Vous êtes sur la page 1sur 48

By.

dr akanksha rastogi
 A break in the continuity of the covering
epithelium of the skin or mucous membrane

 It may either follow molecular death of the


surface epithelium or its traumatic removal.
 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.
 Corneal epithelium- mechanical barrier

 Conjunctiva- cellular & chemical components

 Tear film- biological protective system Major


components of ocular defence system
 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
 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
 Dry eye, Steven-Johnson syndrome, ocular
burn, bullous keratopathy.
 Contact lens use-Increased risk of bacterial
keratitis with use of Extended soft contact
lens corneal hypoxia & decompensation. -
Contamination of CL solution
 Local immune suppression due to topical
corticosteroids
 Ocular surgery- cataract , LASIK.
 1.Malnutrition
 2.Diabetes
 3.Immunosupression-Systemic steroids, AIDS
4.Chronic alcoholism
 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
 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.
 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
 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 enymes
 Necrosis & 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
 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.
 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).
 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.
 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 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 corneal ulcer
 2. Watering due to reflex lacrimation
 3. Photophobia
 4. Pain due to exposed nerve endings
 5. Mucopurulent / purulent discharge
 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.
 1.Visual acuity-reduced
 2.Slit lamp Biomicroscope
 Lids - edema
 Conjunctiva – Ciliary congestion
 -Location of the ulcer
 - central, paracentral , peripheral,total.
 -Size ,
 shape,
 depth,
 margins
 & floor- depends on stage of ulcer.
 -Density and extent of stromal infiltration.
 Anterior chamber - Cells/flare, mobile
Hypopyon.
 Iris- muddy Toxin induced iritis Pupil – miotic
Other: -Sac syringing -corneal sensation -
Fluorescein staining
 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
 1.Staphylococcal
 Central,oval, opaque
 Distinct margins.
 Mild oedema of remaining cornea.
 Stromal abscess in longstanding cases.
 Mild to moderate AC reaction.
 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.
 Affects compromised corneas e.g. Bullous
keratopathy , dry eyes , atopic diseases.
 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.
 Infectious crystalline keratopathy type 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.
 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
 .– 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 .
 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
 Routine – Hemogram BSL HIV Specific –
Corneal scraping Gram stain,
 Culture & Antibiotic sensitivity Culture of
contact lens & solution
 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
 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
 -FLUOROQUINOLONE Indications
 Severe keratitis
 Scleral involvement
 hypopyon
 Impending perforation
 Frank perforation with risk of intraocular
spread
 Infection in children
 P.aeruginosa infection
 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
 Removal of any known cause. ->LOCAL -
>SYSTEMIC
 Mechanical debridement of ulcer.
 Cauterisation of ulcer.
 Bandage soft contact lens.
 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
 -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
 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
 1.Tissue adhesives Cyanoacrylate glue- small
perforations< 3mm -descemetocele
 Patch graft -perforation – 5mm in diameter
 Therapeutic keratoplasty -large areas of
perforation, necrosis -Non-healing ulcer
Thank you

Vous aimerez peut-être aussi