Recurrent corneal erosions yy Dr.Haridas

1. Recurrent corneal
erosions and PTK
DR.HARIDAS

2. Brief History
 This clinical entity was first described by HANSEN in the year
1872 and he named it “intermittent neuralgic vesicular
keratitis”
 the term recurrent corneal erosions was coined by Von Artl
in 1874
 Both recognized antecedent trauma
 Vogt in 1921 described fine white dots on Bowman’s layer ,
fluorescein staining lines , and an irregular epithelial surface
with localized odema using slit lamp

3.  Chandler classified recurrent corneal erosions into 2 main forms
 Chandler’s microform erosions in which minor episodes which
usually last from few minutes to hours and show no obvious
epithelial defect
 Chandler’s macroform erosions are severe episodes may persist
over several days and associated with intolerable pain decreased
vision and photophobia , a frank epithelial defect in slit lamp
examination

4.  Recurrent erosions of the corneal epithelium is a clinical
syndrome of multiple etiologies , characterized by
inadequate epithelial-stromal attachments, resulting in
episodic dys-adhesions and defects of the corneal
epithelium
 The condition occurs across all ages , however the
average age is the mid-fifth decade with a slight female
predominance

6.  The corneal epithelium is firmly adherent to underlying
Bowman layer and stroma by specialized attachment
complexes
• comprised of hemidesmosomes of the basal cells
• Cell adhesion molecules – integrin
• Anchoring fibrils of type VII collagen secreted by basal cells

7. • The long cliliary nerves provide the
perilimbal nerve ring
• Fibres penetrate the cornea in deep
peripheral stroma and Lose their myelin
sheath within a short distance into the
cornea and run parallel to epithelium
• Turn toward the surface penetrating the
Bowman’s layer and basement membrane
forming sub basal plexus and finally
terminate in the wing cells as nerve
endings

8. pathogenesis
 The changes which reduce the adhesion of the corneal
epithelium include
o a deficient basement membrane
o The absence and abnormality of hemidesmosomes
o Loss of anchoring fibrils
Increased level or activity of several members of matrix
metalloproteinase (MMP) including MMP-2 , MMP-9 are reported
in patients having RCE

9. Symptoms
 Repeated episodes of sudden onset of pain usually at
night or upon first awakening
accompanied by
 redness
 photophobia and
 watering of the eyes

10. I. Primary
a) Epithelial basement membrane dystrophy
b) Dystophy involving Bowman’s layer
-Reis-Buckler’s dystrophy
-Thiel-Benke dystrophy
c)Stromal Dystophy
Lattice, Macular and Granular dystrophies
d)Endothelial dystrophy
Etiologies of Recurrent Corneal Erosions

11. II. Secondary
a) Degeneration
Band Keratopathy,Salzmann’s Nodular degeneration
b) Trauma
Epithelial abrasions , Chemical and thermal injury
c) Eyelid pathology
Entropion , ectropion ,lagophthalmos, Meibomian gland dysfunctions,
d) Following Ocular Infections- Bacterial and viral keratitis
e) Following Refractive surgery- LASIK,PRK
f) Systemic causes
Diabetes mellitus, epidermolysis bullosa, juvenile x-linked Alport’s syn
g) Miscellaneous
Keratoconunctivitis sicca, Bullous Keratopathy, idiopathic,

12.  Trauma accounts for 45-69 % of cases
 Epithelial basement membrane dystrophy
accounts for 20-30 % of cases
 Other dystrophic and degenerative diseases
account for a minority of cases

13. Trauma leading to RCE
 Incidence estimates of RCE following traumatic corneal abrasions have
ranged from 5 % - 25 %
 Corneal wound healing occurs in 3 phases
1) Epithelial migration
2) Epithelial proliferation
3) Epithelial adhesion

14. Epithelial migration
 ~3hrs - Neutrophil accumulation (from tear film) occurs along
wound edge and thinning of epithelium to a single layer of
flattened cells
 Latent phase (4-6hrs) – characterized by increased intracellular
protein synthesis, actin filament polymerization and
reorganization from apical to basal region of cells
 Linear phase (4- 5 days) – the flattened cells move across the
defect as a sheet until completely covered
 Lamellopodia & filopodia marks the beginning of cell
migration

15. Epithelial Proliferation
 Basal epithelial cells are the key participants The transient
amplifying basal cells reproduce via mitosis and the new cells
move inwards toward the center of the defect, then upwards
to fill it
 Stem cells at the limbus are responsible for the epithelial cell
replacement by their increased mitosis
 EGF,TGF β and and NGF plays a vital role

