The document provides an overview of the cornea's structure, composition, and associated disorders. It discusses its transparent nature, histological layers, developmental processes, and the mechanisms of corneal nutrition and metabolism. Additionally, the text details various corneal diseases, their clinical features, and the management of bacterial, fungal, and viral infections affecting the cornea.

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CORNEA
STRUCTURE & DISORDERS
Sudeep Chaturvedi
MBBS;MS(Ophtho), Cert. Basics ofHealth Economics(WBI)
Consultant Ophthalmologist, Government Inst. of Medical Sciences, Greater Noida
Consultant Ophthalmologist Promhex Multispecialty Hospital, Greater Noida
Consultant Ophthalmologist GAOne Med.Consult, Greater Noida
General Manager NTPC Ltd (CMO CC-Retd.)
EMAIL- schats1957@gmail.com
The word cornea has come from “Kerato”.
The term “Kerato” in greek means horn or shield like.
Ancient Greek used to believe that cornea is derived
from same material like that of thinly sliced horn of
animal.

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THE CORNEA
The cornea is a transparent avascular
tissue with smooth, convex outer surface
and concave inner surface, which
resembles a small watch-glass.
Radius of curvature of sclera 12mm and
that of cornea is 8mm
It forms anterior 1/6th of the globe
To meet the diverse functional demands
the cornea must be:
- Transparent
- Refract light
- Sustain the intraocular pressure
- Provide a protective interface
DIMENSIONS
Microcornea: when HCD is less than 10mm
Macrocornea: when HCD is more than 13 mm

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Shape :
- Prolate
Surface area:
- About 1.3 cm² (one-sixth of the globe)
Radius of curvature:
-Anterior surface – about 7.8
mm
- Post. Surface – about 6.5
mm
Refractive power: +43.1 D
Refractive index: 1.376

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COMPOSITION OF HUMAN CORNEA
Water: 78 %
Collagen: 15 %
of which: Type-I : 50-55 %
Type-III : 1 %
Type-IV : 8-10 %
Type-VI : 25-30 %
Other protein: 5 %
Keratan sulphate: 0.7 %
Condroitin/dermatan sulphate: 0.3 %
Hyaluronic acid: +
Salts: 1 %
STRUCTURE
TO REMEMBER
A- ANTERIOR EPITHELIUM
B- BOWMAN’S LAYER
C- CORNEAL STROMA
D- DESCEMET’S MEMBRANE
E- ENDOTHELIUM

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DEVELOPMENT
ANTERIOR EPITHELIUM DEVELOPS FROM
SURFACE ECTODERM
THE NEURAL CREST CELLS MIGRATE TOWARDS
SURFACE ECTODERM TO DEVELOP INTO
KERATOCYTES AND ENDODERM
Layers
Thickness
(in µm)
Composition
Epithelium (Ep) 50
Stratified
Squamous
Epithelium
Bowman's
Membrane (BM)
8-14
Compact layer of
unorganised
collagen fibres
Stroma (SP) 500
Orderly
arrangement of
collagen lamellae
with keratocytes
Descemet's
Membrane (DM)
10-12
Consists of
basement
membrane
materials
Endothelium (En) 5
single layer of
simple squamous
epithelium

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EPITHELIUM:
Stratified, squamous and
nonkeratinized
Three types of cells are seen
a.Superficial cells
b.Wing cells
c.Basal cells
- Germinative layer of the
epithelium
-only epithelial layer with mitotic
activity
- Adhesion is achieved by –
desmosomes And
hemidesmosomes
- Desmosomes are tight
junctions between cells
- Hemidesmosomes are tight
junctions between cell and
basal lamina
- - Langerhans cells (cells of
immune system) present
near periphery. They are
almost absent at central
cornea but aggregate in
response to infection
Epithelial Turnover:
-Early studies suggested that the epithelium replaced
approximately weekly by division of basal cells and the oldest
shed from the surface
-It is now recognized that the germinative region lies at the limbus,
the stem cells, and cells migrate at a very slower rate (123
µm/week) to the center of the cornea which may be as long as a
year

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The XYZ hypothesis:
Thoft R. and Friend J.
(1983) proposed that both
limbal basal and corneal
basal cells are the source
for corneal epithelial cells,
and there is a balance
among division, migration
shedding.
Bowman’s layer: (Ant. Limiting lamina)
- Modified region of anterior stroma
- Acellular homogeneous zone
- 8 – 14 µm thick
- It delineates the anterior junction between cornea and limbus
Compact arrangement of collagen gives it great
strength and relatively resistant to trauma both
mechanical and infective.

