Ahmed Abd-Eljalil
4th medical student in Alexandria Uni. - Egypt
Almoroj1994@yahoo.com
References "Kanski_Clinical_Ophthalmology_8th_edition"
"Adler's Physiology of the Eye_ Expert Consult - Online and Print, 11th Edition"
"Atlas Of Clinical Ophthalmology 3rd ed - David J. Spalton et al. (Mosby, 2004)"
Text Book of Alexandria University
3. Aetiology
The Organisms that produce toxins causing tissue
death and pus formation in the Cornea.
StreptococciStaphylococcus
aureus
Pseudomonas
aeruginosa
Bacteria
commensal of the
upper respiratory
tract
commensal of the
nares, skin and
conjunctiva
commensal of the
gastrointestinal
tract
Normal Habit
Infections with
streptococci are
often aggressive.
present with a focal
and fairly well-
defined white or
yellow–white
infiltrate.
The infection is
typically aggressive
and is responsible
for over 60% of
contact lens-related
keratitis.
Disease
5. Pathogenesis
1- Progressive stage :
A- Start with localized necrosis of the anterior layers of
cornea “Epithelium & Bowman’s membrane”.
Necrotic tissue partially cast off into the conjunctival sac
and adheres to ulcer.
B- Saucer-shaped Ulcer due to swelling of the
surrounding Corneal lamellae and project .
C-Surrounding area becomes packed with leucocytes as
gray zone “ground glass appearance”.
D- some toxins produced by the causative organisms
cause irritation of the iris and ciliary body resulting in “
kerato-uveitis”.
Hypopyon
6. Regressive stage
PNL in the cornea ,Dissolve The necrotic tissues .
Infiltration and swelling start disappear.
Floor and edges of the ulcer become smooth and
transparent.
Superficial vascularization from limbus to restore
tissue loss and supply Antibodies.
7. Healing stage
Regeneration of Collagen and formation of fibrous
tissue .
Newly fibers not arranged regular and cause
reflective error.
Mild opacity due to Collagen remodeling
Formed scar are opaque .
Bowman’s membrane never regenerates.
Formed scar tissue fills the tissue gap.
8. Clinical Features
Symptoms : Diminution of Vision ,pain,
photophobia, Ciliary injection , blurred vision and
mucopurulent or purulent discharge.
9. Clinical Features
Signs :
Lid oedema.
epithelial defect with infiltrate involving a larger area.
Hypopyon.
Chemosis.
Loss corneal Lustre
Ulcer can stained by 1% of Fluorescein sodium.
Severe ulceration may lead to descemetocele formation
and perforation, particularly in Pseudomonas infection .
15. General considerations
Hospital admission
Discontinuation of contact lens wear is mandatory
A clear plastic eye shield
Decision to treat
16. Local therapy
Can achieve high tissue concentration and initially
should consist of broad-spectrum antibiotics that
cover most common pathogens.
Antibiotic monotherapy “Ciprofloxacin or ofloxacin”.
Antibiotic duo therapy “combination of two fortified
antibiotics, typically a cephalosporin and an
aminoglycoside”.
Subconjunctival antibiotics.
Mydriatics.
Steroids “are contraindicated until
reepithelizition”
reduce host inflammation, improve comfort,
and minimize corneal scarring.
17. Systemic therapy
Systemic antibiotics are not usually given, but may
be appropriate in the following circumstances:
1-Potential for systemic involvement
2-Severe corneal thinning
3-Scleral involvement
18. Management of apparent treatment failure
If no improvement.
There’s no need to change the initial therapy if
this has induced a favorable response.
However, if Improvement still not
accomplished.
re-scraping performed with inoculation on a
broader range of media.
If cultures remains negative, it might be
necessary to perform a corneal biopsy for
histology and culture.
Excisional keratoplasty.