BACTERIAL KERATITIS

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BACTERIAL KERATITIS

• Dr. Sanjay Shrivastava
• Professor of Ophthalmology
• Regional Institute of Ophthalmology
• Gandhi Medical College
• Bhopal (M.P.)
• drs.rio_at_hotmail.com

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Copy of Power point presentation of Lecture
taken for Junior Final Year students of Gandhi
Medical CollegeBhopal
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Cornea
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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

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Anatomical facts

• Measurements of adult cornea
• Horizontal 11 -12 mm
• Vertical 9-11 mm
• Thickness central 0.5 mm
• peripheral 0.7 1 mm

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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)

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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

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Maintenance 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

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Introduction

• 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.

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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.

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Host Defense and Risk Factors
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Defense 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

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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

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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.

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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

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Risk Factors

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

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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.

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Predisposing Systemic Conditions

• Malnutrition
• Diabetes
• Collagen vascular diseases
• Chronic alcoholism

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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)

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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)

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Classification

• I. According to location
• a. Superficial
• b. Deep
• II. According to Etiology
• a. Infective
• b. Immune mediated
• c. Traumatic
• d. Neoplastic
• e. Degenerative

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Bacterial Keratitis

• Two forms
• Central Keratitis
• Peripheral Keratitis.

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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

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Corneal 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

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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)

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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)

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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.

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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.

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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

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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

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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.

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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)

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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.

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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

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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

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Corneal Ulcer
Central Corneal ulcer involving Lower periphery
also
Peripheral Corneal Ulcer
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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

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Examination

• Visual acuity
• An external ocular examination
• Facial appearance, eyelids, lid closure
• Conjunctiva, 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, stromal infiltrates/ulcerati
  on, thinning or perforation)

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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

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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 of
  infiltrates
• Fungal
• Protozoal
• Nematodes
• Viral infections, HSV, VZV, EBV
• Contact lens infiltrates
• Collagen Vascular Diseases

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Differential Diagnosis

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

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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

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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

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Complications 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

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

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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

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Complications 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.

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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

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Complications of Corneal Ulcer

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

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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

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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

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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

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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.

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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

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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

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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

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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

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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

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Systemic 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

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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)

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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

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Indolent / Non-healing Ulcer

• Consider debridement of necrotic corneal stroma
  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 (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

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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

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Adjunctive Therapy

• Cyanoacrylate tissue glue
• Therapeutic Contact Lenses

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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