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STROMA: (SUBSTANTIA PROPRIA)
Stroma: (Substantia propria)
-About 500 µm thick (about 90% of
corneal thickness)
-Consists of regularly arranged
lamellae of collagen bundles, lie in
proteoglycan ground substance
with –
-200 – 300 bundles – centrally
-500 bundles – peripherally
-Small population of cells –
keratocytes present
-The keratocytes occupy 2.5 – 5 % of total
stromal volume and is responsible for synthesis
and maintaining of collagen proteoglycan
substance of stroma.
-There are stellate processes extending for great
distance and frequent contacts are made with other
keratocytes in same horizontal plane forming gap
junctions

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DESCEMET’S
MEMBRANE: (POST.
LIMITING LAYER)
- It is the basal lamina of
corneal endothelium
- First appears at 2nd month
of gestation and synthesis
continue throughout adult
life
Thickness
at birth :- 3 – 4 µm
at childhood :- about5µm
at adult :- 10 – 12 µm
-It is a strong resistant sheet
-It thickens with age and in some corneal
degenerative conditions
- The peripheral rim of DM is the internal
landmark of corneal limbus and also it is
the anterior limit of drainage angle,
called Schwalbe’ line
- This if too prominent is called posterior
Embryotoxan , condition in which a
thickened and anteriorly displaced
Schwalbe's line is visible on external
examination
Endothelium:
-It is a single layer of hexagonal,
cuboidal cells attached to the
posterior aspect of DM
-It is mesenchymal in origin
-Corneal endothelial cells
production is relatively fixed and
limited
-There is about 0.3% to 0.6%
loss per year
-Cell count keeps reducing with
age and trauma

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Endothelial cells density
- If cells density falls below 500 cells/mm² corneal oedema devlops
and transparency reduced
Endothelium is rich in subcellular organeles –
-large number of mitochondria, both rough and smooth endoplasmic
reticulum, free ribozomes, these reflects that endothelium is extremely
active metabolically
Nutrition to endothelium:
-Endothelium gets its nutrition O₂ from aqueous
-Essential nutrients (such as glucose amino acids) pass across
its surface to supply the cellular needs of all the corneal layers
-It maintains deturgescence of cornea through an active pump
mechanism
-When the hydration of the stroma is ~3.5 mg H2O/mg dry tissue or
less, the stroma is relatively transparent

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Endothelial Repair:
- Physical chemical damage to endothelium results in
loss of cells
- Neighboring cells move over to fill the gap by sliding
process and enlargement of cells occur (polymegathism)
- Thus, after injury, the endothelial cell density falls, the cell
area increases and the cell height decreases
LIMBAL STEM CELLS:
Only 5% to 15% of the cells in the limbus are stem cells
The basal cells of limbal epithelium comprises the limbal
stem cells.
They are the precursor for all other cells of the tissue
They have a self maintaining population
They account for only a small portion of total cells of the
tissue
In vivo,they show slow cycling,but when placed in cell
culture,they demonstrate high potential to proliferate.
They can not be differentiated from rest of the cells
of tissue.

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BLOOD SUPPLY TO CORNEA:
In normal condition, cornea does not contain any blood
vessels
Anterior ciliary artery, a branch of ophthalmic
artery forms a vascular arcade in the limbal
region and helps in corneal metabolism and
wound repair by providing nourishment.
Absence of blood vessel in cornea is one of the
contributing factors for its transparency.
NERVE SUPPLY OF CORNEA:
Density of the nerve ending in
cornea is about 300 times of
that of skin.
The ophthalmic division of the
trigeminal nerve has three
parts: the frontal nerve, the
lacrimal nerve, and the
nasociliary nerve.
The nasociliary nerve provides
sensory innervation to
cornea.

