bacterial kert

7/29/2019 bacterial kert.

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BACTERIAL KERATITIS

CH.HARIKRISHNATITANS BATCH 2007

MAMATA MEDICAL COLLEGE,KHAMMAM,ANDHRAPRADESH


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CLASSIFICATIONIt is difficult to classify and assign a group to each and every case of

keratitis; as overlapping or concurrent findings tend to obscure the

picture. Topographical (morphological) classification

(A) Ulcerative keratitis (corneal ulcer)

Corneal ulcer can be further classified variously.

1. Depending on location(a) Central corneal ulcer

(b) Peripheral corneal ulcer

2. Depending on purulence

(a) Purulent corneal ulcer or suppurative corneal ulcer (mostbacterial and fungal corneal ulcers are suppurative).

(b) Non-purulent corneal ulcers (most of viral, chlamydial andallergic corneal ulcers are non-suppurative).


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3. Depending upon association of hypopyon

(a) Simple corneal ulcer (without hypopyon)

(b) Hypopyon corneal ulcer4. Depending upon depth of ulcer

(a) Superficial corneal ulcer

(b) Deep corneal ulcer(c) Corneal ulcer with impending perforation

(d) Perforated corneal ulcer

5. Depending upon slough formation

(a) Non-sloughing corneal ulcer

(b) Sloughing corneal ulcer


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(B) Non-ulcerative keratitis

1. Superficial keratitis

(a) Diffuse superficial keratitis

(b) Superficial punctate keratitis (SPK)

2. Deep keratitis

(a) Non-suppurative

(i) Interstitial keratitis

(ii) Disciform keratitis

(iii) Keratitis profunda

(iv) Sclerosing keratitis(b) Suppurative deep keratitis

(i) Central corneal abscess

(ii) Posterior corneal abscess


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Etiological classification

1. Infective keratitis

(a) Bacterial

(b) Viral(c) Fungal

(d) Chlamydial

(e) Protozoal

(f) Spirochaetal

3. Trophic keratitis

(a) Exposure keratitis

(b) Neuroparalytic keratitis

(c) Keratomalacia

(d) Atheromatous ulcer

2.Allergic keratitis(a) phlyctenular keratitis

(b) Vernal keratitis

(c) Atopic keratitis


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4. Keratitis associated with diseases of skin andmucous membrane.

5. Keratitis associated with systemic collagenvascular disorders.

6. Traumatic keratitis, which may be due tomechanical trauma, chemical trauma, thermal

burns, radiations

7. Idiopathic keratitis e.g.,

(a) Mooren's corneal ulcer(b) Superior limbic keratoconjunctivitis

(c) Superficial punctate keratitis of Thygeson


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Bacterial Keratitis

Bacterial Keratitis is most common cause ofsuppurative corneal ulceration. There areno specific clinical signs to help confirm a

definite bacterial cause in BacterialKeratitis.

Identification ofrisk factors and

assessment of the distinctive cornealfindings will help in determination ofpotential etiologies.


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Host Defense and Risk Factors


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Defense of Ocular Surface

Normal Defense mechanisms:1. Eyelids

2. Tear film proteins (Secretory immunoglobulins,

complement components, and various enzymesincluding lysozyme, lactoferrin, betalysins,orosomucoid and ceruloplasmin have antibacterialeffect)

3. Corneal epithelium

4. Normal ocular flora5. Conjunctival mucosal associated lymphoid tissue

(MALT) which is present in subepithelium


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Risk Factors

1. Compromised normal ocular surface

2. Chronic colonization and infection of theeyelid margin and lacrimal outflowsystem can predispose cornea

3. Chronic epiphora by reducingconcentration of certain antibacterialsubstances.

4. Dry eye


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Risk Factors

5. Presence of N Gonorrhoeae, C Diphtheriae,Hemophilus Aegyptius and ListeriaMonocytogenes they can penetrate intactcorneal epithelium.

6. Compromised corneal epithelium as in casesof contact lenses users, corneal trauma,

corneal surgery bullous keratopathy.

7. Absence of normal conjunctival flora.


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Risk Factors

8 Biofilm- is a slimy layer composed oforganic polymers produced by embeddedbacteria on contact lens, it protects

bacteria from antibacterial substances andprovide a nidus for infection.

