Title: BACTERIAL KERATITIS
1BACTERIAL KERATITIS
- Dr. Sanjay Shrivastava
- Professor of Ophthalmology
- Regional Institute of Ophthalmology
- Gandhi Medical College
- Bhopal (M.P.)
- drs.rio_at_hotmail.com
2Copy of Power point presentation of Lecture
taken for Junior Final Year students of Gandhi
Medical CollegeBhopal
3Cornea
4 Anatomical facts
- The anterior 1/6th transparent avascular
structure covered anteriorly by tear film and
exposed to external environment . The posterior
surface is in contact with aqueous humour.
Corneal epithelium is continuous - The junction of cornea and sclera is represented
by highly vascularized limbus which contains stem
cells which serves as reservoir of pluripotential
cells
5Anatomical facts
- Measurements of adult cornea
- Horizontal 11 -12 mm
- Vertical 9-11 mm
- Thickness central 0.5 mm
- peripheral 0.7 1 mm
6 Optical properties of Cornea
- Dependant on
- Transparency
- Smoothness of surface
- Contour
- Refractive index
- Refractive power of Cornea is 40 44 Diopter
(i.e. 2/3rd of total refractive power of eye)
7 Maintenance of corneal integrity
- Maintenance of normal corneal integrity
- 1. Role of environmental (Chemical/ biological
agents/physical events of outside world affect
integrity) - 2. Epithelial maintenance limbal stem cells and
basal cells are capable of proliferation
8Maintenance of corneal integrity
- 3. Epithelial movement intracellular signal,
transduction, fibronectine integrin system,
proteolytic enzymes, hyaluronin and growth factor
play an important role in wound healing - 4. Neural regulation
- 5. Stromal maintenance
9Introduction
- Microbial Keratitis is defined as infectious
Corneal ulcer due to proliferation of
microorganisms (including bacteria, fungi,
viruses and parasites) associated with
inflammation and corneal tissue destruction. - It is potentially sight threatening condition and
should be considered as ocular emergency.
10 Bacterial Keratitis
- Bacterial Keratitis is most common cause of
suppurative corneal ulceration. There are no
specific clinical signs to help confirm a
definite bacterial cause in Bacterial Keratitis. - Identification of risk factors and assessment of
the distinctive corneal findings will help in
determination of potential etiologies.
11Host Defense and Risk Factors
12Defense of Ocular Surface
- Normal Defense mechanisms
- Eyelids
- Tear film proteins (Secretory immunoglobulins,
complement components, and various enzymes
including lysozyme, lactoferrin, betalysins,
orosomucoid and ceruloplasmin have antibacterial
effect) - Corneal epithelium
- Normal ocular flora
- Conjunctival mucosal associated lymphoid tissue
(MALT) which is present in subepithelium
13 Risk Factors
- Compromised normal ocular surface
- Chronic colonization and infection of the eyelid
margin and lacrimal outflow system can predispose
cornea - Chronic epiphora by reducing concentration of
certain antibacterial substances. - Dry eye
14Risk Factors
- 5. Presence of N Gonorrhoeae, C Diphtheriae,
Hemophilus Aegyptius and Listeria Monocytogenes
they can penetrate intact corneal epithelium. - 6. Compromised corneal epithelium as in cases of
contact lenses users, corneal trauma, corneal
surgery bullous keratopathy. - 7. Absence of normal conjunctival flora.
15 Risk Factors
- 8 Biofilm- is a slimy layer composed of organic
polymers produced by embedded bacteria on contact
lens, it protects bacteria from antibacterial
substances and provide a nidus for infection. - 9. Corneal anaesthesia
- 10. Abuse of topical anaesthetic solution
16 Risk Factors
- 11. Local immune suppression as due to topical
corticosteroids - 12. Previous viral infection
- 13. Drugs used in viral keratitis
- 14. Corneal hypesthesia
17 External Risk Factors
- Trauma (Nocardia)
- Exposure to contaminated water or solutions
- Chronic abuse of topical anaesthetic solution
- Crack Cocaine smoking (disrupting corneal
epithelium via associated cellular and neuronal
toxicity.
18Predisposing Systemic Conditions
- Malnutrition
- Diabetes
- Collagen vascular diseases
- Chronic alcoholism
19 Etiological Factors
- Inflammation of Cornea (Keratitis) may develop as
a result of - 1. Exogenous infection Mostly traumatic, the
object causing injury may carry infection to
cornea or may come from conjunctival sac
(infecting abraded cornea) - 2. Endogenous Infection (inflammation) this is
immunological in nature eg. Phlyctenular
keratitis caused by tubercular or staphylococcal
hypersensitivity and interstitial keratitis
related to measles or syphilis. These conditions
are commonly noticed at corneal margin (Marginal
Keratitis or Marginal Corneal Ulcer)
20 Etiological Factors
- 3. Spread of Infection from neighboring
structures due to anatomical continuity. - From conjunctiva to corneal epithelium (eg.
