Corneal oedema

cornea
Thickness of the cornea in
the centre is 0.52mm
While at periphery is
0.67mm.
Epithelium is 50-90m
thick
BM 8-14m
Stroma 0.5mm thick &
constitute most of cornea.
Dm is 10-12m
Endothelium 18-20m
with 2400-3000cells/mm2

CORNEA
To perform its primary function of refraction
of light the cornea must be relatively thin &
dehydrated with smooth anterior surface.
In normal cornea, optical transparency is
directly related to the state of hydration of
the tissue.
If cornea swells, it increases its thickness ,
its surface becomes irregular both changes
downgrades its optic properties.

CORNEAL HYDRATION
Cornea is relatively in dehydrated state
for its transperancy.
Water content of cornea is 80% which is
highest of any connective tissue in body.
If hydration becomes above 80% its
central thickness increases &
transperancy reduces.
Cornea swells only in the direction of its
thickness therefore, corneal thickness &
hydration are linearly related.

CORNEAL HYDRATION
Hydration is maintained by:A}Factors draw water in to the cornea:1)Swelling pressure of stromal matrix
( GAGs).
2)Intraocular pressure.
B} factors which prevent flow of water
into the cornea:1)Mechanical barriers.
2) Na+-K+ active pump of endothelium.

stromal
pressure

Na-k
pump

barrier

Hydrati
on

IOP

Evaporation

{A} Stromal swelling

pressure
Pressure exerted by corneal stroma
mainly GAGs is stromal pressure (SP).
Sp is 60 mmhg, is a keystone of
corneal biophysics.
Anionic charges on GAGs molecule
expands the tissue, draws fluid with
equal but negative pressure called
imbibation pressure.

Contd.....
In vivo imbibation pressure is reduced by
IOP, so IP= IOP SP
IP= 17- 60, IP = -43mmhg.
In vitro IP = SP
Sp generates interfibrillar tension may
be biophysical mechanism to maintain
fibrils normal arrangement.
Cornea has an swelling pressure, which
is maintained by endothelial metabolic
pump

{B} Barrier mechanism

Both epithelium & endothelium acts
as a barrier for excessive flow of water
& diffusion of electrolytes into stroma.
As compare to endothelium,
epithelium offers twice resistance.
Endothelium allows diffusion of small
solutes like NaCl & urea, while
epithelium produces hypertonicity of
the solution bathing the cornea.

Barrier mechanism
Endothelial cells are attached to each
other by discontinuous tight
junctions i.e maculae occludentes.
Endothelial barrier function is mainly
calcium dependent.
A calcium free solution will reduce
the barrier function & cause stromal
edema.

{C} Na - K pump
+

Present in endothelium, several fold more

active than its epithelium counterparts.
Activated ATPase mediates active
extrusion of Na from stroma to the
aqueous.
It causes diffusion gradient for water.
Na conc in aqueous is more compare to
stroma, which draws water from the
stroma.

Sodium activity across

endothelium
stroma
Na 134
meq/l

Na-K pump

Aqueous
humour

 Bicarbonate dependent ATPase has also

been reported in the endothelial cells.
Depletion of bicarbonates induces
swelling.
Carbonic anhydrase enzyme has also
been implicated in fluid transport, CAE
inhibitors decreases flow of fluid from
stroma to aqueous ( found only in
endothelium).

Wounded
cornea

142.3meq/l
Aqueous
humour

NA
149.8
Meq/l
H2O

{D} EVAPORATION
Evaporation of water from precorneal
tearfilm increases its osmolarity
relative to cornea.
Hypertonicity of tear film could draw
water from cornea.
However this water loss is readily
replaced by aqueous, it results in
only a little corneal dehydration.

{E} Intra ocular pressure

Most of early writers assume corneal
edema is due to mechanical forcing of
aqueous into the cornea.
But experimental event found out that
to achieve this,effect pressure required
is 200mmHg.
More likely explanation is that the
determining factor is endothelial
damage.

