CORNEAL ULCERS

A. VIRAL KERATITIS
HERPES SIMPLEX KERATITIS

Etiology:
- Herpes simplex virus (HSV), DNA virus, human as natural host.
- Extremely common ocular ionfection & constitute herpetic keratoconjuctivitis
- Major cause os unilateral scarring worldwide
- Most common infectious cause of corneal blindness in developed countries.
Mode of infection:
-HSV-1 :acquired by kissing or coming in close contact w pt suffering from herpes
labialis cause infection above waist/ upper body
-HSV-II :transmitted to eyes of neonates from infected maternal genitalia / from
genital infection cause infection below waist (herpes genitalis)
Ocular lesions: -2 forms:i)
-

Primary Ocular Herpes

Involves non-immunine person
Age: children (6months to 5years old) & teenagers
C/F:
Skin lesions (of lids, periorbital region & lid margin a.k.a vesicular
blepharitis)
Acute follicular conjunctivitis
Keratitis (fine or course epithelial punctate keratitis, dendritic ulcer)

ii) Recurrent Ocular Herpes

-Virus which lies dormant in trigeminal ganglion, reactivaes & cause recurrent
infection.
- due to predisposing stress stimuli (eg. Fever due to malaria, flu, UV exposure,
general ill health, mild trauma etc.)
-types:1. Active epithelial keratitis
- punctate epithelial keratitis
- dendritic ulcer
-geographical ulcer
2. Stromal keratitis
3. Trophic keratitis
4. Herpetic iridocyclitis
Epithelial Keratitis
Symptoms:
Redness
Pain

 Photophobia
Tearing / watering
Decreased vision
Signs:
Superficial punctate lesions (fine or course)

Dendritic ulcer of an irregular, zigzag linear branching

Geographical ulcer- branches of dendritic ulcer which enlarge

Treatment:
-Antiviral (topical 3% ACICLOVIR eye oitment 5x day)
-mechanical debridement

Stromal keratitis
Types:
1. Disciform keratitis

- Rx: steroid eye drops 5x day & antiviral (ACICLOVIR 3%)

2. Diffuse stromal necrotic keratitis

-caused by active viral invasion & tissue destruction

- Rx: Antiviral drugs & keratoplasty (but results unsatisfactory)

HERPES ZOSTER OPHTHALMICUS (HZO)

Etiology:
- An acute infection of Gasserian ganglion of 5th cranial nerve by varicella-zoster
virus (VZV)
- Reactivation, after reamin dormant for decades.
- Frontal nerve more frequently affected than lacrimal & nasociliary nerves.

Lesions strictly limited to one side of midline of head.

Hutchinsons sign
- Involvement of external nasal branch of nasociliary nerve which supplies sides of
tips & root of nose.

Acute phase lesions: ~ totally resolve within few weeks

General features: sudden onset with fever, malaise, severe neuralgic pain
Cutaneous lesions: red, oedematous & vesicle formation, later form pustules
and crusting ulcers; with severe neuralgic pain
Ocular lesions:
Conjuctivitis
Zoster keratitis
Epithelial keratitis
Episcleritis
Scleristis
Iridocyclitis
Acute retinal necrosis
Ant. Segment necrosis
Secondary glaucoma
Rx: antiviral (ACICLOVIR), steroids (PREDNISOLONE) &symptomatic
relief by antiseptics, drying, cold compress.

Chronic phase lesions: ~ persist for years

Post herpetic neuralgia pain which persist even rash has healed
Lid lesions ptosis, trichiasis(abnormally positioned eyelashes that grow
back toward the eye, touching the cornea or conjunctiva), entropion(eyelid
is rolled inward against the eyeball) and notching.
Conjuctival lesions conjuctivitis
Corneal lesions:
Neuroparalytic ulceration
Exposure keratitis
Mucuos plaque keratitis
Scleritis
Uveitis
Lid scarring
Lipid degeneration

Relapsing phase lesions: ~ where acute or chronic lesions reappear few years later
Nummular keratitis
Mucuos palque keratitis
Scleristis

 Episcleritis
Secondary glaucoma

Treatment for Herpes Zoster Ophthalmicus (HZO):

Systemic therapy
-oral antiviral drugs (ACYCLOVIR)
-analgesics
-sys.steroids
-Amitriptyline
Local therapy for skin lesions
-antibiotic-corticosteroid skin oitment/lotions
Local therapy for ocular lesions
-topical steroids
-topical ACYCLOVIR
-cycloplegics
*ref. AK Khurana 5th ed. Page 102
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B. ACANTHAMOEBA KERATITIS

Etiology: Acanthamoeba castellani (free lying amoeba found in soil, fresh water, well
water, sea water, sewage and air)
Mode of infection:
Contact lens wearers using home-made saline from contaminated tap water
Mild trauma a/w contaminated vegetable matter, salt water diving, wind
blown cotaminant, hot tube use and exposure to muddy water.
Opportunistic infection - in patients with herpetic keratitis, bacterial keratitis,
neuroparalytic keratitis.
Symptoms:
May be asymptomatic
Foreign body sensation
Disproportionate pain

