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
Diseases of
the Cornea
BY
Amr Mounir.MD

1.OUTER COAT
2.MIDDLE COAT
3.INNER COAT
Three Coats of Eye Ball


Tough Fibrous Coat
Post 5/6th
of Globe
White & Opaque
Sclera
Radius---12mm
Outer Coat

Tough Fibrous Coat
Ant 1/6th of Globe
Transparent
Cornea
Radius---8mm
Outer Coat

Corneoscleral Limbus

Vertical-------10.6 mm
Horizontal---11.7 mm
Thickness
Central portion----0.52 mm
Peripheral portion----1 mm
Size of Cornea

Three Layers
1.Epithelium & its Basement
2.Stroma & its ant condensation ( Bowman Zone(
3.Endothelium & its Basement (Descemet Membrane(
Structure


From Anterior to Posterior
1.Epithelium
2.Bowman Zone
3.Stroma
4.Descemet Membrane
5.Endothelium
Structure

50-60µm thick
Covers the stroma anteriorly
Continuous with epithelium of conjunctiva
Life of epithelial cells is 7 days
Prevent aqueous solutions to penetrate
Epithelium

Surface cell layer
Wing cell layer
Basal cell layer
Basement membrane
Epithelium

90%of the corneal thickness
Bowman Zone
Lamellar Stroma
Once deformed its typical structure is not restored
Stroma

Descemet membrane
)Regenerates(
Endothelium
Single layer of cells
Cells are tightly bound together
Responsible for dehydration
Never regenerates
Inner Lining

Central cornea is avascular
Corneoscleral limbus is generously supplied by
anterior conjunctival branches of the anterior ciliary
arteries
Aqueous humor and tear film provides nutrients
Blood supply

Branches of the ophthalmic division of
trigeminal nerve and are solely sensory
Most are concentrated in the anterior stroma
beneath the Bowman zone and send branches
forward into epithelium
Descemet membrane and endothelium are not
innervated
Nerve Supply

The microvilli of the anterior surface of the
squamous cell layer are wet by the mucin of tear film
These cells are joined by tight junctions that exclude
water soluble substances
Cornea

Tight junctions of the epithelial cells
Endothelial pump mechanism
Absence of blood vessels
Absence of pigments
Scarcity of cell nuclei in stroma
Regular structure of stroma
Transparency

Superficial
1.Punctate epithelial erosions
Tiny ,slightly depressed, epithelial defects
which stain with flourescein but not with
rose Bengal
PEE are non specific and may develop in a
wide variety of keratopathies
Signs of Corneal Disease


Superficial
2.Punctate epithelial keratitis
It is the hallmark of viral infections.
Swollen epithelial cells
Visible unstained
Stains with rose bengal
Signs of Corneal Disease

Superficial
3.Epithelial Oedema
Sign of
Endothelial decompensation
Severe acute elevation of IOP
Signs of Corneal Disease


Superficial
4.Filaments
Small coma shaped mucus strands lined with
epithelium.
One end attached with epithelium
Signs of Corneal Disease

Superficial
5.Pannus
Inflammatory or degenerative ingrowth of fibro
vascular tissue from limbus
Signs of Corneal Disease


Stromal Lesions
1.Infiltrates
Focal areas of active stromal inflammation
2.Edema
Increased corneal thickness
Decreased transparency
3.Vascularization
Signs of Corneal Disease

Lesions of Descemet Membrane
1.Breaks
Corneal enlargement
Keratoconus
Birth trauma
2.Folds (Striate Keratopathy(
Surgical trauma
Ocular hypotony
Stromal oedema
Signs of Corneal Disease


Def: Corneal ulcers are defect in the corneal epithelium
with or without stromal infiltration.
Types:
A) Infectious ulcerative keratitis
B) Non infectious ulcerative keratitis
Corneal ulcers

Bacteria and
Fungi
Bacteria and
Fungi VirusesViruses AcanthamoebaAcanthamoeba
Systemic
Autoimmune/
Inflammatory
Systemic
Autoimmune/
Inflammatory
Local ToxicLocal Toxic
InfectiousInfectiousNon infectiousNon infectious
EtiologyEtiology

Causes:
Local causes:
Punctate marginal keratitis: Staphylococci, Streptococci, hypersensitivity to
medications
Peripheral keratitis associated with blepharitis:
Systemic causes:
Generally manifestation of systemic, immune-mediated disease
Most common: Rheumatoid arthritis, Wegener’s granulomatosis and
polyarteritis nodosa
Non Infectious Ulcerative Keratitis

INFECTIOUSINFECTIOUS Non INFECTIOUSNon INFECTIOUS
Pain No pain
Discharge No discharge
AC reaction: present AC reaction: absent
Central Peripheral
Trauma: ++++ Trauma: -------



Infectious keratitis
 A corneal ulcer is an ocular emergency that
raises high stakes of questions about
diagnosis and management.
 When a large corneal ulcer is staring you in
the face time isn't in your side.
 Despite varying etiologies and presentations,
as well as different treatment approaches ,
corneal ulcers have one thing in common : the
potential to cause devastating loss of vision.
Important Facts

1-Control of infection
2-Control of inflammation
3-Promotion of re-epithelialization –
lubrication – lid
closure – bandage
soft contact lens
4-Prevention of perforation
– tissue adhesive glue
– conjunctival flap
– systemic immunosuppressive agents
Corneal grafting
PRINCIPLES OF MANAGEMENT
OF CORNEAL DISEASE

Ocular surface disease: Trauma, post-herpetic
corneal disease, bullous keratopathy, corneal
exposure, dry eye and diminished corneal sensation.
Contact lens wear
MICROBIAL KERATITIS
( Bacterial(

