CORNEAL ULCERS-SOLANKI RIDDHI

2ND YEAR (B.OPTOM)

CLASSIFICATION INFECTIVE KERATITIS:I. BACTERIAL CORNEAL ULCERSi. Hypopyon corneal ulcerii. Marginal catarrhal ulceriii. Mycotic corneal ulcerII. VIRAL CORNEAL ULCERSiv. Herpes simplex keratitisv. Herpes zoster ophthalmicusIII. PROTOZOAL KERATITISvi. Acanthamoeba keratitis

ALLERGIC KERATITIS:I. PHLYCTENULAR KERATITISII. VERNAL KERATITISIII. ATOPIC KERATITIS

TROPHIC:I. NEUROPARALYTIC KERATITISII. EXPOSURE KERATITIS

KERATITIS ASSOCIATED WITH DISEASES OF SKIN & MUCOUS MEMBRANE:

I. ROSACEA KERATITIS

KERATITIS ASSOCIATED WITH SYSTEMIC COLLAGEN VASCULAR DISEASES

IDIOPATHIC KERATITIS:I. MOOREN’S ULCER

INFECTIVE KERATITIS:I. BACTERIAL CORNEAL ULCER: Being the most ant. part of eyeball, the

cornea is exposed to atmosphere & hence prone to get infected easily.

At the same time cornea is protected from the defence mechanisms present in tears in the form of lysozyme, betalysin, & other protective proteins.

Infective corneal ulcer may develop when:

Either the local ocular defence mechanism is jeopardised, or

The causative organism is very virulent.

ETIOLOGY: Following 3 pathogens can invade the

intact corneal epithelium & produce ulceration:

i. Neisseria gonorrhoeaeii. Corynebacterium diphtheriae iii. Neisseria meningitidis. 1. Corneal epithelial damage: It may occur in

following conditions:i. Corneal abrasionii. Epithelial dryingiii. Necrosis of epitheliumiv. Desquamation of epithelial cellsv. Epithelial damage due to trophic changes

2. Source of infection include: i. Exogenous infectionii. From the ocular tissueiii. Endogenous infection

3. Causative organism: common bacterias associated with corneal ulceration are:

i. Staphylococcus aureusii. Pseudomonas pyocyaneaiii. Streptococcus pneumoniaeiv. E. coliv. N. gonorrhoeavi. N. meningitidis vii. C. diphtheriae.

BACTERIAL CORNEAL ULCER

[A] PATHOLOGY OF LOCALISED CORNEAL ULCER

1. Stage of progressive infiltration:

It is characterised by the infiltration of polymorphonuclear &/or lymphocytes into the epithelium from the peripheral circulation supplemented by similar cells from the underlying stroma if this tissue is also affected.

Subsequently necrosis of the involved tissue may occur.

2. Stage of active ulceration: Active ulceration results from necrosis &

sloughing of the epithelium, bowman’s membrane & the involved stroma.

During this stage, accumulation of purulent exudates on the cornea.

There occurs vascular congestion of the iris & ciliary body & some degree of iritis due to absorption of toxins from the ulcer.

3. Stage of regression:

Regression is induced by the natural host defence mechanisms.

A line of demarcation develops around the ulcer.

The digestion of necrotic material may result in initial enlargement of the ulcer.

This process may be accompanied by superficial vascularization that increases the humoral & cellular immune response.

The ulcer now begins to heal & epithelium starts growing over the edges.

4. Stage of cicatrization: In this stage, healing continues by

progressive epithelization which forms a permanent covering.

Beneath the epithelium, fibrous tissue is laid down partly by the corneal fibroblasts & partly by the endothelial cells of the new vessels.

The degree of scarring from healing varies. If the ulcer is very superficial & involves the

epithelium only, it heals without leaving any opacity behind.

When ulcer involves bowman’s layer& few superficial stromal lamellae, the resultant scar is called a ‘nebula’.

PATHOLOGY OF CORNEAL ULCER

[B] PATHOLOGY OF PERFORATED CORNEAL ULCER Perforation of corneal ulcer occurs when the

ulcerative process deepens & reaches up to descemet’s membrane.

This membrane is tough & bulges out as Descemetocele.

At this stage, any exertion on the part of patient, such as coughing, sneezing, straining for stool etc. will perforate the corneal ulcer.

Immediately after perforation, the aqueous escapes, IOP falls & the iris-lens diaphragm moves forward.

When the perforation is small & opp. to iris tissue, it is usually plugged & healing by cicatrization proceeds rapidly.