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CORNEAL NUTRITION METABOLISM
Cornea requires energy for normal metabolic
activities as well as for maintaining
transparency and dehydration
Energy is generated by the breakdown of
glucose in the form of ATP
Most actively metabolizing layers are
epithelium endothelium
Sources of Nutrients:
- Oxygen – mainly from atmosphere through
tear film, with minor amounts supplied by the aqueous
and limbal vasculature
- Glucose, amino acid, vitamins, and other nutrients
supplied to cornea by aqueous humor, a lesser amounts
from tears or limbal vessels.
- Glucose also derived from glycogen stores in corneal
epithelium.
- Epithelium consumes O₂ 10 times faster than stroma.

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CORNEAL TRANSPARENCY
The cornea transmits nearly
100% of the light that enters
it. Transparency achieved by
1. Arrangement of stromal
lamellae
Two theories –
i)Maurice (1957): The transparency
of the stroma is due to the lattice
arrangement of collagen fibrils.
He explained, because of their
small diameter and regularity of
separation, back scattered light
would be almost completely
suppressed by destructive
interference
ii) Goldman et al. (1968):
Proposed that lattice
arrangement is not a
necessary factor for stromal
transparency . Cornea is
transparent because fibrils
are small in relation to light
and do not interfere with light
transmission unless they are
larger than one half of a
wavelenght of light(2000 A).
Both theories failed to explain
why there is corneal clouding
with raised IOP and why there
is corneal clearing on
reduction of IOP.
Other factors of corneal transparency –
2. Corneal epithelium tear film
• Epithelial non-keratinization
• Regular uniform arrangement of corneal epithelium
•Junctions between cells its compactness and also
tear film maintain a homogenicity of its refractive index
3. Relative deturgescence state of normal cornea.
4. Corneal avascularity
5. Non myelenated nerve fibres

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Signs of Corneal Disease
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 like
Rosacea.
Dry-eye syndrome.
Blepharitis.
Acute bacterial conjunctivitis.
Trauma.
Exposure keratopathy from poor eyelid
closure.
Ultraviolet or chemical burn.
Contact lens-related disorder such as
toxicity or tight lens syndrome
2.Punctate epithelial keratitis
It is the hallmark of viral infections.
Swollen epithelial cells
Stains with Rose Bengal, till break
down occurs
Can occur in
1. A viral infection.
2. A bacterial infection (including
trachoma)
3. Dry eyes.
4. Strong chemicals splashed in the
eye.
5. Exposure to ultraviolet light
(sunlight, sunlamps, or welding
arcs)
6. Prolonged use of contact lenses.
7. An allergy to eye drops.

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3. Corneal Ulcer is relatively
a corneal epithelial defect
with underlying inflammation
(which soon results in
necrosis of corneal tissue)
due to invasion by bacteria,
fungi, viruses, or
Acanthamoeba. It can be
initiated by mechanical
trauma or nutritional
deficiencies
Signs of Corneal Disease
4. Epithelial Oedema
Sign of Endothelial
decompensation
Severe acute elevation of IOP
Endothelial Dystrophy
5. Filaments
Small coma shaped mucus
strands lined with epithelium.
One end attached with
epithelium
Common in Dry eye disease

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6. Pannus( Chronic
Superficial Keratitis)
Inflammatory or
degenerative in-growth of
fibro vascular tissue from
limbus
No known cause for its
formation
May be caused by chronic
inflammation like in Contact
Lens wearers, Viral
Keratitis, Trachoma and as
congential abnormality.
Signs of Corneal Disease
Stromal Lesions
1.Infiltrates
Focal areas of active stromal
inflammation
2. Oedema
Increased corneal thickness
Decreased transparency
3. Vascularization
Lesions of Endothelium
Endothelial Dystrophy/
Degeneration
Reduced cell count
Epithelial oedema

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“STUMPED” Classification
(Congenital)
S – Sclerocornea
T – Tears in descemet’s membrane
U – Ulcer
M – Metabolic (rarely present at birth)
P – Posterior corneal defect
E – Endothelial dystrophy- usually
effects at a later age
D- Dermoid
SCLEROCORNEA
TEARS IN DESCEMETS
MEMB
POSTERIOR CORNEAL
DEFECT
LIMBAL DERMOID

