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

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  .(B) Non-ulcerative keratitis 1. Superficial keratitis (a) Diffuse superficial keratitis (b) Superficial punctate keratitis (SPK) 2.

Trophic keratitis (a) Exposure keratitis (b) Neuroparalytic keratitis (c) Keratomalacia (d) Atheromatous ulcer .Etiological classification 1.Allergic keratitis (a) phlyctenular keratitis (b) Vernal keratitis (c) Atopic keratitis 3. Infective keratitis (a) Bacterial (b) Viral (c) Fungal (d) Chlamydial (e) Protozoal (f) Spirochaetal 2.

radiations 7. 5. Idiopathic keratitis e. Keratitis associated with systemic collagen vascular disorders. 6.4. chemical trauma.. (a) Mooren's corneal ulcer (b) Superior limbic keratoconjunctivitis (c) Superficial punctate keratitis of Thygeson . Keratitis associated with diseases of skin and mucous membrane. thermal burns. Traumatic keratitis. which may be due to mechanical trauma.g.

Identification of risk factors and assessment of the distinctive corneal findings will help in determination of potential etiologies.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. .

Host Defense and Risk Factors .

orosomucoid and ceruloplasmin have antibacterial effect) Corneal epithelium Normal ocular flora Conjunctival mucosal associated lymphoid tissue (MALT) which is present in subepithelium . lactoferrin. Eyelids 2. Tear film proteins (Secretory immunoglobulins. 4.Defense of Ocular Surface Normal Defense mechanisms: 1. 5. betalysins. complement components. 3. and various enzymes including lysozyme.

Risk Factors 1. 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 . 2. 3.

corneal trauma. C Diphtheriae.Risk Factors 5. . 7. 6. Presence of N Gonorrhoeae. Compromised corneal epithelium as in cases of contact lenses users. Absence of normal conjunctival flora. Hemophilus Aegyptius and Listeria Monocytogenes – they can penetrate intact corneal epithelium. corneal surgery bullous keratopathy.

it protects bacteria from antibacterial substances and provide a nidus for a slimy layer composed of organic polymers produced by embedded bacteria on contact lens. 9. Abuse of topical anaesthetic solution .Risk Factors 8 Biofilm. Corneal anaesthesia 10.

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

. 2. 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. 3. 4.External Risk Factors 1.

3.Predisposing Systemic Conditions 1. Malnutrition Diabetes Collagen vascular diseases Chronic alcoholism . 4. 2.

Etiological Factors Inflammation of Cornea (Keratitis) may develop as a result of: 1. Exogenous infection – Mostly traumatic. Endogenous Infection (inflammation): this is immunological in nature eg. These conditions are commonly noticed at corneal margin (Marginal Keratitis or Marginal Corneal Ulcer) . the object causing injury may carry infection to cornea or may come from conjunctival sac (infecting abraded cornea) 2. Phlyctenular keratitis caused by tubercular or staphylococcal hypersensitivity and interstitial keratitis related to measles or syphilis.

Sclerosing Keratitis) and From Uveal tract to corneal endothelium (eg. Trachoma and Vernal Keratoconjunctivitis) From Sclera to corneal stroma (eg. Herpetic Uveitis causing endothelitis) . Spread of Infection from neighboring structures due to anatomical continuity.Etiological Factors 3. From conjunctiva to corneal epithelium (eg.

gonorrhoeae & C. Such purulent keratitis is usually exogenous due to infection by pyogenic bacteria such as pseudomonas. staphylococcus aureus and albus.Corneal Ulcer  Superficial Purulent Keratitis (Bacterial Corneal Ulcer) Caused by organisms which produce toxins causing tissue death i. diphtheriae . necrosis characterised by pus formation.e. pneumococcus. N.

Corneal Ulcer  Causative organisms: Presence of N Gonorrhoeae. C Diphtheriae. Otherwise most of the bacteria including Pneumococcus is capable of producing corneal ulcer when epithelium is damaged . Hemophilus Aegyptius and Listeria Monocytogenes – they can penetrate intact corneal epithelium.

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

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

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

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

Newly formed fibres are laid down irregularly. Some vessels may persist in large scar . Therefore this fibrous tissue reflects light irregularly. Vascularisation is followed by cicatrization due to regeneration of collagen and formation of fibrous tissue 14.Pathogenesis 13. The scar tissue is more or less opaque. not conforming to normal pattern of stromal fibres.

Bowman’s 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 corneal facet may be transparent and may be associated with marked diminution of vision .Pathogenesis 13. The scar tissue usually fill the gap exactly. but some deficiency may remain giving rise to formation of corneal facet. The vascularization plays part in clearing corneal opacity 15.

Diffusion of bacterial toxins into the anterior chamber leads to hyperaemia and inflammation of the iris and ciliary body (Keratouveitis).Pathogenesis 16. . Polymorphonuclear cells coming out from the uveal tissue may gravitate to bottom of anterior chamber to form hypopyon.

Difficulty in opening eyes especially in bright light (photophobia and blepharospasm) 4. depending on location of corneal ulcer 2. they are: 1.Symptoms of Corneal Ulcer  Symptoms are usually marked. Pain and foreign body/ gritty sensation 5. Diminution of vision. There may be discharge (Mucopurulent / purulent) . Watering (lacrimation) 3.