9. Corneal anaesthesia

10. Abuse of topical anaesthetic solution


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Risk Factors

11. Local immune suppression as due totopical corticosteroids

12. Previous viral infection

13. Drugs used in viral keratitis

14. Corneal hypesthesia


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External Risk Factors

1. Trauma (Nocardia)

2. Exposure to contaminated water orsolutions

3. Chronic abuse of topical anaestheticsolution

4. Crack Cocaine smoking (disruptingcorneal epithelium via associated cellularand neuronal toxicity.


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Predisposing Systemic Conditions

1. Malnutrition

2. Diabetes

3. Collagen vascular diseases4. Chronic alcoholism


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Etiological FactorsInflammation of Cornea (Keratitis) may develop as

a result of:1. Exogenous infection Mostly traumatic, the objectcausing injury may carry infection to cornea or maycome from conjunctival sac (infecting abraded cornea)

2. Endogenous Infection (inflammation): this isimmunological in nature eg. Phlyctenular keratitis causedby tubercular or staphylococcal hypersensitivity andinterstitial keratitis related to measles or syphilis. These

conditions are commonly noticed at corneal margin(Marginal Keratitis or Marginal Corneal Ulcer)


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Etiological Factors

3. Spread of Infection from neighboringstructures 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)


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Corneal Ulcer

Superficial Purulent Keratitis (Bacterial CornealUlcer)

Caused by organisms which produce toxins

causing tissue death i.e. necrosis characterisedby pus formation.

Such purulent keratitis is usually exogenous dueto infection by pyogenic bacteria such aspseudomonas, staphylococcus aureus and albus,pneumococcus, N. gonorrhoeae & C. diphtheriae


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Corneal Ulcer

Causative organisms:

Presence of N Gonorrhoeae, C Diphtheriae,Hemophilus Aegyptius and ListeriaMonocytogenes they can penetrateintact corneal epithelium.

Otherwise most of the bacteria includingPneumococcus is capable of producingcorneal ulcer when epithelium is damaged


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PathogenesisSteps

1. Corneal abrasion2. Infection by microorganism in presence of

predisposing factor(s).3. The predisposing factors are trauma, long term

use of steroids, misdirected eye lashes, mal-apposition of lids, entropion, lagophthalmos,contact lens wear, bullous keratopathy, poorhygienic condition.

4. malnutrition, ocular surface disorders, vitamin Adeficiency, causing corneal necrosis(Keratomalacia), corneal edema and trigeminalnerve paralysis (Neurotropic keratitis)


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Pathogenesis

5. Localized necrosis of superficial layers ofcornea

6. Formation of sequestrum withdisintegration. It cast off in conjunctivalsac

7. Desquamation of corneal epithelium anddamage to Bowmans membrane (area ofepithelial and Bowmans denudation islarger than ulcer)


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Pathogenesis

8. Epithelial regeneration, at times itcovers the edges and floor area

9. A saucer shaped defect with projecting

walls above the normal surface due toswelling of tissue resulting from fluidimbibition by corneal stroma

10. Surrounding area is packed byleucocytes, seen as gray zone ofinfiltration. This is progressive stage.


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Pathogenesis

11. Necrotic material fall off- ulcerbecomes larger -> infiltration and swellingreduce and disappears -> margin becomes

smooth, floor also looks smooth andtransparent. This is regressive stage.

12. Vascularization develops from limus to

corneal ulcer to restore lost tissue and tosupply antibodies.


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Pathogenesis

13. Vascularisation is followed bycicatrization due to regeneration ofcollagen and formation of fibrous tissue

14. Newly formed fibres are laid downirregularly, not conforming to normalpattern of stromal fibres. Therefore thisfibrous tissue reflects light irregularly. Thescar tissue is more or less opaque. Somevessels may persist in large scar


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Pathogenesis

13. Bowmans membrane never regenerates andwhenever it is destroyed some degree of cornealopacity remains

14 Corneal opacity may clear with time especially ifit is not dense. The vascularization plays part inclearing corneal opacity

15. The scar tissue usually fill the gap exactly, but

some deficiency may remain giving rise toformation of corneal facet. The corneal facetmay be transparent and may be associated withmarked diminution of vision


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Pathogenesis

16. Diffusion of bacterial toxins into theanterior chamber leads to hyperaemia andinflammation of the iris and ciliary body

(Keratouveitis). Polymorphonuclear cellscoming out from the uveal tissue maygravitate to bottom of anterior chamber to

form hypopyon.