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Bacterial keratitis
Fungal keratitis
Viral keratitis
Microbial Keratitis Predisposing Factors
The pathogens able to produce corneal infection
in the presence of an intact epithelium are
Neisseria gonorhoae,
Corynebacterium diphtheriae,
Listeria sp. and
Haemophilus sp.
Other bacteria are capable of producing
keratitis only after loss of corneal epithelial
integrity
Bacterial Keratitis

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Predisposing Factors for Epithelial breaks
1.Contact lens wear.The infection is often caused by
pseudomonas aeruginosa which requires an epithelial
defect for corneal invasion.Such defects occur in all
contact lens wearers at times.
2.Ocular surface disease which disrupts defence
mechanisms, such as
trauma,
bullous keratopathy,
corneal exposure,
dry eye and
diminished corneal sensation.
Bacterial Keratitis Clinical Features
1.Staph. aureus and
Strep.pneumoniae tend to
produce oval, yellow-white,
densely opaque stromal
suppuration surrounded by
relatively clear cornea.
2.Pseudomonas typically causes
thick mucopurulent exudate, diffuse
liquefactive necrosis and semi-
opaque “ground-glass” appearance
of adjacent stroma. The infection
may progress rapidly and result in
corneal perforation within 48 hours
3.Enterobacteriacea usually
causes a shallow ulceration,
grey-white pleomorphic
suppuration and diffuse stromal
opalescence.
Bacterial Keratitis

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Management
A bacterial corneal ulcer is a sight-thereatening
condition demanding urgent identification and
eradication of the causative organism. This is best
performed with the patient hospitalized
Bacterial Keratitis
Clinical Features
1.Flamentous fungal keratitis is most
prevalent in agricultural areas and
typically preceded by ocular trauma,
most frequently involving organic
matter such as wood.
2.Candida keratitis usually develops in
association with pre-existing chronic
corneal disease or in an
immunocompromised or debiliated
patient. It is characterized by a yellow-
white ulcer associated with dense
suppuration
Fungal Keratitis

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Viral Keratitis
Herpes Simplex Keratitis
Herpes Zoster Keratitis
Herpes simplex virus
(HSV) is a DNA virus with
humans as the only host.
Infection with HSV is extremely
common and about 90% of the
population are seropositive for HSV
antibodies.
Primary ocular infection
Recurrent ocular infection
-Dendritic ulcer
-Disciform keratitis(endothelitis)
Herpes Simplex Keratitis

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Herpes simplex keratitis
Primary ocular infection
Recurrent ocular infection
-Dendritic ulcer
-Disciform keratitis(endothelitis)
Primary ocular infection
typically occurs in children
between the ages of 6 months
and 5 years
1.Blepharoconjunctivitis is usually
benign and self limited and, in
children, it may be the only
manifestation of primary herpetic
infection.
2.Keratitis is uncommon. It is
characterized by fine epithelial
punctate keratitis which may be
transient.
Herpes Simplex Keratitis
Primary Ocular Infection

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Sign in chronological order
a)Early cases shows opaque cells
arranged in a coarse, punctate
or stellate pattern
b)Following central
desquamation a linear-
branching ulcer begins to form.
The bed of the ulcer stains with
fluorescein.
c)Occasionally, the continued
enlargement of a dendritic ulcer
leads to much larger epithelial
defect which has a geographical
or “amoeboid” configuration
Herpes Simplex Keratitis
Dendritic Ulcer
Disciform Keratitis
Herpetic disciform keratitis is a
primary endotheliitis resulting in
both stromal and epithelial edema
in a round (disciform) distribution
with keratic precipitates underlying
the area of edema. The corneal
edema and keratic precipitates
appear to be out of proportion to
the degree of anterior chamber
inflammation, in contrast to uveitis
with secondary corneal
decompensation.
Disciform keratitis may be caused
by both herpes simplex and
herpes zoster viruses.