Trachoma and Vernal Keratoconjunctivitis) - From Sclera to corneal stroma (eg. Sclerosing
Keratitis) and - From Uveal tract to corneal endothelium (eg.
Herpetic Uveitis causing endothelitis)
21 Classification
- I. According to location
- a. Superficial
- b. Deep
- II. According to Etiology
- a. Infective
- b. Immune mediated
- c. Traumatic
- d. Neoplastic
- e. Degenerative
22Bacterial Keratitis
- Two forms
- Central Keratitis
- Peripheral Keratitis.
23 Corneal Ulcer
- Superficial Purulent Keratitis (Bacterial Corneal
Ulcer) - Caused by organisms which produce toxins causing
tissue death i.e. necrosis characterised by pus
formation. Such purulent keratitis is usually
exogenous due to infection by pyogenic bacteria
such as pseudomonas, staphylococcus aureus and
albus, pneumococcus, N. gonorrhoeae and C.
diphtheriae
24Corneal Ulcer
- Presence of N Gonorrhoeae, C Diphtheriae,
Hemophilus Aegyptius and Listeria Monocytogenes
they can penetrate intact corneal epithelium. - Otherwise most of the bacteria including
Pneumococcus is capable of producing corneal
ulcer when epithelium is damaged
25 Pathogenesis
- Steps
- Corneal abrasion
- Infection by microorganism in presence of
predisposing factor(s). The predisposing factors
are trauma, long term use of steroids,
misdirected eye lashes, mal-apposition of lids,
entropion, lagophthalmos, contact lens wear,
bullous keratopathy, poor hygienic condition,
malnutrition, ocular surface disorders, vitamin A
deficiency, causing corneal necrosis
(Keratomalacia), corneal edema and trigeminal
nerve paralysis (Neurotropic keratitis)
26 Pathogenesis
- 3. Localized necrosis of superficial layers of
cornea - 4. Formation of sequestrum with disintegration.
It cast off in conjunctival sac - 5. Desquamation of corneal epithelium and damage
to Bowmans membrane (area of epithelial and
Bowmans denudation is larger than ulcer)
27 Pathogenesis
- 6. Epithelial regeneration, at times it covers
the edges and floor area - 7. A saucer shaped defect with projecting walls
above the normal surface due to swelling of
tissue resulting from fluid imbibition by corneal
stroma - 8. Surrounding area is packed by leucocytes,
seen as gray zone of infiltration. This is
progressive stage.
28 Pathogenesis
- 9. Necrotic material fall off- ulcer becomes
larger -gt infiltration and swelling reduce and
disappears -gt margin becomes smooth, floor also
looks smooth and transparent. This is regressive
stage. - 10. Vascularization develops from limus to
corneal ulcer to restore lost tissue and to
supply antibodies.
29 Pathogenesis
- 11. Vascularisation is followed by cicatrization
due to regeneration of collagen and formation of
fibrous tissue - 12. Newly formed fibres are laid down
irregularly, not conforming to normal pattern of
stromal fibres. Therefore this fibrous tissue
reflects light irregularly. The scar tissue is
more or less opaque. Some vessels may persist in
large scar
30 Pathogenesis
- 13. Bowmans membrane never regenerates and
whenever it is destroyed some degree of corneal
opacity remains - 14 Corneal opacity may clear with time especially
if it is not dense. The vascularization plays
part in clearing corneal opacity - 15. The scar tissue usually fill the gap exactly,
but some deficiency may remain giving rise to
formation of corneal facet. The corneal facet may
be transparent and may be associated with marked
diminution of vision
31 Pathogenesis
- 16. Diffusion of bacterial toxins into the
anterior chamber leads to hyperaemia and
inflammation of the iris and ciliary body
(Keratouveitis). Polymorphonuclear cells coming
out from the uveal tissue may gravitate to bottom
of anterior chamber to form hypopyon.
32 Symptoms of Corneal Ulcer
- Symptoms are usually marked, they are
- 1. Diminution of vision, depending on location
of corneal ulcer - 2. Watering (lacrimation)
- 3. Difficulty in opening eyes especially in
bright light (photophobia and blepharospasm) - 4. Pain and foreign body/ gritty sensation
- 5. There may be discharge (Mucopurulent /
purulent)
33 Presentation
- Clinical signs and symptoms are variable
dependent on the virulence of the organism,
duration of infection, pre-existing corneal
conditions, immune status of host and previous
use of antibiotics/ steroid - Acanthamoeba can cause masquerading syndrome
mimicking bacterial keratitis.
