glaucoma should be anticipated
and treated with 0.5% timolol maleate, B.I.D.
eye drops and oral acetazolamide.
• Source of infection, i.e., chronic dacryocystitis
if detected, should be treated by
1. Toxic iridocyclitis.
• It is usually associated with cases of
purulent corneal ulcer due to
absorption of toxins in the anterior
2. Secondary glaucoma.
• It occurs due to fibrinous exudates
blocking the angle of anterior
chamber (inflammatory glaucoma).
• Some ulcers caused by virulent organisms
extend rapidly up to Descemet's
membrane, which gives a great
resistance, but due to the effect of
intraocular pressure it herniates as a
transparent vesicle called the
descemetocele or keratocele.
4. Perforation of corneal ulcer
• Sudden strain due to cough, sneeze or
spasm of orbicularis muscle may convert
impending perforation into actual
5. Corneal scarring.
• It is the usual end result of healed corneal
ulcer. Corneal scarring leads to permanent
visual impairment ranging from slight blurring
to total blindness.
• Depending upon the clinical course of ulcer,
corneal scar noted may be nebula, macula,
leucoma, ectatic cicatrix or kerectasia,
adherent leucoma or anterior staphyloma.
Management of a case of corneal
• [A] Clinical evaluation
• [B] Laboratory investigations
• [C] Treatment
[A] Clinical evaluation
• 1. Thorough history taking to elicit mode of
• 2. General physical examination
• Immunocompromising disease.
• 3. Ocular examination
• i. Diffuse light examination
• ii. Regurgitation test and syringing
• iii. Biomicroscopic examination
1. Gram and Giemsa stained smears for possible identification
of infecting organisms.
ii. 10 per cent KOH wet preparation for identification of
iii. Calcofluor white (CFW) stain preparation is viewed under
fluorescence microscope for fungal filaments, the walls of
which appear bright apple green.
iv. Culture on blood agar medium for aerobic organisms.
v. Culture on Sabouraud's dextrose agar medium for fungi.
• I. Treatment of uncomplicated corneal ulcer
• II. Treatment of non-healing corneal ulcerof
uncomplicated corneal ulcer
• III. Treatment of impending perforation
• IV. Treatment of perforated corneal ulcer
I. Treatment of uncomplicated corneal
• 1. Specific treatment for the cause.
• 2. Non-specific supportive therapy.
• 3. Physical and general measures.
1. Specific treatment for the cause.
• Topical antibiotics. Initial therapy should be with
combination therapy to cover both gram-negative
and gram-positive organisms.
• Ciprofloxacin (0.3%) eye drops, or
• Ofloxacin (0.3%) eye drops, or
• Gatifloxacin (0.3%) eye drops.
• Systemic antibiotics are usually not required.
However, a cephalosporine and an
aminoglycoside or oral ciprofloxacin may be given
in perforation and when sclera is involved.
2. Non-specific supportive therapy.
• (a) Cycloplegic drugs 1 percent atropine eye
ointment or drops should be used to reduce pain
from ciliary spasm and to prevent the formation
of posterior synechiae from secondary
• (b) Systemic analgesics and anti-inflammatory
drugs such as paracetamol and ibuprofen relieve
the pain and decrease oedema
• (c) Vitamins (A, B-complex and C) help in early
healing of ulcer.
3. Physical and general measures.
• (a) Hot fomentation. Local application of heat
(preferably dry) gives comfort, reduces pain
and causes vasodilatation.
• (b) Dark goggles may be used to prevent
• (c) Rest, good diet and fresh air may have a
II. Treatment of non-healing corneal
ulcerof uncomplicated corneal ulcer
• 1. Removal of any known cause of non-healing
i. Local causes.
Ii. Systemic causes:
• 2. Mechanical debridement of ulcer
• 3. Cauterisation of the ulcer
• 4. Bandage soft contact lens
• 5. Peritomy
Treatment of perforated corneal ulcer
• Best is to prevent perforation. However, if
perforation has occurred, immediate measures
should be taken to restore the integrity of
• Depending upon the size of perforation and
availability, measures like use of tissue adhesive
glues, covering with conjunctival flap, use of
bandage soft contact lens or therapeutic
keratoplasty should be undertaken.
• Best is an urgent therapeutic keratoplasty.