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Herpes zoster is a common infection caused by human herpes
virus
Usually occurs in infected individuals who have had Chicken Pox in
past
Virus lies dormant in Ganglions and erupts in compromised
individuals
Approximately 15% of all cases of herpes zoster affect the
ophthalmic division of the trigeminal nerve
Herpes Zoster Ophthalmicus
1.The Rash (one side of midline)
2.Conjunctivitis
3.Acute Epithelial Keratitis,
4.Dendritic Epithelial Lesions
5.Nummular Keratitis
5.Disciform Keratitis
6.Anterior Uveitis
6.Secondary Glaucoma
Serious Eye involvement if
nasociliary branch affected-
Vesicle on side of nose/
Hutchinson’s Sign
Peripheral Corneal Lesions
Dellen: saucer like thinning of peripheral cornea
causes: raised limbal lesion, use of hard
contact lenses/ dehydration, ideopathic in
elderly
Necrotising Keratitis: Herpes Simplex, Rare in
Zoster
Marginal Keratitis ( Catarrhal Ulcer): supposed to
be hypersensitivity reaction to staph exotoxins
Common with chronic ulcerative blepharitis
Starts as subepithelial infiltrate spreading
circumferentially and finally epithelium breaks
down to form an ulcer

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PRINCIPLES OF TREATMENT OF CORNEAL ULCER
1. IDENTIFICATION OF CAUSATIVE AGENT-
CLINICAL PATHOLOGICAL(CS DISCHARGE/
SCRAPING)
2. ANTIBIOTICS/ CAUTERISATION
3. REST TO PART- RELIEVE PAIN- PROTECT
FROM PERFORATION- PB, CYCLOPLEGIA,
BCL(BANDAGE CONTACT LENS)
4. RESTORATION OF VISION-
GLASSES/TATTOOING/CORNEAL GRAFT
5. THERAPEUTIC CORNEAL GRAFTING FOR
NON HEALING ULCERS
Rosacea keratitis:
•In association with skin lesion on face
•Usually between 30-50 yr age,
•In females commonly
•Symmetrical distribution on face
•Unknown reason
•Increases with stress, alcohol and tobacco
consumption
•Common in fair skin persons
•Three stages:
•1- Erythema;
•2- papules/pustules;
•3- nodules and furunculoid lesions;
•Rhinophyma(rare, most advanced form)
•Corneal involvement: Punctate
keratitis/Peripheral vascularisation/gross
ulceration/ thinning
•Emollients, Immune modulators,
vasoconstrictors applied locally
•Oral antibiotics Doxy/ Metronidazole

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Phlyctenular keratoconjunctivitis:
•also known as phlyctenulosis
•is an inflammatory syndrome
caused by a delayed hypersensitivity
reaction to one or more antigens.
•The triggering antigen is usually a
bacterial protein particularly from
Staphylococcus aureus but may also
be a virus, fungus (particularly
Candida albicans or Nematode.
•Initially was considered a
hypersensitivity reaction to tubercular
protein alone.
•It may be in association with
conjunctival lesion or may occur
astride limbus
•May ulcerate rarely
KERATITIS IN SYSTEMIC COLLAGEN DISEASES
Cornea is affected in systemic
collagen diseases like
Rheumatoid Arthritis, SLE,
Polyartritis Nodosa, Wegner
Granulomatosis
Presentation can be Sclerosing
Keratitis, Peripheral Corneal
Thinning, Stromal Keratitis,
Peripheral Ulcerations, Corneal
Melting
A tongue shaped corneal opacity
with apex towards center, and a
clear margin from limbus,
corresponding scleritis nodule
present

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Keratoconus (conical
cornea) is a fairly
common, progressive
disorder in which the
cornea assumes an
irregular conical shape.
The hallmark of keratoconus is
central or paracentral stromal
thinning, apical protrusion and
irregular astigmatism.
The onset is at around puberty and
progresses slowly thereafter,
although it may become stationary
at any time
Corneal Ectasias
Keratoconus
1. SPECTACLE CORRECTION
2. CONTACT LENSES
3. PENETRATING KERATOPLASTY
FOR PROGRESSIVE LESION
AND SCARRING
4. C3R( CROSS LINKING WITH
RIBOFLAVIN) PROCEDURE
Treatment
Decreased visual acuity
Rizutti’s sign
Munson sign
Fleischer ring
Corneal scarring
Features
Keratoglobus (from Greek kerat
o- horn, cornea;
and Latin: globus round), is a
degenerative non-
inflammatory disorder of the
eye in which structural changes
within the cornea cause it to
become extremely thin and
change to a more globular shape
than its normal gradual curve. It
causes corneal thinning, primarily
at the margins, resulting in a
spherical, slightly enlarged eye.