34 Signs
- Visual acuity may be affected, depending on
location of corneal ulcer - Edema of lids of affected eye, in severe cases
- Blepharospasm
- Ciliary and conjunctival congestion
- Hazyness / pus may be present in anterior chamber
35 Signs
- 6. Colour and pattern of iris may be disturbed
- 7. Cornea loss of transparency the ulcer appears
yellowish/ grayish pale lesion of varying shape
/size, breach in continuity of corneal surface,
ulcer with irregular floor and margins, floor
appears grayish / grayish pale/ grayish yellow,
zone of infiltration with projecting swollen
edges. The surrounding cornea may appear ground
glass like due to corneal edema
36Corneal Ulcer
Central Corneal ulcer involving Lower periphery
also
Peripheral Corneal Ulcer
37 Clinical Examination
- Evaluation of predisposing and aggravating
Factors - A detailed history
- Prior ocular history
- Review of related medical problems, current
ocular medications and history of medication
allergy
38 Examination
- Visual acuity
- An external ocular examination
- Facial appearance, eyelids, lid closure
- Conjunctiva, Nasolacrimal apparatus, corneal
sensation
39 Examination
- 3. Slit Lamp Biomicroscopy For
- Eyelid margin
- Tear film
- Conjunctiva
- Sclera
- Cornea (epithelial defects, punctate
keratopathy, edema, stromal infiltrates/ulcerati
on, thinning or perforation)
40Slit Lamp Examination Contd
- Location of lesion
- Density, Size , shape , depth, colour
- Endothelium
- Anterior chamber
- Loose or Broken sutures
- Signs of corneal dystrophy
- Signs of previous inflammation
41 Slit Lamp Examination Contd
- Anterior Vitreous
- Fluorescein
- Rose Bengal staining
42Differential Diagnosis
- Differentiate from Non-infectious causes of
infiltrates - Fungal
- Protozoal
- Nematodes
- Viral infections, HSV, VZV, EBV
- Contact lens infiltrates
- Collagen Vascular Diseases
43 Differential Diagnosis
- 7. Sarcoidosis
- 8. Severe Rosacea
- 9. Allergic Conditions
- 10. Corneal Trauma , FB and Loose sutures
44 Complications of Corneal Ulcer
- Spread of ulcer horizontally and depth-wise,
leading to thinning of cornea - Bulging of descemets membrane (Keratocele or
Descemetocele). This appears as transparent
vesicle surrounded by grayish zone of
infiltration. Bulging of descemets membrane
represents condition of impending perforation of
cornea
45Complications of Corneal Ulcer
- 3. Perforation of ulcer is generally caused by
sudden exertion such as coughing, sneezing,
straining at stool or firm closure of eyes.
Exertion causes rise of blood pressure and
results in increase in intra-ocular pressure
(IOP). Weak area of ulcer is unable to support
the increased IOP , gives way and perforation
develops
46Complications of Corneal Ulcer
- PERFORATION OF CORNEAL ULCER
- Complications of perforation may be serious and
sight threatening - Peripheral perforation Iris is thrown forward
-gt opening is occluded -gt anterior chamber is
formed , scarring takes place - a. Iris may be pushed back to normal position or
47Complications of Corneal Ulcer
- b. Iris may remains adherent to corneal scar
(anterior synechia) - If peripheral perforation is large the
pupillary border of iris prolapse through
opening. Exudation takes place on prolapsed
tissue -gt an adherent leucoma forms (it may be
flat or bulging)
48 Complications of Corneal Ulcer
- B. Central perforation small central
perforation -gt anterior chamber collapse - -gt lens comes in contact with corneal
endothelial surface -gt anterior capsular cataract
-gt repeated healing and perforation leading to
corneal fistula formation
49Complications of Corneal Ulcer
- C. Sloughing of whole cornea prolapse of iris
-gt pupillary block and exudation on iris -gt
pseudocornea formation (iris covered with
exudates , formation of fibrous tissue and
formation of scar tissue) -gt anterior chamber
anatomy is lost , angle of anterior chamber is
occluded leading to secondary glaucoma -gt
anterior staphyloma (an ectatic cicatric with
incarceration of iris). Anterior staphyloma may
be partial or total.
