Presentation outline

 Brief anatomy of the cornea

 Definition of corneal ulcers
 Classifications and types of corneal ulcers
 Clinical features of some corneal ulcers
 Management of corneal ulcers
 Complications of corneal ulcers

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 The cornea is a transparent, dehydrated
and avascular structure, and forms 1/6th of
the outer fibrous coat of the eyeball. It
receives its nutrients from the tear film at
the outside and the aqueous humour from
the inside.
 Its nerve supply is from the ophthalmic
division of the trigeminal nerve (cranial
nerve V).
 Dimensions of the cornea
 Anterior vertical diameter……… 11mm
 Anterior horizontal diameter..……12mm
 Posterior diameter ………….11.5mm
 Refractive index …………....1.33
 Refractive power …………….43D
 Thickness
 At the centre……………….. 0.52mm
 At the periphery ……………….......1mm
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 Layers of the corner
 The cornea consist of 5 and or 6 layers,
namely
 Anterior epithelium this is made up of
stratified squamous cells and this layer
replaces itself once a week.
 Bowman’s membrane – is a thin and
dense fibrous layer of connective tissues
that lies beneath the cornea epithelium,
once damaged or destroyed does not
regenerate.
 Corneal stroma- constitutes 90% of the
cornea total thickness and consists of
collagen fibres which are arranged in
regular layers that enable the cornea to be
clear.
 Pre Decesmet’s membrane (Dua’s layer,
discovered in 2013) is about
15micrometer thick acellular structure
which is very strong and impervious
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(unaffected or immune to damage) to air.
 Decesmet’s membrane- is separates the stroma from the underlying endothelial layer,
once destroyed it regenerates.
 Endothelium- the innermost layer of the corner and its back is constantly bathed in
the clear aqueous humour. It’s the most active layer of the cornea with cell density of
about 6,000/mm2 in young adults

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 An ulcer is an open sore of the skin, eye or mucous membrane, often caused by an
initial abrasion and generally by an inflammation and or an infection.
 Corneal ulcer is a break in the integrity or continuity of any layer(s) of the corner.

CLASSIFICATIONS OF CORNER ULCERS

 Basically, corneal ulcers are grouped into two (2) types namely;

Ulcerative keratitis:
 Under this ulcers are grouped

 depending on the location thus central or peripheral

 Depending on purulence thus purulent and non- purulent

 Depending on association of Hypopyon thus simple and Hypopyon corneal ulcers

 Depending on slough formation

 Based of aetiology we have the Infective and non-infective/sterile

Non-ulcerative keratitis: here the epithelium is intact.

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In ulcerative keratitis there is a break in the continuity of the epithelium. The types
of ulcers under this category include;
 Bacterial corneal ulcers

 Fungal corneal ulcers

 Marginal corneal ulcers (catarrhal ulcer)

 Idiopathic corneal ulcers (Mooren’s ulcer)

 Atheromatous corneal ulcers

 Ulcers associated with malnutrition, which also include;

 Central marasmic corneal ulcer

 Keratomalacia corneal ulcers

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 CORNEAL ULCERS UNDERGO FOUR STAGES
 Stage of infiltration: this stage cornea inflammation begins with the
migration of lymphocytes into the cornea from the limbal vessels; if the
lesion is superficial and does not involve the Bowman’s membrane it heals
easily and faster without leaving any opacity. But if it extends into the deep
layers of the corner and destroyers the Bowman’s membrane then it
indicates the progression of the lesion.
 Stage of progression or active ulceration; the margins of the ulcer swells
as the floor and margin of the ulcer are packed with inflammatory cells and
they appear gray. Enzymes released by lymphocytes exacerbate necrosis
and toxins may diffuse in the anterior chamber and cause damage to the
corneal endothelium and induce iritis.
 Stage of regression; sloughs are cut off and the ulcer appears large with
smooth edges, limbal blood vessels extend and invade the ulcer and healing
begins as the epithelium starts growing over the edges to bridge the gap.
 Stage of cicatrisation; healing continues and fibrous tissue are laid down
(corneal fibroblast and endothelial cells) thus after healing, cornea
becomes opaque at the site of ulceration.

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 ETIOLOGY
1. Exogenous infection thus invasion by
organisms such as;
 staphylococcus aureus
 pseudomonas aeruginosa
 Neisseria gonorrhoea
 streptococcus pneumoniea
 streptococcus haemolyticus
2. Risk factors that disturbs the corneal
epithelium
 Trauma
 Foreign body
 contact lens wear
 Prolong use of corticosteroids
 Impaired defence mechanism
Clinical features of bacterial corneal
ulcers
 The ulcer may be round, oval or
irregular in shape
 Epithelial defect with large infiltrate
and conjunctival injection
 Pain and irritation
 Tearing and discharges
 Eyelid swelling
 Blurred vision
 The margins of the ulcer is
oedematous
 Small superficial vessels grow from
the limbus towards the margins of the
ulcer
 Hypopyon in the anterior chamber
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This frequently occurs in warm and humid climates following trauma to the cornea by
vegetable material, indiscriminate use of corticosteroids, contact lens wear, and keratitis
sicca and cornea surgery.
Symptoms
 Foreign body sensation

 Increasing eye pain or discomfort

 Sudden blurry vision

 Unusual redness of the eye

 Eyelid swelling.