EDEMA
Word edema is derived from greekword
odma 1400bc , means "swelling.
Formerly known as dropsy or
hydropsy which means accumulation
of excessive fluid.
Etiology of corneal edema:
SECONDARY CAUSES
PRIMARY CAUSES

CORNEAL EDEMA

[I] Mechanical trauma

1) Blunt non penetrating injury causes
edema by injury to endothelium, mostly
it is reversible.
2) Perforating injuries cause direct
damage to the cornea, intra ocular FB in
AC can cause edema mainly in inferior
periphery where FB mainly settles.
3) Forceps delivery cause pressure on
globe, may cause edema due to DM
tear.

DESCEMETs TEAR

Mechanical trauma
4) Noxious chemicals mainly alkalies which
penetrates cornea cause endothelium
damage.
5)Intraocular sx can cause acute endothelial
loss most notably in superior & central
cornea.
6) BROWN McLEAN syndrome: peripheral
edema with brown black discolouration of
underlying endothelium seen in ICCE,
ECCE,CCPE, pars plana vitrectomy.

Brown Mclean Syndrome

Mechanical trauma
7)Cold induced reversible corneal edema has
been reported in trigeminal nerve
dysfunction.
8) Certain systemic medications like
amantadine & cefaclor can cause edema.
9) Lasers used for iridotomy can cause focal
corneal edema.
10) High altitude corneal decompensation has
been reported causing hypoxia induced
corneal edema.

[ II ] GLAUCOMA
Acute rise in IOP which exceeds swelling
pressure of stroma causes epithelial
edema.
Hypoxic Endothelial decompensation
occurs due to diminished aqueous flow.
When corneal endothelium is compromised,
edema occurs even @ lower level of IOP.
Chronic elevation of IOP permanently
damages the endothelium.
Irreversible corneal edema may occur.

GLAUCOMA

GLAUCOMA
Penetrating keratoplasty is the only
treatment of choice in irreversible corneal
edema, but IOP must be first controlled.
In hypotony, AC is shallow or flat. Mechanical
trauma by cornea iris or iris corneal touch
leads to edema.
Normal human volunteers experiment study
can be explained by hypotony induced
edema,
(corneal edema occurs in tightly patched eye).

[ III ] Contact lenses

Most common cause of corneal edema is
prolonged use of contact lens.
It is mainly due to insufficient supply of
oxygen to epithelium.
Edema presents as microcystic epithelial
edema near the center of resting
position of the lens.
It is best seen with scattered
illumination of slit lamp referred as
Sattlers veil.

Contd....
If allowed to continue, itll cause stromal
edema, descemets membrane folds.
Edema easily clears if contact lens is
removed.
Even altering the fit of contact lens is also
successful in reducing edema if it provides
sufficient oxygen to the epithelium.
The response & recovery from edema is
independent of age.

[IV] ICE syndrome

Iridocorneal endothelial syndrome is
basically spectrum of disorders that
includes
A) Progressive iris atrophy.
B) Chandlers syndrome.
C) Iris nevus syndrome
( Cogan Reese)

Chandler syndrome
Corneal endothelial abnormalities
(hammered silver).
Presents with blurred vision & haloes
due to corneal edema
Corectopia may be mild to moderate
Glaucoma may be less severe & but at
presentation IOP may be normal.
Chandler syndrome have more severe
edema.

Cogan Resse syndrome

Characterised by diffuse
naevus Which covers
iris or iris nodule.
Iris atrophy may be
absent in
50% of patients,
but corectopia &
Glaucoma
May be severe.

