Corneal edema occurs when the cornea swells and increases in thickness due to an abnormal accumulation of fluid in the stroma. The key causes of corneal edema include mechanical trauma, glaucoma, contact lens overuse, endothelial dystrophies, and bullous keratopathy. Corneal edema is evaluated using slit lamp examination, pachymetry, and imaging modalities like OCT and specular microscopy which measure corneal thickness and endothelial cell density. Treatment depends on the underlying cause but may include controlling IOP, removing contact lenses, or performing keratoplasty in severe cases.

1. CORNEAL EDEMA
Dr. Kishore Khade

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

3. 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.

4. 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.

5. 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.

6. stromal barrier
pressure
Hydration
IOP
Na-k
pump
Evaporation

7. {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.

8. 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

9. {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.

10. 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.

11. {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.

12. Sodium activity across
endothelium
stroma
Na-K pump
Na 134
meq/l
Aqueous
humour

13. • 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).

15. Wounded
cornea 142.3meq/l
Aqueous
NA humour
149.8
Meq/l
H2O

16. {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.

17. {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.

18. EDEMA
• Word edema is derived from greek word
oídēma 1400bc , means "swelling“.
• Formerly known as dropsy or hydropsy which
means accumulation of excessive fluid.
• Etiology of corneal edema:
 SECONDARY CAUSES
 PRIMARY CAUSES

19. CORNEAL EDEMA

20. [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.

21. DESCEMET’s TEAR

22. 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.

23. Brown Mclean Syndrome

24. 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.

25. [ 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.

26. GLAUCOMA

27. 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).

28. [ 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 Sattler’s veil.

29. Contd....
• If allowed to continue, it‘ll cause stromal
edema, descemet’s 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.

30. [IV] ICE syndrome
• Iridocorneal endothelial syndrome is basically
spectrum of disorders that includes
A) Progressive iris atrophy.
B) Chandler’s syndrome.
C) Iris nevus syndrome ( Cogan Reese)

31. 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.

32. 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.

33. 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

34. [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.

35. 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 Fuch’s
dystrophy.

36. [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.

37. PRIMARY CAUSES
A) Primary endothelial dystrophies: dystrophies
involving endothelium & descemet’s
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 fuch’s dystrophy.

38. 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
descemet’s membrane & endothelium is
present, it presents with congenital corneal
edema.

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

40. FUCH’s 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.

41. 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.

42. 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.

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

44. 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.

45. 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.

46. Coloured haloes

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

48. Slit lamp examination
Slit lamp examination reveals
cornea guttata, stromal
density,
Descemet’s 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.

49. 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.

50. Pachymetry

51. Pachymetry
• Corneal pachymetry;- is the process of measuring
the thickness of the cornea. It can be done using
contact methods, such as ultrasound and 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).

52. 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.

53. 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.

54. 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

55. 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.

56. 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.

57. 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 .

58. 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 bowman’s membrane.
• This produces adhesion between stroma &
basal layer of epithelium preventing formation
of bullae.

59. 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.

60. 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.

61. keratoplasty

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

63. Keratoprosthesis

64. THANKYOU