 Increased light sensitivity

. Signs of fungal ulcers

 Corneal lesion have a white/grey stromal infiltrate with indistinct fluffy margins

 Feathery branching like extensions or borders.

 May be satellite lesions with hypopyon and conjunctiva injection as well as purulent
secretions.

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10
  Peripheral ulcerative keratitis is a shollow ulcer on the surface of the cornea, on the edges
of the cornea.
 Most often seen in the older people and thought to be caused by staphylococcal blepharo-
conjunctivitis where antigen presenting cells at the limbus stimulate the T lymphocytes to
produce peripheral infiltrates with or without ulcerations.
SYMPTOMS
 Red eye

 Photophobia

 Blurry of vision

 Pain

SIGNS
 Circumferential progression of associated marginal infiltrates with associated limbal
hyperemia and conjunctivitis
 Loss of corneal epithelium; ulcerations in the marginal zone seperated from the limbus
by a clear corneal zone
 Unilateral or bilateral peripheral curvilinear infiltrates in superficial cornea where lids
cross the corneal periphery.
 Staphylococcal blepharitis and meibomitis are often also present.

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 These are painful, chronic progressive ulcers of unknown cause, but believed that
autoimmunity plays a role. Ancylostoma duodenale infestation, accidental trauma
and surgery are considered risk factors. This usually occurs in two forms; benign
(unilateral) ulcers in old males, and virulent bilateral progressive ulcer of young
patients and is much painful.
 Destruction of the cornea generally affects stromal tissue leaving behind an intact
endothelium and epithelium. No inflammation is seen in the sclera adjacent to the
peripheral ulcer.
 CLINICAL FEATURES
 Pain, lacrimation, photophobia and impaired vision
 Ulcers start at the periphery and slowly spread circumferentially and centripetally
 Intense pain in the affected eye(s).
 Inflammation of the uvea
 Non-inflamed sclera

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ATHEROMATOUS CORNEAL ULCERS
 This generally occurs as an old leukoma (scar) undergo degenerative changes with
calcareous deposits. The devitalisation and the insensitivity of the cornea make it
vulnerable to infection hence it quickly perforates.
CORNEAL ULCERS ASSOCIATED WITH MALNUTRITION
 This involves central marasmic and Keratomalacia corneal ulcers; the latter is
associated with xerosis of the conjunctiva and vitamin A deficiency while the former is
as a result of protein-energy malnutrition.
CLINICAL FEATURES OF KERATOMALACIA
 Keratomalacia is seen in children less than 5yrs of age in underprivileged families

 They look very ill and suffer from infective diarrhoea

 Night blindness

 Cornea becomes dull and insensitive and a keratinized plaque may cover the surface

 The ulcer is oval or round with dense yellowish-white infiltration near the central part
of the cornea
 Usually devoid of inflammatory reaction

 13
  An ulcer occurring in the layers of the cornea but the epithelium is intact. Broadly,
non-ulcerative keratitis is divide into two (2) groups; superficial and deep.
Superficial keratitis involves the corneal epithelium, bowman’s membrane and
superficial corneal stroma. This category is further divided in the following….
 Superficial punctate keratitis

 Thygeson’s superficial punctate keratitis

 Superior limbic keratitis

 Filamentary keratitis

 Recurrent corneal erosions

 Photophthalmia

Deep non ulcerative keratitis

 Interstitial keratitis

 Keratitis profunda; usually unilateral and associated with iridocyclitis and often
affects adults
 Disciform keratitis; often associated with viral infection and characterized by the
appearance of a disc-shaped dense grayish infiltration in the deep layer of the central
cornea
 Sclerosing keratitis; as a result of a complication of scleritis and manifest as a
tongue-shaped opacity that develops at the margin of the cornea. 14
We have
 Herpes Simplex Keratitis and

 Herpes Zoster Ophthalmicus

HERPES SIMPLEX KERATITIS

 Caused by the herpes simplex virus, the disease spreads through direct contact between two
persons. Has 2 strains as HSV-1 and HSV-2, the former affects the upper part of the body
mostly the mouth, lids and eyes whiles the latter attracts the anogenital region.
Reoccurrence is most like to resurface with an upper respiratory infection as individuals
affected become carriers.
 The HSV infection occurs in two forms primary herpetic infection usually found in non-
immune subjects thus children less than 3 yrs of age owning to close contact. This presents
with mild fever, malaise and non-suppurative preauricular lymphadenopathy, lesions
develop on the lips and the periorbita. Usually is self-limiting.
 Recurrent infection, here the virus during primary infection reaches dormancy at the
trigeminal ganglion where it lies dormant for many years. Reactivation occurs following
stress, trivial trauma, attack of flu, use of corticosteroids and immunosuppressive agents.
Clinical manifestation
 Reduced corneal sensation