PERFORATED CORNEAL ULCER

I. BACTERIAL CORNEAL ULCER

i. HYPOPYON CORNEAL ULCER Causative Organisms: i. Staphylococciii. Streptococciiii. Gonococciiv. Moraxella v. Pseudomonas pyocyanea vi. Pneumococcus. Source Of Infection: For

pneumococcal infection is usually the chronic dacryocystitis.

Clinical features: Symptoms: i. Painii. Foreign body sensationiii. Watering iv. Photophobiav. Blurred visionvi. Redness of eye. Signs: i. Lids are swollenii. Blepharospasmiii. Conjunctiva is chemosed iv. Hyperaemia & ciliary congestion.

HYPOPYON

Complications Of Corneal Ulcer:

1. Toxic iridocyclitis: usually associated with cases of purulent corneal ulcer.2. Secondary glaucoma: occurs due to fibrinous exudates blocking the angle of ant. chamber (inflammatory glaucoma) 3. Descemetocele: occurs when virulent organisms extends upto descemet’s memb.4. Perforation Of Corneal Ulcer: occurs due to sudden strain due to cough, sneeze or spasm of orbicularis muscle.5. Corneal Scarring: It is the usual end result of healed corneal ulcer.

DESCEMETOCELE

TREATMENT: i. Topical antibiotics: Ciprofloxacin or

Ofloxacin or Gatifloxacin (0.3%) eye drops,

ii. Cycloplegic drugsiii. Systemic analgesics iv. Anti-inflammatory drugs such as

paracetamol & ibuprofenv. Vitamins ( A, B-complex & C)vi. Hot fomentation vii. Removal of any known cause of non-

healing ulcerviii. Peritomy

ii. MARGINAL CATARRHAL ULCER

These superficial ulcers situated near limbus are frequently seen especially in old people.

ETIOLOGY: Marginal catarrhal ulcer is thought to be

caused by a hypersensitivity rxn to staphylococcal toxins.

It occurs in association with chronic staphylococcal blepharoconjunctivitis.

Moraxella & Haemophilus are also known to cause such ulcers.

Clinical Features: i. Patient usually presents with mild

ocular irritation, pain, photophobia & watering.

ii. The ulcer is shallow, slightly infiltrated & often multiple, usually associated with staphylococcal conjunctivitis.

iii. Recurrences are very common.Treatment: iv. Topical corticosteroid v. Antibiotic therapy iii. Treatment of associated blepharitis &

chronic

MARGINAL CATARRHAL ULCER

iii. MYCOTIC CORNEAL ULCER The incidence of suppurative corneal ulcers

caused by fungi has increased in the recent years due to injudicious use of antibiotics & steroids.

ETIOLOGY:1. Causative fungi: i. Aspergillusii. Fusariumiii. Alternariaiv. Penicillium.v. Candida & Cryptococcus.

CLINICAL FEATURES: Symptoms: i. Painii. Foreign body sensationiii. Watering iv. Photophobiav. Blurred visionvi. Redness of eye.Signs: vii. Dry-lookingviii. Greyish whiteix. Delicate feathery finger-like extensions x. A sterile immune ring may be presentxi. Multiple, small satellite lesions may be

present

TREATMENT:i. Antifungal drugsii. Natamycin, Fluconazol, Nystatiniii. Therapeutic penetrating keratoplasty

MYCOTIC CORNEAL ULCER

II. VIRAL CORNEAL ULCERSi. HERPES SIMPLEX KERATITIS Ocular infections with herpes simplex virus

(HSV) are extremely common & constitute herpetic keratoconjunctivitis & iritis.

ETIOLOGY: Herpes simplex virus (HSV): It is a DNA virus. Its only natural host is man. According to different clinical &

immunological properties, HSV is of two types: HSV type I typically causes infection above the waist & HSV type II below the waist (herpes genitalis).

Mode Of Infection: 1. HSV-I infection: It is acquired by kissing

or coming in close contact with a patient suffering from herpes labialis.

2. HSV-II infection: It is transmitted to eyes of neonates through infected genitalia of the mother.

Ocular Lesions Of Herpes Simplex: [A] Primary herpes:3. Skin lesions4. Conjunctiva-acute follicular

conjunctivitis5. Cornea

[B] Recurrent herpes:1. Epithelial keratitis:i. Punctuate epithelial keratitisii. Dendritic ulceriii. Geographical ulcer

2. Stromal keratitisi. Disciform keratitis ii. Diffuse stromal necrotic keratitis

3. Metaherpetic keratitis

[A] Primary Ocular Herpes Primary infection (first attack) involves a

nonimmune person. It typically occurs in children betn 6

months & 5 yrs & in teenagers.Clinical Features:1. Skin lesions: Vesicular lesions may

occur involving skin of lids, periorbital region & the lid margin.

