CORNEA
Švehlíková G.
Department of Ophthalmology LF UPJS v
Košiciach
Prednosta: prof. MUDr. Juhás T., DrSc.
ANATOMY OF THE CORNEA
Epitelium
 Stroma
 Endotelium

CLINICAL EVALUATION
SLIT-LAMP BIOMICROSCOPY
Fluorescein staining of
the cornea
CORNEA
Keratometry - measuring the curvature of
the anterior surface of the cornea,
particularly for assessing the extent and axis
of astigmatism
Corneal Topography Map
CORNEA
keratoscopy
Normal cornea
Pachymetry - corneal
thickness
keratoconus
SPECULAR MICROSCOPE
Normal endothelial cells
Pathologic endothelium
DEVELOPMENTAL ANOMALIES
MICROCORNEA
rare, hereditary,
 horizontal corneal
diameter is 10 mm or
less
 otherwise normal
structure
 other ocular abnorm.
– glaucoma, cataract,
iris abnorm...

MEGALOCORNEA
rare, bilat.
 corneal diameter is 13
mm or more
 structure is normal
 high myopia,
astigmatism

DEGENERATIVE CHANGES OF
THE CORNEA
Occur with age or secondary to exogenous
noxious agents
Often more pronounced in one eye
ARCUS LIPOIDES - SENILIS
yellow-white circular
opacity in the
peripheral cornea
 consist of lipids
deposited in the
corneal stroma
 high prevalence –
arcus senilis

BAND KERATOPATHY
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deposition of calcium salts in the
subepitelial space
causes - chronic iridocyclitis,
phtisis bulbi, metabolic –
increased serum calcium , chronic
renal failure
Treatment:
- repeated application of calcium
binding agent EDTA
(ethylenediaminetetraacetic acid)
- Excimer laser phototherapeutic
keratectomy has been effectively
performed to treat more
extensive cases
SPHEROID DEGENERATION
yellow subepitelial
and stromal deposits
 visual impairment,
severe fotofobia, pain
 frequent exposure to
sunlight

SALZMANN´S NODULAR DERENERATION
multiple bluish-white
superficial nodules
 occurs secondary to
chronic keratitis and
trauma

CORNEAL DYSTROPHIES
Progresive, usualy bilateral, genetically
determined disorders
Age of presentation – 1. – 4. decade
CORNEAL DYSTROPHIES
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Classification
1. anterior D. – Cogan microcystic D, ReisBucklers D, Meesman D, Schnyder D
2. stromal D. – latice D, granular D, macular D
3. posterior D. – Fuchs endotelial, posterior
polymorphous D
COGAN MICROCYSTIC DYSTROPHY
map-dot-fingerprint D
 four types of lesion are
seen either in
isolation or in
combination : dots,
microcysts, map-like,
fingerprint-like
 often asymptomatic
 10% recurent cornela
erosions

MEESMANN DYSTROPHY
AD
 rare,
 multiple
intraepithelial cysts
across the entire
cornea
 symptoms – foreign
body sensation,
photophobia
 usually no th

LATTICE DYSTROPHY
AD
 subepitelial and
intrastromal
branching lattice
figures
 accumulation of
amyloid material
 complication –
recurent epitelial
breaks

GRANULAR DYSTROPHY
AD
 multiple grey-white,
snowflake-like,
sharply demarcated
opacites
 beginning in the
epithelium, later in
the entire stroma
 histology – hyaline
deposits

MACULAR DYSTROPHY
systemic disorder of
keratan sulfate
metabolism
 AR
 progresive, greyish
opacification

FUCHS ENDOTELIAL DYSTROPHY

slowly progresive disease

Signs:
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Asymmetrical, bilateral, presents
in the fifth or sixth decade
bilateral primary cornea guttata
and a reduced endothelial cell
density
advanced stage:
endothelial cell pump
decompensation results in corneal
edema
bullous keratopathy
histology shows a thickened
Descemet’s membrane and
endothelial cell loss.