Iris atrophy
Essential iris atrophy
characterised by distortion
Of pupil, peripheral anterior
synechie & iris atrophy
With full thickness holes.
Glaucoma commonly
present in the involved eye.
Unilateral occurs in 4th & 5th
Decades of life in caucasians

[V] Essential corneal

edema
Idiopathic , episodic & often cyclic may be
unilateral.
Presents with typical features of corneal
edema like fb sensation,diminished vision &
haloes which persists for months then
disappears.
Recurrent erosions on cornea may be noted.
It may progress to the formation of bullae
with ciliary injection & urgent symptoms of
pain & photophobia.

Essential corneal edema

Pupils may be semidilated &
sluggishly reacting to light.
If secondary infection does not set up
attack passes of & the condition
eventually cleans up.
Some of these cases may be early
presentation of dystrophic changes
like Fuchs dystrophy.

[VI] Metabolic disorders

Some vague concepts suggested by
corneal edema occuring in some
metabolic conditions like myxedema.
It has also seen in hypercholesterolemia.
In malaria mainly in patients taking
mepacrine for its treatment, in this
condition edema is limited to basal layer
of epithelium & superficial layer of
stroma.

PRIMARY CAUSES
A) Primary endothelial dystrophies:
dystrophies involving endothelium &
descemets membrane causes
symmetrical marked stromal edema
which is gradually progressive over a
period of years.
B) Primary endothelial dystrophy which
develop later in life are fuchs
dystrophy.

Primary Endothelial
Dystrophy
Congenital hereditary endothelial
dystrophy: characterised by diffuse edema
at birth or soon thereafter, without
significant anterior segment
abnormalities.
Posterior polymorphous dystrophy: B/L
vesicular or linear lesions at the level of
descemets membrane & endothelium is
present, it presents with congenital
corneal edema.

FUCHs dytrophy
AD pattern of inheritance,
Earliest changes are limited
To posterior cornea &
presents with central B/L
asymmetrical corneal
Guttata.
In fuchs dystrophy
endothelial cells transform
into fibroblast
Like cells capable of
secreting collagen fibrils.
Contribute to BM thickening.

FUCHs dytrophy
Progressive endothelial decompensation
leads to stromal & epithelial edema.
Fluid in the stroma permeates the
epitelial layer causes microcystic
epithelial edema.
Individual epithelial cells burst,
intercellular edema occurs & typical
blisters or bullae formed.
These changes are confined to centre of
cornea initially.

Bullous keratopathy
It represents the terminal
stage of severe or
Prolonged epithelial
edema.
In the affected area the
epithelium is steamy
Irregular & on its surface
one or more large bullae
Appears, raised in the
form of blebs.

Bullous keratopathy
After 2-3 days the bullae rupture only to
reappear, the cycle associated with
considerable irritation & pain.
Treatment is extremely difficult; retrobulbar
injection of alcohol, removal of endothelium
by scraping, cauterisation of cornea by
tincture iodine, trichloro-acetic acid.
Bandage contact lens to relieve pain.
Lamellar grafting, if measures of therapy
fails & if recurrence persists treatment is
enucleation.

Manifestations of edema
Depends upon cause & degree of the
condition.
Mild discomfort in conditions like
fuchs dystrophy.
Severe neuralgic pain is seen in
bullous keratopathy.
Colour haloes.
Severe visual loss.

Visual acuity
Small amount of epithelial edema can
result in substantial reduction in visual
acuity.
Although 70% stromal edema is
compatible with normal visual acuity.
Decreased acuity is more severe in early
morning.
IOP, iritis glaucoma & optic nerve changes
may contribute to reduced acuity.

Pain & discomfort

As edema increases epithelium is
detached from basement membrane to
form bullae.
This rupture of bullae causes severe
pain, photophobia, epiphora &
narrowing of palpebral fissure.
Photophobia is due to light scattering in
the edematous cornea.
Coloured haloes.

Coloured haloes

Evaluation of corneal
morphology
Slit lamp examination.
Specular biomicroscopy.
Pachymetry.
Optical coherence tomography.
Scheimpflug camera.
Orbscan.