2. Acute follicular conjunctivitis with regional lymphadenitis is the usual.

3. Keratitis: Cornea is involved in about 50% of the cases. The keratitis can occur as a coarse punctuate or diffuse branching epithelial.

[B] Recurrent Ocular Herpes The virus which lies dormant in the

trigeminal ganglion, periodically reactivates & causes recurrent infection.

1. Epithelial keratitis:i. Punctuate epithelial keratitis: The initial epithelial lesions of recurrent

herpes resemble those seen in primary herpes & may be either in the form of fine or coarse superficial punctuate lesions.

ii. Dendritic ulcer: Dendritic ulcer is a typical lesion of recurrent

epithelial keratitis. The ulcer is of an irregular, zigzag linear

branching shape.

iii. Geographical ulcer: Sometimes, the branches of dendritic

ulcer enlarge & coalesce to form a large epithelial ulcer with a ‘geographical’ or ‘amoeboid’ configuration, hence the name.

Symptoms i. Photophobiaii. Lacrimation iii. Pain.

Treatment same as of epithelial keratitis.

2. Stromal Keratitis: i. Disciform keratitis: Endothelium damage results in corneal

oedema due to imbibation of aqueous humour.

Signs: i. Focal disc-shaped patch of stromal oedema

w/o necrosisii. Folds in descemet’s membiii. Keratic precipitatesiv. Ring of stromal infiltratev. Corneal sensations are diminishedvi. IOP may be raised.Treatment: consists of diluted steroid eye drops (acyclovir 3%).

ii. Diffuse Stromal Necrotic Keratitis: It is a type of interstitial keratitis caused by

active viral invasion & tissue destruction.Symptoms: i. Painii. Photophobia iii. RednessSigns: iv. Necroticv. Blotchyvi. Cheesy white infiltratesTreatment: Keratoplasty.

3. Metaherpetic Keratitis: It is not an active viral disease, but is a

mechanical healing problem which occurs at the site of a previous herpetic ulcer.

Clinically it represents as an indolent linear or ovoid epithelial defect.

Treatment i. Lubricants (artificial tears)ii. Bandage soft contact lensiii. Lid closure (tarsorrhaphy).

LESIONS OF RECURRENT HERPES SIMPLEX KERATITIS

ii. HERPES ZOSTER OPHTHALMICUS

Herpes zoster ophthalmicus is an acute infection of Gasserian ganglion of the Vth cranial nerve by the varicella-zoster virus (VZV).

It constitutes approx 10% of all cases of herpes zoster.

ETIOLOGYVaricella-zoster virus: It is a DNA virus & produces acidophilic

intranuclear inclusion bodies. It is neurotropic in nature.

Clinical Featuresi. Frontal nerve is more frequently

affected than the lacrimal & nasociliary nerves.

ii. About 50% cases of herpes zoster ophthalmicus get ocular complications.

iii. The Hutchinson’s rule, which implies that ocular involvement is frequent if the side or tip of nose presents vesicles, is useful but not infallible.

iv. Lesions of herpes zoster are strictly limited to one side of the midline of head.

Clinical Phases of H. zoster ophthalmicus are:i. Acute, which may totally resolve.ii. Chronic, which may persist for years.iii. Relapsing, where the acute or chronic

lesions reappear sometimes years later.Treatment:iv. Oral antiviral drugsv. Cimetidinevi. Amitriptylinevii. Antibiotic-corticosteroid skin ointment

or lotionsviii. Keratoplasty

HERPES ZOSTER OPHTHALMICUS KERATITIS

III. PROTOZOAL KERATITISi. ACANTHAMOEBA KERATITIS Acanthamoeba keratitis has recently

gained importance because of its increasing incidence, difficulty in diagnosis & unsatisfactory treatment.

ETIOLOGY Acanthamoeba is a free lying amoeba

found in soil, fresh water, well water, sea water, sewage & air.

It exists in trophozoite & encysted forms.