3. depending on location of corneal ulcer Edema of lids of affected eye.Signs 1. 5. Visual acuity may be affected. in severe cases Blepharospasm Ciliary and conjunctival congestion Hazyness / pus may be present in anterior chamber . 2. 4.

The surrounding cornea may appear ground glass like due to corneal edema . Colour and pattern of iris may be disturbed 7. floor appears grayish / grayish pale/ grayish yellow. Cornea: loss of transparency the ulcer appears yellowish/ grayish pale lesion of varying shape /size. breach in continuity of corneal surface.Signs 6. zone of infiltration with projecting swollen edges. ulcer with irregular floor and margins.

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

moraxella.Hypopyon corneal ulcer Causative organisms: Psuedomonas. stapyhlococcus. streptococcus.  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  . gonococci. pneumococcus.

Clinical features Symptoms:  Same as bacterial corneal ulcer   Signs: Ulcus serpens. secondary glucoma. perforation . tendency to creep over the cornea. iridocyclitis.

A detailed history 2. current ocular medications and history of medication allergy . Prior ocular history 3. Review of related medical problems.Clinical Examination Evaluation of predisposing and aggravating Factors 1.

2. corneal sensation . lid closure Conjunctiva. Visual acuity An external ocular examination Facial appearance. eyelids. Nasolacrimal apparatus.Examination 1.

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

shape . colour Endothelium Anterior chamber Loose or Broken sutures Signs of corneal dystrophy Signs of previous inflammation . depth. Size .Slit Lamp Examination… Contd Location of lesion Density.

Slit Lamp Examination… Contd Anterior Vitreous Fluorescein Rose Bengal staining .

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

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

1. Bulging of descemet’s membrane represents condition of impending perforation of cornea Complications of Corneal Ulcer . leading to thinning of cornea Bulging of descemet’s membrane (Keratocele or Descemetocele). Spread of ulcer horizontally and depth-wise. This appears as transparent vesicle surrounded by grayish zone of infiltration. 2.

gives way and perforation develops . Perforation of ulcer is generally caused by sudden exertion such as coughing. sneezing. Weak area of ulcer is unable to support the increased IOP . Exertion causes rise of blood pressure and results in increase in intra-ocular pressure (IOP).Complications of Corneal Ulcer 3. straining at stool or firm closure of eyes.

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

Complications of Corneal Ulcer b. Exudation takes place on prolapsed tissue -> an adherent leucoma forms (it may be flat or bulging) . Iris may remains adherent to corneal scar (anterior synechia) If peripheral perforation is large the pupillary border of iris prolapse through opening.

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 . angle of anterior chamber is occluded leading to secondary glaucoma -> anterior staphyloma (an ectatic cicatric with incarceration of iris). formation of fibrous tissue and formation of scar tissue) -> anterior chamber anatomy is lost . Anterior staphyloma may be partial or total.

This may lead to vitreous haemorrhage . Intraocular haemorrhage may occur due to dilatation and rupture of intra-ocular blood vessels due to sudden hypotony. Lens and vitreous may prolapse through perforation. sub-retinal or sub-choroidal haemorrhage.Complications of Corneal Ulcer In case of sudden large perforation lens may subluxate or thrown out due to rupture of suspensory ligaments. In elderly patients there may be expulsive haemorrhage . choroidal .

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

based on clinical judgment b. Control of infection with appropriate antibiotic(s) a.Treatment of uncomplicated corneal ulcer LOCAL TREATMENT 1. based on culture and sensitivity report . based on finding of smear examination c.

Collagen shield or soft contact lenses soaked in antibiotics are sometimes used and may enhance drug delivery.Local Antibiotic therapy Antibiotic drops frequently. 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 . ointment may be used at bedtime in less severe cases.

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

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

5 ml. S/c 100 mgm in 0. S/c 100 mgm in 0. Fluroquinolones: 3 mgm/ ml . Ceftazidime : Topical – 50 mgm/ml.5 ml.Gram Negative Cocci Ceftriaxone : Topical – 50 mgm/ml.

Treatment of uncomplicated corneal ulcer 2. prevent dangerous results of iridocyclitis. breaks adhesions and prevent synechia formation . relieves pain. Cycloplegic and mydriatic drug: atropine 1% or cyclopentolate 1% or Homatropine 2%. These drugs prevents ciliary spasm.

Protection of eye from external environment with dark glasses .Treatment of uncomplicated corneal ulcer 3. Application of heat: provides comfort and causes vasodilatation 5. Cleanliness: Irrigation with luke warm normal saline or 2% luke warm boric acid solution to remove conjunctival discharge and necrotic material 4.

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 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 1.

Supportive treatment 4. Analgesic anti-inflammatory 3.Systemic Treatment 2. 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  .

blowing of nose etc must be avoided . atropine. All forced expiration like coughing. add topical antiglaucoma medication (like Timolol or Betaxolol) or add systemic acetazolamide. bandage contact lens is beneficial. sneezing.Treatment of Keratocele or Descemetocele  Continue use of local antibiotics.

blowing of nose etc must be avoided Use of tissue adhesive (Glue): N-butyl 2-ethyl cyanoacrylate Therapeutic penetrating keratoplasty or conjunctival flap . firm bandage or bandage contact lens All forced expiration like coughing.Treatment of perforated corneal ulcer      Rest Continue treatment of corneal ulcer with modification. i. sneezing.e.

2. Cyanoacrylate tissue glue Therapeutic Contact Lenses .Adjunctive Therapy 1.

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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