BACTERIAL KERATITIS

CH.HARIKRISHNA TITANS BATCH 2007 MAMATA MEDICAL COLLEGE, KHAMMAM, ANDHRAPRADESH

CLASSIFICATION
It 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 (most bacterial and fungal corneal ulcers are suppurative). (b) Non-purulent corneal ulcers (most of viral, chlamydial and allergic corneal ulcers are non-suppurative).

3. Depending upon association of hypopyon (a) Simple corneal ulcer (without hypopyon) (b) Hypopyon corneal ulcer 4. 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

(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

Etiological classification 1. Infective keratitis (a) Bacterial (b) Viral (c) Fungal (d) Chlamydial (e) Protozoal (f) Spirochaetal

2.Allergic keratitis (a) phlyctenular keratitis

(b) Vernal keratitis (c) Atopic keratitis

3. Trophic keratitis (a) Exposure keratitis (b) Neuroparalytic keratitis (c) Keratomalacia (d) Atheromatous ulcer

4. Keratitis associated with diseases of skin and mucous membrane. 5. Keratitis associated with systemic collagen vascular disorders. 6. Traumatic keratitis, which may be due to mechanical 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

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.

Host Defense and Risk Factors

Defense of Ocular Surface

Normal Defense mechanisms: 1. Eyelids
2.

3. 4. 5.

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

Risk Factors
1.

2.

3.

4.

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

Risk 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.

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

Risk Factors
11. Local immune suppression as due to topical corticosteroids 12. Previous viral infection 13. Drugs used in viral keratitis 14. Corneal hypesthesia

External Risk Factors

1.

2.
3. 4.

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.

Predisposing Systemic Conditions

1.

2.
3. 4.

Malnutrition Diabetes Collagen vascular diseases Chronic alcoholism

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)

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)

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 & C. diphtheriae

Corneal Ulcer
Causative

organisms: 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

Pathogenesis
Steps 1. Corneal abrasion 2. Infection by microorganism in presence of predisposing factor(s). 3. The predisposing factors are trauma, long term use of steroids, misdirected eye lashes, malapposition of lids, entropion, lagophthalmos, contact lens wear, bullous keratopathy, poor hygienic condition. 4. malnutrition, ocular surface disorders, vitamin A deficiency, causing corneal necrosis (Keratomalacia), corneal edema and trigeminal nerve paralysis (Neurotropic keratitis)

Pathogenesis
5. Localized necrosis of superficial layers of cornea 6. Formation of sequestrum with disintegration. It cast off in conjunctival sac 7. Desquamation of corneal epithelium and damage to Bowmans membrane (area of epithelial and Bowmans denudation is larger than ulcer)

Pathogenesis
8. Epithelial regeneration, at times it covers the edges and floor area 9. A saucer shaped defect with projecting walls above the normal surface due to swelling of tissue resulting from fluid imbibition by corneal stroma 10. Surrounding area is packed by leucocytes, seen as gray zone of infiltration. This is progressive stage.

Pathogenesis
11. Necrotic material fall off- ulcer becomes larger -> infiltration and swelling reduce and disappears -> margin becomes smooth, floor also looks smooth and transparent. This is regressive stage. 12. Vascularization develops from limus to corneal ulcer to restore lost tissue and to supply antibodies.

Pathogenesis
13. Vascularisation is followed by cicatrization due to regeneration of collagen and formation of fibrous tissue 14. 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

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

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.

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)

Signs
1. 2. 3. 4.

5.

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

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

Corneal Ulcer

Peripheral Corneal Ulcer

Central Corneal ulcer involving Lower periphery also

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

Clinical features
Symptoms: Same as bacterial corneal ulcer

Signs: Ulcus serpens, tendency to creep over the cornea, iridocyclitis, secondary glucoma, perforation

Clinical Examination
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 medication allergy

Examination
1.

2.

Visual acuity An external ocular examination Facial appearance, eyelids, lid closure Conjunctiva, Nasolacrimal apparatus, corneal sensation

Examination
3. Slit Lamp Biomicroscopy: For Eyelid margin Tear film Conjunctiva Sclera Cornea (epithelial defects, punctate keratopathy, edema, stromal infiltrates/ulceration, thinning or perforation)

Slit 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

Slit Lamp Examination Contd

Anterior Vitreous Fluorescein Rose Bengal staining

Differential Diagnosis
Differentiate from Non-infectious causes of infiltrates 1. Fungal 2. Protozoal 3. Nematodes 4. Viral infections, HSV, VZV, EBV 5. Contact lens infiltrates 6. Collagen Vascular Diseases

Differential Diagnosis
7. Sarcoidosis 8. Severe Rosacea 9. Allergic Conditions 10. Corneal Trauma , FB and Loose sutures

1. 2.

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

Complications of Corneal Ulcer

Complications 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

Complications of Corneal Ulcer

PERFORATION OF CORNEAL ULCER Complications of perforation may be serious and sight threatening A. Peripheral perforation: Iris is thrown forward -> opening is occluded -> anterior chamber is formed , scarring takes place: a. Iris may be pushed back to normal position or

Complications 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 -> an adherent leucoma forms (it may be flat or bulging)

Complications of Corneal Ulcer

B. Central perforation: small 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

Complications of Corneal Ulcer

C. Sloughing of whole cornea: prolapse of iris -> pupillary block and exudation on iris -> pseudocornea formation (iris covered with exudates , formation of fibrous 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 of iris). Anterior staphyloma may be partial or total.

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

Complications of Corneal Ulcer

D. Intra-ocular purulent infection: due to perforation bacteria enter in the eye and causes purulent iridocyclitis, endophthalmitis and panophthalmitis

Treatment 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

Local 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

Therapeutic 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
1.

Therapeutic 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.

Gram 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

Gram 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

Treatment 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

Treatment 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

Treatment 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

Systemic Treatment
1.

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

Systemic 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)

Non-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

Indolent / Non-healing Ulcer

Consider debridement of necrotic corneal stroma and Frequent lubrication and/or Temporary tarsorrhaphy

Treatment 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

Treatment 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

Adjunctive Therapy
1.

2.

Cyanoacrylate tissue glue Therapeutic Contact Lenses

Surgical Treatment
1.

2.

Conjunctival flap; Penetrating Keratoplasty (PKP): Large central ulcer , presenting late History of previous ocular surgery Injudicious use steroid treatment

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