CLINICAL FEATURESSymptoms : i. Very severe painii. Wateringiii. Photophobiaiv. Blepharospasm v. Blurred vision.Signs : vi. Initial lesions in the form of Limbitis,

Coarse, Opaque Streaks, Fine Epithelial & Sub-Epithelial Opacities & Radial Kerato-neuritis.

vii. Advanced cases shows a central or paracentral ring-shaped lesion with stromal.Hypopyon may also be present.

Treatment :It is usually unsatisfactory:i. Non-specific treatment is on the

general lines for corneal ulcer.ii. Specific medical treatment includes:

propamidine isethionate(0.1%), neomycin drops, polyhexamethylene biguanide (0.01-0.02%).

iii. Penetrating keratoplasty is frequently required in non-responsive cases.

ACANTHAMOEBA

ALLERGIC KERATITISI. PHLYCTENULAR KERATITIS

Corneal involvement may occur secondarily from extension of conjunctival phlycten; or rarely as a primary disease.

It may present in 2 forms:A. Ulcerative phlyctenular keratitis B. Diffuse infiltrative keratitis

A. Ulcerative Phlyctenular Keratitis May occur in the following 3 forms:1. Sacrofulous ulcer:• Is a shallow marginal ulcer formed due to

breakdown of small limbal phlycten. • Such an ulcer usually clears up without leaving

any opacity.2. Fascicular ulcer:• It has a prominent parallel leash of blood vessels.• This ulcer usually remains superficial but leaves

behind a band-shaped superficial opacity after healing.

3. Miliary ulcer:• In this form multiple small ulcers are scattered

over a portion of or whole of the cornea.

ULCERATIVE PHLYCTENULAR KERATITIS

B. Diffuse Infiltrative Phlyctenular Keratitis

It may appear in the form of central infiltration of cornea with characteristic rich vascularization from the periphery, all around the limbus.

It may be superficial or deep. Recurrences are very common.

Treatment i. Topical steroidsii. Antibiotic drops & ointmentsiii. Atropine (1%) eye ointment.

DIFFUSE INFILTRATIVE PHLYCTENULAR KERATITIS

II. VERNAL KERATITIS Corneal involvement in VKC may be

primary or secondary due to extension of limbal lesions.

Vernal keratitis includes following 5 types of lesions:

1. Punctuate epithelial keratitis2. Ulcerative vernal keratitis (shield

ulcertaion)3. Vernal corneal plaques 4. Subepithelial scarring5. Pseudogerontoxon

1. Punctuate epithelial keratitis • Involving upper cornea is usually associated with

palpebral form of disease. 2. Ulcerative vernal keratitis• Presents as a shallow transverse ulcer in upper

part of cornea.• The ulceration results due to epithelial

macroerosions.3. Vernal corneal plaques • Result due to coating of bare areas of epithelial

macroerosions with a layer of altered exudates.4. Subepithelial scarring • Occurs in the form of a ring scar.5. Pseudogerontoxon • Is characterised by a classical ‘cupid’s bow’

outline.

Treatment

i. Topical steroidsii. Mast cell stabilizersiii. Topical antihistaminicsiv. Acetyl cysteinev. Topical cyclosporinevi. Supratarsal injectionvii. Cryo applicationviii. Surgical excision

VERNAL KERATITIS

III. ATOPIC KERATITIS It is an adult equivalent of vernal keratitis & is

often associated with atopic dermatitis. Most of the patients are young atopic adults,

with male predominance.Symptoms include:i. Itching, soreness, dry sensationii. Mucoid dischargeiii. Photophobia or blurred visionSigns iv. Lid margins are chronically inflammed with

rounded posterior borders.v. Tarsal conjunctiva has milky appearance.vi. Cornea may show punctuate epithelial

keratitis.

Treatment is often frustrating

i. Treat facial eczema & lid margin disease.

ii. Sodium cromoglycate drops, steroids & tear supplements may be helpful for conjunctival lesions.

ATOPIC KERATITIS

TROPHIC CORNEAL ULCERS Trophic corneal ulcers develop due to

disturbance in metabolic activity of epithelial cells.

This group includes:I. Neuroparalytic KeratitisII. Exposure Keratitis

I. NEUROPARALYTIC KERATITIS Neuroparalytic keratitis occurs due to

paralysis of the sensory nerve supply of the cornea.