16. Epithelial Adhesion
 Reformation of the adhesion complexes occur gradually starting
from periphery to centre
 Focal contacts at the leading edge of epithelium form by
linkages from cytoplasmic actin filament to extracellular matrix
proteins like fibronectin , laminin.
 Trauma predispose to RCE either because the basal epithelial
cells fail to produce proper basement membrane complexes to
attach to the Bowman layer or because of defective epithelial
adhesion

17. Epithelial basement Membrane
Dystrophy (EBMD)
 Cogan’s Microcystic (Map Dot Fingerprint) Dystrophy
pathophysiologic hallmark is an abnormality in the formation
and maintenance of the epithelial basement membrane adhesion
complex of the corneal epithelium
a history of recurrent erosions should suggest this diagnosis,
especially if they are bilateral and occur in multiple sites

18. pathogenesis
Epithellial cells produce abnormal multilaminar basement
membrane , both in normal location and intra- epithelially
Blocks the normal migration of epithelial cells toward the surface
Trapped epithelial cells degenerate to form intraepithelial
microcysts, which slowly migrate to the surface

19.  With continued cycles of epithelial breakdown and
aborted efforts at the development of a stable
epithelial basement membrane adhesion complex,
morphological changes eventually develop, which lead
to the classic "map-dot-fingerprint" epithelial and
subepithelial findings.

20. Map changes Dot changes

21. Inadequate formation of
hemidesmosomes by the basal
epithelial cells results in
compensatory aberrant
regeneration and duplication of
the epithelial basement
membrane, a change that is
clinically manifested by the
"fingerprint" lines.
Fingerprint like changes

22. Diagnosis of RCE
 A history of prior corneal abrasions , especially a
shearing injury as from a tree branch or a fingernail
scratch can often be elicited
 In patients lacking a cause for erosions , examination
done under fluorescein staining and retroillumination
for EBMD in asymptomatic eyes

23. Adhesion test
 In cases where a erosion is suspected but lacks the evidence of
epithelial defect in slit lamp examination , the presence of an
occult epithelial adhesion is detected by use of dry cellulose
surgical sponge rubbed gently and tangentially over the
suspected area after topically anesthetizing the cornea.
 If the intact epithelial sheet is moveable ( +ve adhesion test) then
the lack of adequate epithelial stromal adhesion is certain.

24. Management
 Conservative management aims mainly in resolution of the
epithelial defect
A)For relatively small (less than 1 quadrant of cornea) and clean
(without infiltrate) defect
1) Lubrication
This is considered first-line therapy
frequent application of preservative-free artificial tears
combined with
2) mild antibiotic eye ointment at bedtime (or more frequently)
to prevent the eyelid from adhering to the corneal epithelium and
antibiotic prophylaxis.

25. Topical immunomodulators
such as 0.05% cyclosporine-A
(Restasis), reduce the likelihood of
RCEs by improving the lacrimal and
mucin tear layer quality by inhibiting
lacrimal gland T-lymphocyte
proliferation and increasing goblet
cell numbers, which can help
decrease corneal friction.

26.  Hypertonic (5%) sodium chloride
will promote the epithelial adherence
by increasing the the tear osmolarity ,
thereby decreasing the epithelial odema
and promoting epithelial adherence.
These agents should be continued for a
few months as it takes few months for
the adhesion complexes to build up

27. B) If the epithelial defect is larger and patient is extremely
uncomfortable then continuous pressure patching (24-
72hrs) is employed .
C) In the presence of corneal stromal infiltrate and/or
anterior chamber reaction , a concomitant infection must
be suspected thereby microbiological cultures are
performed

28. Therapeutic Contact lens
provide symptomatic relief and encourage healing of the
epithelium by protecting them from the ‘windshield wiper’
debridement action of the blinking eyelids
Diadvantages – increase the risk of microbial keratitis
hence a topical antibiotic(flouroquinolones) should be used
once/twice daily

29. a relatively flat (base curve
>8.6mm), plano or low minus
power , high water content
SCL are preferred
The lens can be worn from
few weeks to several months,
replacing it every 2 weeks

30.  Any signs of underlying blepharitis should be treated with lid
hygiene measures (hot compresses and eyelid scrubbing) with
additional oral doxycycline in more severe cases.
 Combination therapy with topical lubrication, oral tetracyclines,
and a topical corticosteroid particularly for patients with
meibomian gland dysfunction
 Both doxycycline and methylprednisolone inhibit matrix
metalloproteinase-9, which is implicated in cleaving scaffolding
proteins in the corneal epithelial basement membrane.
 This inhibition can aid the recovery and reattachment of the
corneal epithelium following RCE.

