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