bacterial corneal ulcer drbp
TRANSCRIPT
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
• Bony orbital rim,eyelids,• Intact corneal & conjunctival
epithelium
Anatomical
• Tear film-mucus layer• Lacrimal system
Mechanical
• Tear film constitutes-IgA, complement components, and enzymes lysozyme, lactoferrin, betalysins have antibacterial effect
• CALT
Antimicrobial
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.AureusS.Epidermidis
Gram positive cocci 1.Most common organism2.Eyelid diseases3.Dry eye, bullous keratopathy, atopic disease.
Streptococcus S.PneumoniaeS. Viridans
Gram positive cocci chronic Dacryocystitis.Corneal grafts .
Pseudomonas P. Aeruginosa Gram negative bacilli
1.Contact Lens users2.Comatose pt.3.Pt on mechanical ventillator4.HIV
Moraxella M.Lacunata Gram negative diplobacilli
Malnourished, alcoholics , diabetes
Nocardia,Actinomycets
Gram positive bacilli Ocular trauma contaminated by soil
Atypical Mycobacteria
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, 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
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-reduced2.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 Moderate Severe
Size <2mm 2-5mm >5mm
Depth of ulcer
<20% 20-50% >50%
Stromal infiltrate1.Density2.Extent
DenseSuperficial
DenseUpto mid- stroma
DenseDeep stromal
Scleral involvement
present
Harrison SM. Grading corneal ulcers. Ann Ophthalmol 1975;7:537-9, 541-2.
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 ANTIBIOTICS-FLUOROQUINOLONE
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 .
1. Straining should be avoided.
2. Pressure bandage
3. Lowering of IOP
4. Tissue adhesive glue (cynoacrylate)
5. Conjunctival flap
6. Soft contact lens Bandage
7. Penetrating keratoplasty
TREATMENT OF IMPENDING PERFORATION
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, perforationTreatment Re-evaluate for
Drug toxicityNon-infectious causes orUnusual 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..