BACTERIAL CORNEAL

ULCER..

Dr. Bhushan Patil.

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.

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

Anatomical

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

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.

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

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

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.

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.Pneumonia
e
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 positive cocci

Gram negative
diplobacilli

Gram positive bacilli Ocular trauma contaminated

by soil
M. Chelonae

Acid fast bacilli

Following LASIK

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 enymesNecrosis & sloughing of
epithelium, Bowmans 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
epithelium.
Infective organism multiplies release toxins
and enzymes.

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.

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
smooth.
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
forms opacity.

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

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

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.

OCULAR EXAMINATION
1.Visual acuity-reduced
2.Slit lamp Biomicroscope
Lids - edema

Conjunctiva Ciliary congestion

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.

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

Grading of corneal ulcer

Features

Mild

Size

<2mm

Depth of
ulcer

<20%

Stromal
infiltrate
1.Density
2.Extent

Dense
Superficial

Moderate

Severe

2-5mm

>5mm

20-50%

>50%

Dense
Upto midstroma

Dense
Deep stromal

Scleral
involvement
Harrison SM. Grading corneal ulcers. Ann Ophthalmol 1975;7:537-9, 541-2.

present

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.

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.

BACTERIAL ULCER WITH HYPOPYON

HYPOPYON.

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.

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.
Seen in following corneal
grafts , prolonged use of
topical steroid.

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

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 .

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

INVESTIGATIONS

Routine Hemogram
BSL
HIV

Specific Corneal scraping

Gram stain, Culture &
Antibiotic sensitivity
Culture of contact lens & solution

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

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.

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

SYSTEMIC ANTIBIOTICSFLUOROQUINOLONE
Indications
Severe keratitis
Scleral involvement
hypopyon
Impending perforation
Frank perforation with risk of intraocular spread
Infection in children
P.aeruginosa infection

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 .

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

TREATMENT OF NON HEALING

ULCER
Removal of any known cause.
->LOCAL
->SYSTEMIC
Mechanical debridement of ulcer.
Cauterisation of ulcer.
Bandage soft contact lens.

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

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
-re-epithelization
-corneal vascularization

Antibiotic frequency-tapered to 4hrly after 72 hrs

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

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

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

2. Patch graft
-perforation
5mm in diameter

3 . Therapeutic keratoplasty
-large areas of perforation, necrosis
-Non-healing ulcer

Thank you..