Image obtained by
specular microscopy
shows destruction of
the endothelial cells
(right side of image).
In comparison, the left
side and the middle
(magnified view) of
the image show an
intact endothelium
with a clearly visible
honeycomb structure
KERATOCONUS


degenerative, non-inflammatory
disorder of the cornea
number of patients affected varies
between 1 in 3,000 and 1 in 10,000
depending on geographic location

asymetrical progresive thinning

manifestation between the age of 10-20
the causes of keratoconus are poorly
understood
- increased activity of proteinase
enzymes and a reduced activity in
the proteinase enzyme inhibitors.
This imbalance can destroy the
structural proteins and supporting
substrates within the cornea,
resulting in thinning and loss of
the normal mechanical strength.
Early signs
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irregular astigmatism
slit-lamp examination:
- Vogt lines - very fine,
vertical lines in the cornea
- Fleishers ring - yellowbrown ring of iron pigment
seen at the base of the
cone beneath the
epithelium
corneal topography is
the most sensitive method
for detecting very early
keratoconus by identifying
subtle, inferior corneal
steepening
Late signs
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progressive corneal
thinning, with poor
vision from marked
irregular astigmatism
the apex of the cone is
the thinnest area and
is usually displaced
inferiorly just below
the centre
corneal protrusion
causing bulging of the
lower lid on looking
down (Munson sign).
Acute Hydrops
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in advanced cases,
spontaneous ruptures of the
Descemet's membrane can
occur, causing a tear near the
apex of the cone
the rupture allows aqueous to
pass into the cornea resulting
in significant corneal oedema
and opacification
although the break usually
heals within 6-10 weeks and
the corneal oedema clears, a
variable amount of corneal
scarring may develop
corneas that do not recover
transparency may require a
corneal transplant
Treatment
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depends of the degree of
ectasia
early and mild cases can be
treated with astigmatic
spectacle correction and
soft toric contact lenses
as the disease progresses rigid contact lenses
10-25% of patients with
keratoconus progress –
surgical intervention
Surgical options include:
1. Corneal Collagen Crosslinking with Riboflavin
2. Corneal transplantation
3. Intra-corneal ring
segment insert
Corneal Collagen Cross-linking with
Riboflavin
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new treatment modality,
stabilize the process
the aims of the treatment are to
increase the mechanical stability of
the cornea by inducing cross linkage
between the corneal collagen fibres
under topical anaesthesia
as riboflavin does not penetrate the
corneal epithelium this is removed and
riboflavin (vitamin B2) is applied as a
photosensitiser
the tissue is then exposed to UVA
(370nm) light for about 30 minutes
this allows the generation of additional
connections, so-called cross-linkings,
between the individual collagen fibres
of the cornea.
Corneal transplantation

Corneal transplantation (grafting) replaces the
central 7-8 millimeters of the cornea with a donor
cornea that has been prepared by an eye bank
Corneal transplantation

different types:
Penetrating Keratoplasty
 Lamellar Keratoplasty
 Decemet’s Stripping with Endothelial
Keratoplasty (DSEK)

Corneal transplantation
Penetrating
Keratoplasty
Lamellar
Keratoplasty
Decemet’s
Stripping with
Endothelial
Keratoplasty
(DSEK)
Indications
-
to improve vision
to reduce pain
or to maintain the structural integrity of the eye
Disorders:
- Bullous keratopathy (pseudophakic or aphakic,
Fuchs' endothelial dystrophy)
- Keratoconus
- Keratitis or postkeratitis (caused by viral,
bacterial, fungal, or Acanthamoeba infection or
perforation)
- Corneal stromal dystrophies
PENETRATING KERATOPLASTY ( PK)
full thickness corneal transplantation, PK is the
commonest type of corneal graft
 the sutures are normally removed 1 to 2 years
after surgery

PK
PK
PK
Suturing techniques
Interrupted
sutures
Single running
suture
Double running
suture
Stp. PK
LAMELLAR KERATOPLASTY
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in DLK a central disc of
tissue including the front
95% of the cornea is
replaced with a transplant
tissue
importantly, the
endothelial cell layer is left
in place
performed as an
alternative to PK in
keratoconus, because this
cell layer remains healthy
in keratoconus
LAMELLAR KERATOPLASTY
Advantages for DLK include:
 fewer problems with rejection
- the endothelial cell layer is the main target of immunological
attack in corneal transplant rejection reactions, and damage to
this layer during graft rejection can cause the graft to fail
- leaving the original endothelial layer in place with a DLK avoids
most rejection problems
Disadvantages for DLK include
 reduced visual clarity - some visual clarity is lost as a result of
light scatter at the interface between the transplant and the host
tissue in all partial thickness corneal grafting techniques
 technical difficulty
DECEMET’S STRIPPING WITH
ENDOTHELIAL KERATOPLASTY (DSEK)
partial-thickness corneal transplant that replaces
only the endothelial layer
 instead of replacing the entire cornea the surgeon
strips-away a delicate membrane along the
backside of the cornea
 thin piece of donor tissue containing the
endothelial cell layer is inserted onto the back
surface of the patient’s cornea
 can be performed with topical anesthesia and
small incisions
 no stitching is required