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Symptoms of Corneal Ulcer

Symptoms are usually marked, they are:

1. Diminution of vision, depending on location ofcorneal ulcer

2. Watering (lacrimation)3. Difficulty in opening eyes especially in brightlight (photophobia and blepharospasm)

4. Pain and foreign body/ gritty sensation5. There may be discharge (Mucopurulent /purulent)


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Signs

1. Visual acuity may be affected, dependingon location of corneal ulcer

2. Edema of lids of affected eye, in severecases

3. Blepharospasm

4. Ciliary and conjunctival congestion

5. Hazyness / pus may be present inanterior chamber


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Signs

6. Colour and pattern of iris may be disturbed

7. Cornea: loss of transparency the ulcer appearsyellowish/ grayish pale lesion of varying shape

/size, breach in continuity of corneal surface,ulcer with irregular floor and margins, floorappears grayish / grayish pale/ grayish yellow,zone of infiltration with projecting swollen

edges.The surrounding cornea may appear groundglass like due to corneal edema


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Corneal Ulcer

Peripheral Corneal UlcerCentral Corneal ulcer involving

Lower periphery also


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Hypopyon corneal ulcer

Causative organisms:

Psuedomonas, pneumococcus, stapyhlococcus,

streptococcus, gonococci, moraxella.

Source of infection:

Chronic dacryocystitis

Predisposing factors:

Virulence of organism and resistance of host tissue

Mechanism of development of hypopion

corneal ulcer with iritis diffusion of bacterial toxin

gravitate to the bottom of AC to form hypopion


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Clinical features Symptoms:

Same as bacterial corneal ulcer

Signs:

Ulcus serpens,

tendency to creep over the

cornea,iridocyclitis,

secondary glucoma,

perforation


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Clinical Examination

Evaluation of predisposing and aggravatingFactors

1. A detailed history

2. Prior ocular history

3. Review of related medical problems,current ocular medications and history ofmedication allergy


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Examination

1. Visual acuity

2. An external ocular examination

Facial appearance, eyelids, lid closureConjunctiva, Nasolacrimal apparatus,corneal sensation


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Examination

3. Slit Lamp Biomicroscopy: For

Eyelid margin

Tear film

Conjunctiva

Sclera

Cornea (epithelial defects, punctate

keratopathy, edema, stromalinfiltrates/ulceration, thinning orperforation)


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Slit Lamp Examination Contd

Location of lesion

Density, Size , shape , depth, colour

EndotheliumAnterior chamber

Loose or Broken sutures

Signs of corneal dystrophySigns of previous inflammation


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Slit Lamp Examination Contd

Anterior Vitreous

Fluorescein

Rose Bengal staining


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Differential Diagnosis

Differentiate from Non-infectious causes ofinfiltrates

1. Fungal

2. Protozoal3. Nematodes

4. Viral infections, HSV, VZV, EBV

5. Contact lens infiltrates6. Collagen Vascular Diseases


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Differential Diagnosis

7. Sarcoidosis

8. Severe Rosacea

9. Allergic Conditions10. Corneal Trauma , FB and Loose sutures

Complications of Corneal Ulcer


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Complications of Corneal Ulcer1. Spread of ulcer horizontally and depth-wise,

leading to thinning of cornea

2. Bulging ofdescemets membrane (Keratoceleor Descemetocele). This appears astransparent vesicle surrounded by grayish

zone of infiltration. Bulging ofdescemetsmembrane represents condition of impendingperforation of cornea


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3. Perforation of ulcer is generally caused bysudden exertion such as coughing,sneezing, straining at stool or firm closure

of eyes.

Exertion causes rise of blood pressure andresults in increase in intra-ocular pressure

(IOP). Weak area of ulcer is unable tosupport the increased IOP , gives way andperforation develops


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PERFORATION OF CORNEAL ULCER

Complications of perforation may be seriousand sight threatening

A. Peripheral perforation: Iris is thrownforward -> opening is occluded ->anterior chamber is formed , scarring

takes place:a. Iris may be pushed back to normalposition or


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b. Iris may remains adherent to cornealscar (anterior synechia)

If peripheral perforation is large thepupillary border of iris prolapse throughopening. Exudation takes place onprolapsed tissue -> an adherent leucoma

forms (it may be flat or bulging)


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B. Central perforation: small centralperforation -> anterior chamber collapse

-> lens comes in contact with corneal

endothelial surface -> anterior capsular

cataract -> repeated healing and

perforation leading to corneal fistula

formation



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Complications of Corneal UlcerC. Sloughing of whole cornea: prolapse of iris ->pupillary block and exudation on iris -> pseudocornea

formation (iris covered with exudates , formation offibrous tissue and formation of scar tissue) -> anterior

chamber anatomy is lost , angle of anterior chamber is

occluded leading to secondary glaucoma -> anterior

staphyloma (an ectatic cicatric with incarceration ofiris).Anterior staphyloma may be partial or total.


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In case of sudden large perforation lens maysubluxate or thrown out due to rupture ofsuspensory ligaments.