Pathogens which can produce corneal infection in intact
epithelium.
1.Neisseria gonorrhoeae
2.Corynebacterium diphtheriae
3.Listeria
4.Haemophilus
MICROBIAL KERATITIS
( Bacterial(

Oval, yellow-white, densely opaque stromal
suppuration surrounded by relatively clear cornea
Staph. aureus and strep.
pneumoniae

Bacterial ulcer

History
Clinical examination (including staining and
sensitivity(
Hospitalization
Corneal scrapping
Treatment
MANAGEMENT
 Acute painful injected eye.
 Profuse tearing and discharge.
 Decrease visual acuity.
 Large F.B
 Stromal invasion with epithelial excavating
edge.
Differentiators
1. Fluroquinolones 
 Every 5 mins / hour
 Hour / 24 hs
 2 hour / 24 hs
2. Fortified eye drops  ulcer < 2 ws ,
improvement not obvious.
(N.B)Don’t miss resistant bacteria.
1. Steriods
Treatment

Wrong diagnosis
Wrong treatment
Drug toxicity
Poor response to
treatment

Filamentous fungal keratitis
–Aspergillus
- Fusarium
FUNGAL KERATITIS

Greyish-white ulcer with indistinct margins
Surrounded by feathery infilterates
Ring infilterate
Endothelial plaque
Hypopyon
History of vegetable matter
injury
 Dull grey infiltrate.
 Satellite lesions.
 Awareness of those ulcers resembling bacterial
keratitis
 Awareness of those caused by yeast  better
defined borders
 Real flags
Differentiators

Fungal Keratitis


Usually develops in pre-existing corneal disease or
immunocompromised patient
Yellow-white ulcer
Dense suppuration
Candida keratitis


Suppurative bacterial keratitis
Herpetic stromal necrotic keratitis
D/D of fungal keratitis

Culture
Biopsy
Antifungal therapy – Initially broad-
spectrum econazole 1% topically – Then
depending upon sensitivity natamycin or
imidazole for 6 weeks
Systemic ketoconazole
Therapeutic penetrating keratoplasty
MANAGEMENT

Protozoan –active
(trophozoite) –dormant (cystic(
Common in swimmers and CL wearers
ACANTHAMOEBA
KERATITIS

Blurred vision and disproportionate pain
Patchy anterior stromal infilterates
Perineural infilterates (radial keratoneuritis(
Infilterates coalesce –ring abcess, ulceration
and hypopyon
White satellite lesions
CLINICAL FEATURES

Acanthamoeba Keratitis
 History:
Ulcer simulators resemble HS in shape but ??
Light sensitive ( Jacket- over- the head sign)
 Treatment :
Differentiators


Corneal scrappings stained with calcoflour
white
Corneal biopsy
Treatment with chlorhexidine,
polyhexamethylenebiguanide drops,
dipropamidine and propamidine.
Therapeutic penetrating keratoplasty
MANAGEMENT
Primary ocular herpes: -Primary ocular herpes: -
Blepharoconjunctivitis -Blepharoconjunctivitis -
Keatitis (punctate epithelialKeatitis (punctate epithelial((

Opaque cells arranged in a course punctate
or stellate pattern
Central desquamation leads to a linear
branching ulcer. –Fluorescein
stain – Rose Bengal stain
–Diminished corneal
sensitivity
Anterior stromal infilterates
Geographical or amoeboid ulcer
DENDRITIC ULCER



Herpes zoster keratitis
Healing corneal abrasion
Pseudodendrites due to soft contact lens
Acanthamoeba keratitis
Drug toxicity
Differential diagnosis
 Dentritic ulcer.
 Loss of corneal sensation.
 Photophobia.
Types of HSV keratitis:
 Primary
 Recurrent
 Dentritic , Geographic , Metaherptica
 Diabetic foot in the eye  Neurotrophic
Differentiators

Antiviral therapy –
Acycloguanosine 3% ointment –
Trifluorothymidine 1% drops –
Adenine arabinoside 3% ointment, 0.1%
drops
Idoxuridine
Debridement (with sterile cotton-tipped bud
2mm beyond the edge of ulcer(
TREATMENT

Stromal necrotic keratitis
Disciform keratitis
OTHER ENTITIES

Predominantly affects children
Etiology –
Tuberculosis – Delayed
hypersensitivity reaction to staphylococcal or other
bacterial antigen
PHLYCTENULOSIS

Photophobia, lacrimation and
blepharospasm.
PRESENTATION

Conjunctival: Pinkish-white nodule surrounded by
hyperaemia
Corneal: May resolve spontaneously or extend
radially to the cornea. May cause severe ulceration or
perforation.
SIGNS


Short course of topical steroids
Topical antibiotics
TREATMENT

keratoconjunctivitis sicca (KCS(:
Or
keratitis sicca: is a multifactorial disease of the tears and
the ocular surface disturbance with corneal
manifestations
Causes:
1-Dry eye
2-Vitamin A deficiency
Keratoconjunctivitis
Sicca


Exposure keratopathy (EK) is the cornea damage that
occurs from prolonged exposure of the ocular surface to
the outside environment.
EK can lead to ulceration, microbial keratitis, and
permanent vision loss from scarring
Causes:
1-Lagophthalmos
2-Proptosis
3-Lid malposition
Exposure Keratopathy


is a degenerative disease of the cornea caused by
damage of the trigeminal nerve which results in
impairment of corneal sensitivity, spontaneous corneal
epithelium breakdown, poor corneal healing and
development of corneal ulceration, melting and
perforation
Diagnosis:
by placing a cotton wad or cotton thread in contact with
the corneal surfaceCorneal sensitivity test:
Neurotrophic keratitis


Thank you

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