 Staining of the cornea reveals dendric ulcer

 Discomfort to light

 Redness and blurred vision 15

 This is characterized by multiple vesicles on one side of the face along the
ophthalmic division of the trigeminal nerve (usually involving the supraorbital,
supratrocheal and infratrochear branches of the nasal branch of the trigeminal
nerve), preceded with severe neuralgia. This is caused by the varicella zoster virus
believed to remain dormant after infection of chicken pox in young age and gets
activated later causing HZO.
 Clinical features
 Neuralgic pain along the trigeminal nerve associated with fever, nausea, vomiting
and malaise.
 Appearance of crops vesicles on one side of the forehead and the scalp
 The lids are edematous and cornea lesions may vary from small infiltrates to a big
vesicle which may ulcerate.
 The dendrites of the herpes Zoster are smaller without central ulceration and
terminal bulbs, whiles that of herpes simplex have central ulceration and terminal
bulbs.

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 Stain with fluorescein
 Discharges can be taken for culture and sensitivity
test…
 Kimura spatula or sterile disposable blade is used to
take scrapings from the floor of the ulcer after
anaesthetizing the surface, and the material introduced
on blood sugar, chocolate agar and sabouraud agar for
culture and spread over slides for Gram and Giemsa
stains for bacteria, Potassium hydroxide (KOH)
preparation for fungi

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 Reassure and explain all procedures to the client
 Check clients visual acuity
 Check the IOP
 Take a good history
 Proper eye examination should be done
 Lids for swellings
 Conjunctiva for foreign bodies, injection
 Cornea for abrasions, haziness and or edema, stain for ulcers
 A/C for depth, Hypopyon, blood
 Iris for forward displacement
 Pupil-pupillary margin fails to seal the gap if corneal perforation occurs in the centre
 Depending upon the nature of the case, some may need admission.
 Eyelid cleaning and warm compress for marginal ulcer associated with blepharitis
 Irrigation with warm saline 2 to 3 times a day, this removes the discharges and necrotic
materials along with organisms and their toxins. Also warm water prevents vascular
stasis and encourages flow of antibiotics.
 Protect the eye with a pad unless there is copious discharge, eyes discharging can be
protected by glasses. 18
Antibiotics
 With bacterial corneal ulcers broad spectrum antibiotics such fluroquinolone
(moxifloxacin, ciprofloxacin) and cephalosporin (cefazolin 5%) drops are effective for
controlling corneal infection both Gram positive and negative organisms.
 Fungal treat with natamycin 5% suspension with both sysytemic and tropical
amphotericin-B (0.15% drops) is effective against a wide range of fungi. Some other
antifungal agents are fluconazole, ketoconazole, itraconazole and voriconazole.
 With viral corneal ulcers treat with antiviral therapy such as oral famciclovir 5oomg 3
times a day, valacyclovir 1g 3 times a day or acyclovir 800mg 5 times a day for 7 to 10
days but in immune-compromised patients, intravenous acyclovir is preferred. Here
oral corticosteroids reduce pain and prevent crust formation and facilitates early
recovery. Amitriptyline or carbamazepine may be needed to control severe pain.
Anti-glaucoma
 Anti-glaucoma agents are given to reduce IOP that may occur as a result of secondary
glaucoma.
Vitamin A
 In children, corneal ulcers associated with malnutrition should be given Vitamin A
capsule 200,000IU in 3 doses as recommended by WHO.

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 Analgesics and non-steroidal anti-inflammatory
drugs
Cycloplegic such as homoatropin 2% or atropine sulphate
1% drop at least twice a day. Atropine prevents or
relieves ciliary spasm and minimizes the accompanying
complication of anterior uveitis.

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SURGICAL MANAGEMENT
 Debridement is done to remove sloughs that reduces the count of microorganisms and
increases the absorption of medications
 Conjunctiva flapping, amniotic membrane transplantation (AMT) and tectonic corneal
grafting supports the weak cornea preventing corneal perforation while penetrating
therapeutic keratoplasty and cyanoacrylate glue corrects perforated corneal ulcer.
 COMPLICATIONS OF CORNEAL ULCERS

 Corneal necrosis

 Corneal perforation

 Corneal scarring

 Secondary glaucoma

 Secondary cataract

 Blindness

 Anterior synechiae

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 CORNEA SCAR CORNEAL NECROSIS

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