Slit lamp examination

Slit lamp examination reveals
cornea guttata, stromal
density,
Descemets membrane folds.
Bullae are easily observed by
slitlamp. In case of chronic
Corneal edema
neovascularization,pannus
formation or dystrophies
are visible. In case of stromal
edema thickness exceeds 0.6mm.

Specular biomicroscopy
Measures cell density.
Normally endothelial
cell count is 3000 -2000 cells/mm2.
Cell count less <1000
poorly tolerate ocular
Surgery.
Used in assesing cells
in Corneal grafting,
LASIK, dystrophies
corneal edema.

Pachymetry

Pachymetry
Corneal pachymetry;-is the process of
measuring the thickness of the cornea. It can
be done using contact methods, such as
ultrasoundand confocal microscopy
(CONFOSCAN), or noncontact methods such
as optical biometry with a single Scheimpflug
camera (such as SIRIUS or PENTACAM), or
Optical Coherence Tomography (OCT) and
online Optical Coherence Pachymetry (OCP,
such as ORBSCAN).

Optical coherence
tomography

Optical coherence tomography

is an established
medical imaging technique.
It is widely used to obtain
high-resolution images
of the retina and the
anterior segment of the eye.
Corneal thickness can also be
measured.

Scheimpflug camera.
Pentacam trade name,
Is a diagnostic unit able
To perform five functions;
Image of AS.
3D anterior chamber
analyzer.
pachymetry.
Corneal topography.
Cataract analyzer.

ORBSCAN
II
The Orbscan II topographer
analyses the physical
shape / contours of
cornea and allows the surgeon
to decide if it has suitable
shape, is healthy and thick
enough for treatment.
It is the only
topographer currently available
that measures the shape of both
the front and back surface of the
entire cornea (other systems
only measure the front surface)
and can therefore provide
acomplete picture of the thickness of cornea

management
In all cases of corneal edema if documented IOP
is high, its control with topical anti glaucoma
drugs or systemic CAE inhibitors are given.
Even in moderately elevated IOP patients
control may significantly reduces epithelial
edema.
If IOP remains elevated despite maximum
tolerated medical therapy surgical intervention
must be considered.
Cyclocryotherapy/ trabeculectomy are
considered.

Local therapy
Early morning reduced vision can be
improved by exposing eyes to warm air
eg:hair dryer.
Topical application of hyperosmotic
agents like 5%NaCl solution or ointment
can reduce edema to an little extend.
If inflammation is a contributory cause of
corneal edema topical application steroids
may be very helpful.

Local therapy
If the etiology of edema is not
apperent 10 days course of topical
steroids can serve as diagnostic as
well as therapeutic purpose.
In patients with early corneal
decompensation & mild edema a
careful refraction may improve vision.
Therapeutic hydrophilic contact lens
can be used .

Local therapy
Thin hydrophilic lens fitted flat on
cornea allow maximum contact
between lens & irregular cornea.
Application of radiodiathermy or other
forms of electrocautery on bowmans
membrane.
This produces adhesion between
stroma & basal layer of epithelium
preventing formation of bullae.

management
Gundersen conjunctival flap with or
without lamellar keratectomy can be
performed to relieve pain.
Retrobulbar alcohol injection or
tarsorrhaphy also may relieve pain.
In painful blind eye or in absolute
glaucoma enucleation may represent
the optimal procedure.

Penetrating keratoplasty
If visual recovery exists penetrating
keratoplasty is performed before
cauterisation of BM or conjuntival flap
procedure.
In case of multiple graft failure & corneal
thickness exceeds 1.5mm, the use of
keratoprosthesis has been advocated.
Keraoprosthesis is considered as an last
ditch effort for visual rehabilitation.

keratoplasty

Keratoprosthesis
Keratoprosthesis causes
high rate of failure &
Complications.
In case of bilateral corneal
edema
Keratoprosthesis in worst
eye & keratoplasty in
fellow is
Performed.

Keratoprosthesis

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