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Chemical Burn : Acid or Alkali
Corneal Burns- Chemical Corneal Burns- Chemical

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Flash Burn :
•caused by ultraviolet light from
various sources
•sunlamp in salon
•reflection of the sun off the
snow at high elevation (snow
blindness)
•photographer's flood lamp
•lightning that strikes close to
you
•halogen lamp
•welding torch
•direct sunlight
• many times presentation is pain
redness and diminished vision,
after 6-8 hrs of exposure leading
to SPK
CORNEAL DEGENERATION
corneal degeneration refers to the condition in
which the normal cells undergo some
destructive changes under the influence of age
or some pathological/metabolic conditions.

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The corneal dystrophies are a group of
progressive, usually bilateral and mostly
genetically determined corneal opacifying
disorders which develop in the absence of
inflammation.
Corneal Dystrophies DEGENERATION VS DYSTROPHY
• Non - Hereditary and Non -Familial
• Usually Unilateral to start
• Mostly Peripheral
• Commoner than Dystrophy
• Vascularity and Inflammation may be
present

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Corneal
degenerations
Depending
upon
etiology
Age -Related
Pathological
Degeneration
Depending
upon
location
Axial
Peripheral
6
5
Corneal Degeneration Depending upon Location
2. AxialCornealDegenerations
a) FattyDegenerations
b) HyalineDegenerations
c) Amyloidosis
d) CalcificDegenerations
(Band Keratopathy)
e) Salzmann’sNodular
Degeneration
1.Peripheral Degenerations
a) ArcusSenilis
b) Vogt’sWhite LimbalGirdle
c) Hassall–Henle Bodies
d) Terriens’sMarginalDegeneration
e) Mooren’sUlcer
f) PellucidMarginalDegeneration
g) FurrowDegeneration(Senile
MarginalDegeneration)

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Depending upon Etiology
I. AgeRelatedDegenerations
a) ArcusSenilis
b) VogtsWhite LimbalGirdle
c) Hassal- HenleBodies
d) MosaicDegenerations
II. PathologicalDegenerations:
a) FattyDegeneration
b) Amyloidosis
c) CalcificDegenerations (
BandShaped
Keratopathy)
d) Salzmann’sNodular
Degeneration
e) Terrien’sMarginal
Degeneration
f) Mooren’sUlcer
g) PellucidMarginal
Degeneration
h) FurrowDegenerations
i) SpheroidalDegeneration
•ARCUSSENILIS
•It is the annular lipid infiltrations of
the corneal periphery seen in the
elderly.
Age – related degeneration occurring
bilaterallyin60%ofpeopleaged40to60
years.
•Andalmostallindividuals agedover
80years.
•Doesnotaffectvision
AGE RELATED
• Commencesasacrescentric greyor
white arc in the superior and
inferior quadrantandprogressesto
form a ring around thec
ornea,
• 1mm wide ring
• Lucidinterval of Vogt’s–the clear
zonewhich separatesthe ring of
opacityfromthe limbus.
• Peripheral border issharpandinner
borderis diffuse.
• Lipid deposits are found

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ARCUS JUVENELIS
•Similarto ArcusSenilisbut occursin individuals agedless
than 40years.
•Rarecondition
•Associatedwith Hypercholesterolemia
•Diagnosticfeature: Presenceof aline of clear cornea
between opacity andlimbus.
Vogt’s White Limbal Girdle
Agerelated which appearsasa
• Bilateral
• Chalky white opacities in the
inter - palpebral area both
nasally andtemporally.
• Opacity in the Bowman's
Membrane.