50 Complications of Corneal Ulcer
- In case of sudden large perforation lens may
subluxate or thrown out due to rupture of
suspensory ligaments. Lens and vitreous may
prolapse through perforation. Intraocular
haemorrhage may occur due to dilatation and
rupture of intra-ocular blood vessels due to
sudden hypotony. This may lead to vitreous
haemorrhage , choroidal , sub-retinal or
sub-choroidal haemorrhage. In elderly patients
there may be expulsive haemorrhage
51 Complications of Corneal Ulcer
- D. Intra-ocular purulent infection due to
perforation bacteria enter in the eye and causes
purulent iridocyclitis, endophthalmitis and
panophthalmitis
52Treatment of uncomplicated corneal ulcer
- LOCAL TREATMENT
- 1. 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
53Local Antibiotic therapy
- Antibiotic drops frequently, ointment may be used
at bedtime in less severe cases. Collagen shield
or soft contact lenses soaked in antibiotics are
sometimes used and may enhance drug delivery. - Sub-conjunctival antibiotics may be helpful where
there is imminent scleral spread or perforation
or in cases where compliance with the treatment
regimen is questionable
54Therapeutic Agents
- No organism identified or multiple types of
organisms - Cefazolin Topical 50 mgm/ml S/c 100 mgm in
0.5 ml. - With Tobramycin / Gentamicin
- Topical 9-14 mgm/ml S/c 20 mgm in 0.5 ml.
- Fluroquinolones 3 mgm/ ml
55Therapeutic Agents
- 2. Gram Positive Cocci
- Cefazolin Topical 50 mgm/ml S/c 100 mgm in
0.5 ml. - Vancomycin Topical 15 - 50 mgm/ml S/c 25 mgm
in 0.5 ml.
56Gram Negative Rods
- Tobramycin / Gentamicin
- Topical 9-14 mgm/ml S/c 20 mgm in 0.5 ml.
- Ceftazidime Topical 50 mgm/ml S/c 100mgm in
0.5 ml. - Fluroquinolones 3 mgm/ ml
57Gram Negative Cocci
- Ceftriaxone Topical 50 mgm/ml S/c 100 mgm in
0.5 ml. - Ceftazidime Topical 50 mgm/ml S/c 100 mgm in
0.5 ml. - Fluroquinolones 3 mgm/ ml
58Treatment of uncomplicated corneal ulcer
- 2. Cycloplegic and mydriatic drug atropine 1
or cyclopentolate 1 or Homatropine 2. These
drugs prevents ciliary spasm, relieves pain,
prevent dangerous results of iridocyclitis,
breaks adhesions and prevent synechia formation
59Treatment of uncomplicated corneal ulcer
- 3. Cleanliness Irrigation with luke warm normal
saline or 2 luke warm boric acid solution to
remove conjunctival discharge and necrotic
material - 4. Application of heat provides comfort and
causes vasodilatation - 5. Protection of eye from external environment
with dark glasses
60Treatment of uncomplicated corneal ulcer
- Steroids must not be used in presence of active
infected corneal ulcer - In cases of progressive corneal ulcer despite
routine therapeutic treatment, the following
measures be considered - Scraping of ulcer floor followed by cauterization
with pure (100) carbolic acid or 10-20
trichloracetic acid. Povidone Iodine can also be
used for cauterization
61Systemic Treatment
- Systemic Antibiotics consider in sever cases
with scleral or intra-ocular extension of
infection or with impending or frank perforation
of the cornea - Systemic antibiotic therapy is necessary in
cases of Gonococcal keratitis due to its
fulminating nature and systemic involvement
62Systemic Treatment
- 2. Analgesic anti-inflammatory
- 3. Supportive treatment
- 4. Acetazolamide Tab is added in cases of
impending perforation or perforated corneal ulcer
and in cases where there is raised intra-ocular
tension (in dosage of 250 mgm upto four times a
day)
63Non-responsive / Progressive Corneal Ulcer
- TREATMENT
- Re-evaluate for
- Drug toxicity
- Non-infectious causes or
- Unusual organisms such as non-tubercular
mycobacteria, Nocardia or acanthamoeba should be
suspected - Modification of anti-microbial therapy
- Therapeutic keratoplasty may be undertaken
-
64Indolent / Non-healing Ulcer
- Consider debridement of necrotic corneal stroma
and - Frequent lubrication and/or
- Temporary tarsorrhaphy
65Treatment of Keratocele or Descemetocele
- Continue use of local antibiotics, atropine, add
topical antiglaucoma medication (like Timolol or
Betaxolol) or add systemic acetazolamide, bandage
contact lens is beneficial. All forced expiration
like coughing, sneezing, blowing of nose etc must
be avoided
66Treatment of perforated corneal ulcer
- Rest
- Continue treatment of corneal ulcer with
modification, i.e. firm bandage or bandage
contact lens - All forced expiration like coughing, sneezing,
blowing of nose etc must be avoided - Use of tissue adhesive (Glue) N-butyl 2-ethyl
cyanoacrylate - Therapeutic penetrating keratoplasty or
conjunctival flap
67 Adjunctive Therapy
- Cyanoacrylate tissue glue
- Therapeutic Contact Lenses
68 Surgical Treatment
- Conjunctival flap In recalcitrant bacterial
keratitis - Penetrating Keratoplasty (PKP)
- Large central ulcer , presenting late
- History of previous ocular surgery
- Injudicious use steroid treatment