31.  Punctal occlusion
• For chronic dry eye patients whose RCE is resistant to
punctal occlusion may be performed. This simple, one-time
intervention can promote more rapid healing and prevent
attacks by increasing the ocular surface residence time of both
natural and exogenously applied tears.
• As a trial, especially in patients with mild to moderate dry eye, a
dissolvable short-term collagen punctal plug may be used.
• However, in patients with severe tear film insufficiency, longer-
term silicone punctal plugs are recommended.

32.  Autologous serum
 biochemical properties of blood serum are very similar to that
the tear film.
 It is composed of substances necessary for epithelial healing,
such as vit A , EGF,TGF β and fibronectin. The lipids present in
serum acts as a substitute for lipid components produced by
meibomian glands
 Autologous serum generally is accepted as safe
 Disadvantages - costly and cumbersome

33.  Amniotic membrane (AM) patching
 Transplantation of cryo-preserved AM exerts anti- inflammatory,
anti-scarring and anti-angiogenic actions , they contain tissue
inhibitors of MMPs
 Under topical anesthesia, debridement of the loose epithelial
cells by a dry cellulose sponge is done and the corneal surface
covered with AM
 They act as a biological bandage and help in treating RCE

34.  hydrated amniotic tissue PROKERA (Bio-Tissue ,Inc, Miami FL) has been
approved by the FDA as a self retained sutureless medical device to promote
corneal wound healing
This device is an amniotic membrane sheet supported on a 16mm plastic ring. It can be applied
simply as a large-diameter contact lens, though the ring itself is much thicker than a standard
contact lens.

35. Surgical techniques
1) Debridement
2) Superficial epithelial keratectomy
3) Anterior stromal puncture
4) Phototherapeutic Keratectomy

36. Debridement
 Applied in cases with Extensive epithelial deterioration and
residual associated cellular debris
 Mechanical debridement of loosely adhered or nonadherent
epithelium provides a smooth basement membrane to which
healthy epithelium may re-adhere
 This technique requires only a cotton swab or blunt instrument
and can be performed at the slit lamp with topical anesthesia.

37. Devitalised epithelium and debris
adherent to the damaged basement
membrane surface inhibit restoration
of intact basement membrane and
recovery of tight epithelial- stromal
adhesion

38. After the application of topical
anesthetic, a gentle scrub with a dry
cellulose sponge or No 15 BP blade
is performed to sweep aside
nonadherent epithelium and debris.

39. Jeweler’s forceps are employed
to remove loose shards of
marginal epithelium.

40. The surface of the Bowman’s
layer is polished with a dry
cellulose sponge .
Topical antibiotic are applied
followed by pressure patch.
If the defect persist >72hrs,
then patch is replaced with BCL

41.  limitations of this procedure derive from the fact that
no significant modifications to enhance epithelial
adhesion are made in Bowman’s layer or other
deeper corneal structures

42. Superficial keratectomy
The optimum candidate for this procedure
 has spontaneous multiple erosions in different areas of the
cornea,
 no history of trauma and
 severe basement membrane dystrophy, involving visual axis
resulting in poor vision and large areas of loosely adherent
irregular epithelium.
The premise behind superficial keratectomy is that if irregularities
in the epithelium and anchoring complex are removed and allowed
to grow back in a controlled environment, the structures may
normalize as they develop

43.  Under local anesthesia (or, in some highly cooperative patients, the
use of topical anesthetic agents) a lid speculum is inserted to hold
the eye open.
 The area appropriate for debridement is identified with fluorescein
or adhesion test .
 The epithelial and subepithellial debris are removed using dry
cellulose sponge

44. A superficial plane of dissection
using a No 15 BP blade is
established in the perilimbal area
Leaving approximately 1 mm of
intact perilimbal epithelium, the rest
of the epithelium and its basement
membrane, if possible, are lifted and
dissected free. An attempt should
be made to peel and dissect away
the epithelium in a continuous
sheet.

45.  Persistent epithelial fragments may be visualized by instilling fluorescein.
Bowman’s layer should not be incised but should be scraped with a blade
oriented perpendicular to the surface of the cornea, taking care not to
produce linear scars in Bowman’s layer.
 Alternatively a diamond burr may be
used to gently polish Bowman’s layer
to enhance epithelial adhesion
it leaves a smooth surface upon which
new epithelium can grow

46. Anterior stromal puncture (epithelial
reinforcement, corneal micropuncture)
 This technique involved the use of a straight 20-gauge needle to
make multiple shallow penetrations through the epithelium into
anterior corneal stroma to improve epithelial adhesion,
apparently by inciting focal microcicatrization to ‘spot weld’ the
epithelium to stroma.
 This technique performed under topical anesthesia under slit
lamp , and is best suited for those with single erosive areas(from
trauma) in area outside the visual axis

47.  A careful preoperative slit lamp examination should also include
retroillumination. Epithelial reinforcement may be performed
either between erosive episodes or through loose, irregular
epithelium during an active erosion without the need for
debridement.
 Topical nonsteroidal drops should be instilled every 10 to 15
minutes, starting 30 minutes to 1 hour before the procedure to
aid in postoperative pain management. Also, several drops of a
fluoroquinolone, or other broad- spectrum antibiotic drop used
pre operatively.