Watering
Photophobia
Blurred vision
Blepharospasm (involuntary tight closure of eyelids)

Signs:
Initial lesions: Limbitis (94% of cases)
Radial keratoneuritis
Epitheliopathy in any forms
(a) Punctate epitheliopathy
(b) Epithelial ridges
(c) Pseudo or true dendrites
(d) Irregular epitheliopathy
Advance cases: Patchy stromal infiltrates
Satellite infiltrates
Central of paracentral ring infiltrates* with overlying epithelial defects
Hypopyon

*Ring infiltrates

Severe cases: Ring abscess*

Hypopyon & stromal necrosis*

*Ring abscess

*Stromal necrosis

Clinical diagnosis:
-difficult
-made by exclusion, out of non-responsive patients being treated for herpetic, bacterial
or fungal keratitis.

Complications:
Scleritis
Stromal melting
Perforation

Investigations: (corneal scraping)

Confocal microscopy diagnostic; direct visualization of cysts
Potassium hydroxide (KOH) mount
Calcoflour white stain
Lactophenol cotton blue stain
Culture on non-nutrient agar (E.coli enriched) may shows trophozoites &
cysts.
Other mothods: immunohistochemistry, PCR.

Treatment:
Debridement
Topical amoebicide
(a) Diamidines eg. Propamidine isethionate & Hexamidine
(b) Biguanides eg. Polyhexamethylene biguanide(PHMB) & Chlorhexidine
(c) Aminoglycosides eg. Neomycin & Paromycin
(d) Imidazoles eg. Clotrimazole & Miconazole
Long term prophylactic therapy with PHMB
Penetrating keratoplasty (in non-responsive case; after full course of
max.medical therapy & quiescent phase of at least 6 months.

*ref. AK Khurana 5th ed. Page 107

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C. EXPOSURE KERATITIS

When eyes are covered insufficiently by lids and there is loss of protective mechanism
by blinking. (a.k.a. keratitis lagophthalmos)
Causes:
Extreme proptosis (due to any cause will allow inadequate closure of lids)
Bells palsy or any other cause of facial palsy
Simblepharon*
Deep coma (with inadequate closure of lids)
Physiological lagophthalmos (during sleep)
Mustle tone reduction in Parkinsonism
Mechanical lid scarring due to burns, trauma etc.

*Symblepharon, is a partial or complete adhesion of the palpebral conjunctiva

of the eyelid to the bulbar conjunctiva of the eyeball

Symptoms:
Ocular irritation
Burning sensation
Foreign body sensation
Redness

Signs:
Drying of cornea
Punctate epithelial defects
Corneal ulceration, followed by bacterial superinfection

Treatment:
Prophylaxis: Artificial tears
Instillation of ointment
Closure of lids during sleep (bandage/tape)
Bandage contact lenses
Temporary tarsorrhaphy
Treat the cause of exposure
Permanent treatment:

Tarsorrhaphy
Gold plate for upper lid
Conjuctival flap
Proptosis management

*ref. AK Khurana 5th ed. Page 109

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D. NEUROTROPHIC KERATOPATHY

Loss of corneal sensation owing to damage of sensory nerve supplying the cornea
Pathogenesis: unclear.
Disturbance in corneal sensation metabolic activity of corneal epithelium is
disturbed, lead to accunulation of metabolites edema in cells & exfoliation
ulceration & corneal changes.
Causes:
Congenital:
i) Riley-Day Syndrome
ii)Congenital insensitivity to pain

iii)Anhydrotic ectodermal dysplasia

Acquired:
i) Trigeminal nerve damage (following alcohol block or
electrocoagulationof Gasserian ganglion or section of the
sensory root of 5th nerve)
ii) Neoplasm
iii) Infection (by HSV, Herpes Zoster Ophthalmicus)
iv) Syphilitic (leutic) neuropathy
v) Injury to ganglion
vi) Systemic causes: diabetic, leprosy

Symptoms:
red eye
swollen eyelids
defective vision

Signs:
Ciliary congestion
Corneal signs
i) Sensation decreased
ii) Sheen is lost
iii) Punctate epithelial erosions involve interpalpabral area
iv) Franks epithelial defects
v) Corneal ulcer formation (horizontally oval, located in lower one half of
cornea & hv grey heaped-up epithelial border)
Treatment:
Conventional treatment: antioboitics, cycloplegics, lubricating drops &
patching
Special treatment: Topical nerve growth factor drops & autologois serum drops
Amniotic membrane transplantation (in case of large non healing ulcers)
Lateral tarsorrhaphy to promote healing & prevent relapse.

*ref: AK Khurana 5th ed. Page109

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