Causes 1. Congenital i. Familial dysautonomia (Riley-Day syndrome)ii. Congenital insensitivity to pain.iii. Anhidrotic ectodermal dysplasia.2. Acquired i. Following alcohol-block or

electrocoagulation of Gasserian ganglion or section of the sensory root of trigeminal nerve for trigeminal neuralgia.

ii. A neoplasm pressing on Gasserian ganglion.

iii. Gasserian ganglion destruction due to acute infection in herpes zoster ophthalmicus.

iv. Acute infection of Gasserian ganglion by herpes simplex virus.

v. Syphilitic (luetic) neuropathy.vi. Involvement of corneal nerves in

leprosy.vii. Injury to Gasserian ganglion.

Clinical Featuresi. Characteristics features are no pain, no

lacrimation, & complete loss of corneal sensations.

ii. Ciliary congestion is marked.iii. Corneal sheen is dull.iv. Initial corneal changes are in the form

of punctuate epithelial erosions in the inter-palpebral area followed by ulceration due to exofoliation of corneal epithelium.

v. Relapses are very common, even the healed scar quickly breaks down again.

Treatment i. Initial treatment with antibiotic &

atropine eye ointment.ii. Topical nerve growth factor drops &

amniotic membrane transplantation.iii. If, however, relapses occur, it is best

to perform lateral tarsorrhaphy which should be kept for at least one year.

iv. Along with it prolonged use of artificial tears is also recommended.

NEUROPARALYTIC KERATITIS

II. EXPOSURE KERATITIS Normally cornea is covered by eyelids

during sleep & is constantly kept moist by blinking movements during awaking.

When eyes are covered insufficiently by the lids & there is loss of protective mechanism of blinking the condition of exposure keratopathy develops.

Causes1. Extreme proptosis due to any cause will

allow inadequate closure of lids.2. Bell’s palsy or any other cause of facial

palsy.3. Ectropion of severe degree.4. Symblepharon causing lagophthalmos.

Clinical Featuresi. Initial dessication occurs in the

interpalpebral area leading to fine punctuate epithelial.

ii. Bacterial superinfection may cause deep suppurative ulceration which may even perforate.

Treatmentiii. Topical antibioticsiv. Cycloplegic drugsv. Systemic analgesicsvi. Vitamins (A,B-complex & C )vii. Hot fomentation.

EXPOSURE KERATITIS

KERATITIS ASSOCIATED WITH DISEASES OF SKIN & MUCOUS MEMBRANEI. ROSACEA KERATITISClinical Featuresi. The condition typically occurs in elderly

women in the form of facial eruptions presenting as butterfly configuration.

ii. Ocular lesions include chronic blepharoconjunctivitis & keratitis.

iii. Rosacea keratitis occurs as yellowish white marginal infiltrates & small ulcers.

Treatment iv. Topical steroids v. Long course of systemic tetracycline.

ROSACEA KERATITIS

KERATITIS ASSOCIATED WITH SYSTEMIC COLLAGEN VASCULAR DISEASES Peripheral corneal ulceration &/or

melting of corneal tissue is not infrequent occurrence in patients suffering from systemic diseases such as rheumatoid arthritis, systemic lupus rythematosus, polyarteritis nodosa & Wegener’s granulomatosis.

Such corneal ulcers are usually indolent & difficult to treat.

Systemic treatment of the primary disease may be beneficial.

PERIPHERAL CORNEAL ULCER

IDIOPATHIC CORNEAL ULCERSI. MOOREN’S ULCERThe Mooren’s ulcer (chronic serpiginous or rodent ulcer) is a severe inflammatory peripheral ulcerative keratitis.ETIOLOGYExact etiology is not known. Different views are:1. It is an idiopathic degenerative condition.2. It may be due to an ischaemic necrosis

resulting from vasculitis of limbal vessels.3. It may be due to the effects of enzyme

collagenase & proteoglyconase from conjunctiva.

Clinical FeaturesTwo clinical varieties of Mooren’ ulcer have been recognised.1. Benign form which is usually unilateral,

affects the elderly people & is characterised by a relative slow progress.

2. Virulent type also called the proressive form is bilateral, more often occurs in younger patients. The ulcer is rapidly progressive with a high incidence of scleral involvement.

Symptoms i. Severe painii. Photophobiaiii. Lacrimation iv. Defective vision.Signsv. Patches of grey infiltrates which

coalesce to form a shallow furrow over the whole cornea.

vi. Whitish overhanging edge.vii. The ulcer rarely perforates & the

sclera remains uninvolved.

Treatmenti. Topical corticosteroidsii. Immunosuppressive therapyiii. Soft contact lensesiv. Lamellar or full thickness corneal

grafts.

MOOREN’S ULCER

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