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• Drop shapedexcrescencesof
hyalinematerial projecting
into the anterior chamber
around the corneal
periphery
• Arisefrom Descemet’s
membrane
• Commonestsenile change.
• In pathological changes,they
becomelarger and invade the
central areaand theconditions
iscalled ‘CornealGuttata’.
Hassal- HenleBodies Mooren’s Ulcer :
Mooren’s ulceration is characterized by painful
peripheral corneal ulceration of unknown
etiology.
The disease generally begins with intense limbal
inflammation and swelling in the episclera and
conjunctiva.
Corneal changes begin 2-3 mm from the limbus,
first appearing as grey swellings that rapidly
furrow, affecting the superficial one-third of the
cornea and then proceeding circumferentially
and centrally over 4-12 months.
The bed of the furrow becomes vascularized,
with vessels advancing into the base of the
undermined edges of the ulcers
These ulcers are crescent-shaped and can
leave behind either an opaque, edematous
central cornea or alternatively, they can
completely consume the corneal stroma and
replacing it with a thin fibrovascular membrane

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Pellucid marginal degeneration (PMD),
is a degenerative corneal condition,
often confused with keratoconus.
It is typically characterized by a clear,
bilateral thinning in the inferior and
peripheral region of the cornea
Although some cases affect only one
eye.
The cause of the disease remains
unclear.
The term pellucid marginal
degeneration was first coined in 1957
by the ophthalmologist Schalaeppi.
The word pellucid means clear,
indicating that the corneas retain clarity
in pellucid marginal degeneration
1.Anterior dystrophies
-Microcystic (Cogan)
-Reis-Büclers
-Meesmann
-Schnyder
2.Stromal dystrophies
-Lattice I,II, III
-Granular I,II, III
-Macular I, II
3.Posterior dystrophies
-Fuchs endothelial
-Posterior polymorphous
Corneal Dystrophies

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CORNEAL TRANSPLANT/ GRAFTING
Corneal transplantation, also known
as corneal grafting, is a surgical
procedure where a damaged or diseased
cornea is replaced by donated corneal tissue
(the graft).
The graft is taken from a recently dead
individual with no known diseases or other
factors that may affect the chance of
survival of the donated tissue or the health
of the recipient or can be a Bioengineered
Graft Tissue.
When the entire cornea is replaced it is
known as Penetrating Keratoplasty and
when only part of the cornea is replaced it is
known as Lamellar Keratoplasty.
Keratoplasty simply means surgery to the
cornea.
Lamellar Keratoplasty can also be Deep
Anterior Lamellar Keratoplasty(DALK) or
Endothelial Keratoplasty(EK).
There are three forms of EK.
Deep Lamellar Endothelial
Keratoplasty (DLEK) in which the
posterior part of the recipient
cornea is replaced by donor tissue.
Descemet's Stripping (Automated)
Endothelial Keratoplasty
(DSEK/DSAEK) in which the
diseased Descemet’s membrane is
removed and replaced by a healthy
donor posterior transplant.
Descemet Membrane Endothelial
Keratoplasty (DMEK) is the most
recent EK technique in which an
isolated Descemet membrane is
transplanted.

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Examination Of Corneal opacity -
Overview
Clinical History
Clinical Evaluation Of Cornea And External Eye
Bedside Tests
Laboratory Investigations And Corneal Imaging
Evaluation Of Visual Potential And Prognostication
APPROACH TO A CASE OF CORNEAL
OPACITY
HISTORY
Congenital or Acquired
Onset and duration
Unilateral or bilateral
Trauma or chemical injury
Recurrent episodes of pain and redness
Long term topical medication
Contact lens use
Previous ocular surgery
Systemic illness

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Symptoms
Diminution of vision
Pain,
Redness
Photophobia
Examination
Adenexa
Congestion- Presence/absence/Conjunctival/Corneal
Grading
Appearance: demarcated/ diffuse/sharp/dirty
Sensations/ Tenderness
Depth of Opacity
Anterior Chamber Reaction
Pupil Size/reaction
Lens for Cataract/ Position
Intra ocular Pressure

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Grading the Opacity
Nebular: faint opacity due to
superficial scar involving bowman’s
layer and superficial stroma
Macular: Semi dense opacity d/t scar
involving half of stroma.
Leucomatous: Dense white opacity
d/t scarring ofmore than half of stroma
Examination of Corneal Opacity- Tear
Film Evaluation
Tear Film
Function Test
TBUT
Schirmer’s test
Tear Meniscus
Height
Tear Clearance
rate
Tear Osmolarity
And
Composition

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