48. The large gauge needle used to eliminate the risk of perforation , alternatively
bending the tip of the needle like cystatome also helps in producing small
punctures of consistent depth.
The treatment is performed directly over the areas of defective epithelium or
over the dysadhesive areas of cell sheet and should extend 1-2 mm beyond
the erosive focus into normal tissue

49. Flouresein along with anesthetic,
should be applied to help visualize the
puncture marks.

50.  Anterior stromal puncture also done using Nd Yag laser
 Advantages include minute and uniform wound with less corneal
scarring, so the procedure can be repeated whenever necessary

51. Phototherapeutic Keratectomy
 The excimer laser revolutionized corneal refractive surgery in the
1990s.
 PTK was approved by the FDA in 1995.
 The ablation method involves 193nm laser emission with
repetition rate upto 50hz and diameter 6.5mm.
 No more than 4 shots should be performed on one area in order
to preserve the Bowman’s layer

52. FDA approved Indications of PTK
 Superficial corneal dystrophies (including granular, lattice and Reis
Buckler’s dystrophy)
 EBMD and irregular corneal surfaces
 Corneal scars and Opacities

53. Ideal Patient criteria
 Significant visual compromise
 Pathological condition in anterior third of cornea
 Elevated or flat opacity
 Myopic
 Under consideration for corneal transplant
 Quiet, uninflamed eye
 Recurrent corneal erosion that has failed medical therapy

54. Pre operative evaluation
Should be performed no longer than 90 days before the surgery
Medical history (collagen vascular d/s , immunodeficiencies)
 Visual acuity with and without correction
 Intraocular pressures
 Slit lamp examination
 Dilated fundus examination
 Irregular astigmatism should be evaluated by keratometry and corneal
topography
 Preoperative corneal thickness is measured by pachymetry
 Anterior segment OCT used to have detailed view of entire cornea

55. Relative contraindications
 Pathological condition deeper than 1/3rd of cornea
 Thin preoperative cornea
 Active ocular inflammation like uveitis
 Hyperopic refractive error
 Severe Blepharitis
 Lagophthalmos or poorly controlled dry eye
 Collagen vascular disease like RA
 Immunosuppression

56. Technique
 General
1) Remove the bulk of opacity from the central cornea
2) Smooth the central and mid peripheral cornea
3) Remove the least amount of stroma that is required
4) Ablate and check frequently during the procedure to ensure that
only required amount of tissue is removed
5) If the epithelium is helping create a smooth corneal surface , it is
best to perform transepithelial ablation
6) If the epithelium is exacerbating the corneal irregularity , it is
mechanically removed before the laser treatment
7) Masking agents are very helpful in smoothening the cornea

57. For recurrent corneal erosions
 All the loose epithelium is removed with a sharp blade
 A 6.5mm diameter circular PTK ablation is applied centrally for a
depth of 5-6 µm , which is part way through the bowmans
membrane
 If an area larger than the largest ablation zone needs to be treated
, then the central area is treated and a 6.5 mm sponge is placed
centrally to block the previously treated area, the laser ablation
zone diameter is set to 4mm and peripheral areas are treated with
barely overlapping 5-6 µm depth ablation

58. Masking agents
 These are substances that are applied to the cornea
during the treatment to selectively block laser
ablation to create smoother surface
 Saline or artificial tears are used
 the masking agents are applied in areas where no
laser ablation is desired

59. Post operative management
 Initial managements include
1) Epithelial healing
Immediately after the surgery , topical antibiotics are given,
cycloplegic agents are instilled .
The eye can be pressure patched with an antibiotic ointment or BSCL
2)Pain control
Pain reduced by a combination of icepacks over orbit for several days
, oral painkillers and neuropathic pain medications( gabapentin)
The pain diminishes gradually as the epithelial defect resolves

60. complications
 Pain
 Poor epithelial healing
 Haze/scar
 Infection
 Induced hyperopia, regular and irregular astigmatism
 Decreased uncorrected and best corrected vision
 Recurrence of condition (11 percent)

61.  Post operative haze
over the first several weeks after surgery, the treated area may
develop anterior stromal haze.
If it is mild and without any symptoms, it can be followed up and
it diminishes on its own.
If it is more significant , topical steroids are helpful

64. Thank you