Lens and vitreous may prolapse throughperforation. Intraocular haemorrhage may occurdue to dilatation and rupture of intra-ocularblood vessels due to sudden hypotony.

This may lead to vitreous haemorrhage , choroidal, sub-retinal or sub-choroidal haemorrhage. Inelderly patients there may be expulsive

haemorrhage


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D. Intra-ocular purulent infection: due toperforation bacteria enter in the eye andcauses purulent iridocyclitis,

endophthalmitis and panophthalmitis


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Treatment of uncomplicated corneal ulcer

LOCAL TREATMENT

1. Control of infection with appropriateantibiotic(s)

a. based on clinical judgment

b. based on finding of smear examination

c. based on culture and sensitivity report


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Local Antibiotic therapy

Antibiotic drops frequently, ointment may beused at bedtime in less severe cases.Collagen shield or soft contact lenses

soaked in antibiotics are sometimes usedand may enhance drug delivery.

Sub-conjunctival antibiotics may be helpfulwhere there is imminent scleral spread orperforation or in cases where compliancewith the treatment regimen isquestionable


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Therapeutic Agents

1. No organism identified or multiple typesof 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 0.5ml.

Fluroquinolones: 3 mgm/ ml


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Therapeutic Agents

2. Gram Positive Cocci

Cefazolin: Topical 50 mgm/ml; S/c 100mgm in 0.5 ml.

Vancomycin: Topical15 - 50 mgm/ml;S/c 25 mgm in 0.5 ml.


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Gram Negative Rods

Tobramycin / Gentamicin:

Topical 9-14 mgm/ml; S/c 20 mgm in 0.5ml.

Ceftazidime : Topical 50 mgm/ml; S/c100mgm in 0.5 ml.



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Gram Negative Cocci

Ceftriaxone : Topical 50 mgm/ml; S/c 100mgm in 0.5 ml.

Ceftazidime : Topical 50 mgm/ml; S/c 100

mgm in 0.5 ml.



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2. Cycloplegic and mydriatic drug:

atropine 1% or cyclopentolate 1% orHomatropine 2%. These drugs preventsciliary spasm, relieves pain, preventdangerous results of iridocyclitis, breaks

adhesions and prevent synechia formation


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3. Cleanliness: Irrigation with luke warmnormal saline or 2% luke warm boric acidsolution to remove conjunctival discharge

and necrotic material4. Application of heat: provides comfortand causes vasodilatation

5. Protection of eye from externalenvironment with dark glasses


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Steroids must not be used in presence ofactive infected corneal ulcer

In cases of progressive corneal ulcer

despite routine therapeutic treatment, thefollowing measures be considered:

Scraping of ulcer floor followed by

cauterization with pure (100%) carbolic acidor 10-20% trichloracetic acid. Povidone Iodinecan also be used for cauterization


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Systemic Treatment

1. Systemic Antibiotics: consider in severcases with scleral or intra-ocularextension of infection or with impending

or frank perforation of the corneaSystemic antibiotic therapy is necessaryin cases of Gonococcal keratitis due to its

fulminating nature and systemicinvolvement


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Systemic Treatment

2. Analgesic anti-inflammatory

3. Supportive treatment

4. Acetazolamide Tab is added in cases ofimpending perforation or perforatedcorneal ulcer and in cases where there israised intra-ocular tension (in dosage of

250 mgm upto four times a day)


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Non-responsive / Progressive Corneal Ulcer

TREATMENTRe-evaluate for

Drug toxicity

Non-infectious causes orUnusual organisms such as non-tubercularmycobacteria, Nocardia or acanthamoebashould be suspected

Modification of anti-microbial therapyTherapeutic keratoplasty may be undertaken


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Indolent / Non-healing Ulcer

Consider debridement of necrotic cornealstroma and

Frequent lubrication and/or

Temporary tarsorrhaphy


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Treatment of Keratocele or Descemetocele

Continue use of local antibiotics, atropine,add topical antiglaucoma medication (likeTimolol or Betaxolol) or add systemic

acetazolamide, bandage contact lens isbeneficial. All forced expiration likecoughing, sneezing, blowing of nose etc

must be avoided


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Treatment of perforated corneal ulcer

Rest Continue treatment of corneal ulcer with

modification, i.e. firm bandage or bandagecontact 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


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Adjunctive Therapy

1. Cyanoacrylate tissue glue

2. Therapeutic Contact Lenses


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Surgical Treatment

1. Conjunctival flap;

2. Penetrating Keratoplasty (PKP):

Large central ulcer , presenting late

History of previous ocular surgery

Injudicious use steroid treatment


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