DSEK
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is appropriate for patients in which the endothelial cell
layer is dysfunctional in cases of Fuchs’ dystrophy or post
cataract surgery endothelial dysfunction (pseudophakic
bullous keratopathy)
Advantages of DSEK as compaired to standard corneal
transplantation may include:
Better shape – problems with astigmatism are uncommon,
visual recovery is faster
No suture problems - two of the commonest reasons for
graft failure in PK are rejection and infection. Both
problems may be precipitated by suture loosening or
breakage. Because there are no sutures on the corneal
surface after DSEK, these problems are avoided
Disadvantages
technical difficulty
DSEK

Only patients with
endothelial cell problems
are candidates for DSEK
Complications:
Graft rejection
 Infection (intraocular and corneal)
 Wound leak
 Glaucoma
 Graft failure
 High refractive error (especially astigmatism,
myopia, or both)
 Recurrence of disease (with herpes simplex or
hereditary corneal stromal dystrophy).

CORNEAL INFECTIONS
Viruses
Bacteria
Fungi
Protozoa
EPIDEMIC KERATOCONJUNCTIVITIS
Adenovirus
 Epidemic – highly
infectious
 Inicial acute
conjunctivitis, after 3
weeks – subepitelial
opacities –
spontaneously
disappear

HERPES SIMPLEX INFECTION
DNA virus
 infection extremnly
common, 90% of the
population are
seropositive for HSV
antibidies
 most infection are
subclinical
 two types :
HSV-1 ( face, lips, eyes)
HSV-2 (genital)
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HS virus
HSV1 LATENT INFECTION
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primary inf. – subclinical
or mild symptoms
recurent inf. – the virus
travels up the axon of
sensory nerve to its
ganglion, where it lies in a
latent state
in some patients the virus
reactivates, replicates and
travels down the axon to
its target tissue, causing
recurrent lesion
PRIMARY OCULAR INFECTION

Typicaly in children
Blepharoconjunctivitis
- benign, self-limited
- skin lesion involve the lids
and periorbital area
- conjunctivitis – akute,
watery discharge,
preauricular adenopathy.
- Th : topical antiviral
ointment 5x/day
Keratitis
- uncommon, fine epitelial
punctate
- in some patients progress
DENDRITIC KERETITIS
the epithelial infection
of the cornea
 corneal sensitivity is
reduced
 recurens

STROMAL NECROTIC KERATITIS
is caused by active
viral invasion and
destruction
 rare
 may follow epitelial
disease or may be
associated with an
intact epithelium
 Th – difficult
antiviral agents,
lubricant ointments

DISCIFORM KERATITIS
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aetiology is
controversial
either by a reactivated
viral inf. or
hypersensitivity
reakcion to antigen
signs – central zone of
epith. oedema, stromal
thickening, surrounding
ring of precipitates
Th. top. steroids comb.
with antiviral th.
BACTERIAL KERATITIS
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-
Pathogens able to produce
corneal infection of an intact
epithelium are –
Neisseria gonorhoe,
Corynebacterium
diphtheriae, Listeria sp.,
Haemophilus sp.
-
-
Other bacteria only after
loss of corneal epithelial
integrity
Predisposing factors –
contact lens wear, trauma,
corneal exposure, dry eye,
topical steroids, systemic
immunosupresive agents
BACTERIAL KERATITIS
round ulcer with deep
stromal infiltration
 hypopyon
 broad-spectrum ATB

CAUSES
Staph. aureus, Strep.
pneumoniae
 Pseudomonas
 Enterobacteriaceae

FUNGAL KERATITIS

clinical appearance
varies with the
infectious agent and
stage of the disease
1. filamentous fungal
keratitis
2. candida keratitis
FILAMENTOUS FUNGAL KERATITIS
Aspergillus or
Fusarium sp.
 ocular trauma,
organic material –
wood
 greyish – white ulcer
with indistrict
margins

CANDIDA KERATITIS
usualy develops in
association with preexisting chronic corneal
disease or in an
immunocompromised
pacient
 yellow-white ulcer with
dense suppuration

ACANTHAMOEBA KERATITIS
free-living protozoans
- found in air, soil and
water
- exist in both active
( trophozoide ) and
dormant ( cystic ) forms
- cystic forms – able to
survive for prolonged
periods
 contact lens wearer
- keratitis may occur
following a minor
corneal erosion

ACANTHAMOEBA KERATITIS
Presentation
- Early signs : 1-4
weeks limbitis, small
anterior stromal
infiltrates
- infiltrates gradually
enlarge, form central
or paracentral ring
 Th- diamidin and
imidazole derivatives
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QUESTIONS AND DISCUSSION
THANK YOU FOR YOUR ATTENTION !