Indication, contraindication, advantage, disadvantage, types of keratoplasty, complication of keratoplasty and management, corneal graft rejection and failure M.S ophthalmology, sarojini devi eye hospital, regional institute of ophthalmology, osmania medical college, hyderabad, telangana

1. KERATOPLASTY
PRESENTER: SIVARAMAN.G
DISCUSSANT :Dr. SHANTHA
CHAIRMAN: Dr. SRINIVAS PRASAD

2.  DEFINITION
 TYPES
 PREOP EVALUATION
 PROCEDURE
 INDICATIONS, ADVANTAGE, DISADVANTAGE
 COMPLICATIONS
 CORNEAL GRAFT REJECTION AND FAILURE
 MANAGEMENT OF COMPLICATIONS

3. DEFINITION
 Keratoplasty refers to replacement of diseased host
corneal tissue by healthy donor cornea.
 Full thickness (Penetrating keratoplasty)
 Partial thickness (Anterior and Posterior Lamellar
keratoplasty

4. GENERAL INDICATIONS
 Optical
 To restore vision by obtaining clear visual axis
 Tectonic
 To restore corneal integrity and tectonic support in
severe structural changes
 Therapautic
 To remove the infected corneal tissue who are
unresponsive to antimicrobial therapy
 Cosmetic
 Rare
 To improve appearance of eye with whitish corneal scar

5. TYPES

6.  PENETRATING KERTOPLASTY
 LAMELLAR KERATOPLASTY
ANTERIOR
Anterior Lamellar
Keratoplaty(ALK)
Deep Anterior Lamellar
Keratoplasty(DALK
POSTERIOR
Deep Lamellar endothelial
keratoplaty(DLEK)
Descement Stripping Endothelial
Keratoplasty(DSEK)
Descement stripping Automated
Endothelial Keratoplasty(DSAEK)
Deep Membrance Endothelial
Keratoplasty(DMEK)

7. PREOP EVALUATION
 General systemic evaluation – HTN, DM , cardiac disease
 Patient socioeconomic status and compliance for follow up
 Ocular history of present & past illness and ocular
surgeries

8.  Ocular examination of eye and adnexa – slit lamp, details
of corneal vascularization, tear film assessment, IOP,
presence of cataract
 If anterior segment details are not visible-
Ant-seg OCT
 Posterior segment evaluation – Bscan

9. PREOPERATIVE PREPARATION
 Antiinfective agent – reduce the risk of endophthalmitis,
appropriate lid care
 IOP control – good lid and extaocular akinesia, use of
mannitol preoperatively
 Pupil –not dilated, constricting the pupil with 2% pilocarpine
intraoperatively maybe done to reduce lens damage during
trephining of phakic eye

10. PENETRATING KERATOPLASTY
 Full thickness Replacement of corneal tissue with healthy
donor graft
INDICATIONS(Optical & Therapeutic)
 Pseudo/aphakic corneal decompensation
 Stromal corneal dystrophy
 Granular, lattice, macular, Schnyder central crystallin,
central cloudy dystrophy

11.  Primary corneal endotheliopathies
 Fuchs endothelial dystrophy, congenital hereditary
endothelial dystrophy, posterior polymorphous
dystrophy, ICE syndrome.
 Corneal ectasia and thinning
 Keratoconus. Keratoglobus
 Congenital corneal opacity
 Peters anomaly, sclero-cornea, congenital glaucoma

12.  Acquired corneal scars
 Post viral keratitis, healed keratomalacia, post traumatic
corneal scar
 Non infectious ulcerative keratitis
 Posterior Rheumatoid corneal melting
 Exposure keratopathy
 Immune corneal melt d/t systemic vasculitis,
keratoconjunctivitis sicca, mooren’s ulcer

13.  Corneal degeneration
 Failed corneal graft
 Non healing infectious keratitis,
 Infectious keratitis with perforation,
 Post chemical injury and melt

14. CONTRAINDICATIONS
 Epithelial dysfunction – limbal stem cell deficiency
 Stromal vascularization – more than 2 quadrants
 Multiple graft failures

15. ADVANTAGE
 Full thickness transplant
 No interface related visual problem
 Ability to treat all layers
 Anterior segment reconstruction in single procedure

16. DISADVANTAGE
 Corneal surface disease or neurotrophic cornea
leads to prolonged healing or persistent epithelial
defect.
 Irregular or significant regular astigmatism
 Difficulty in determining anterior corneal curvature

17. S/P OKP 2ND POD FOR RE CENTRAL CORNEAL
OPACITY

18. S/P OKP POD 2MONTHS IN 6 YR CHILD

19. S/P OKP 6MONTHS

20. S/P TKP FOR FUNGAL CORNEAL ULCER

21. SUTURE INFILTRATE

22. S/P TKP 3RD POD

23. COMPLICATIONS

24.  Intraoperative complication
 Scleral perforation d/t bridle suture or sclear fixation ring
Trephination problem
 Small size trephine of donor cornea leads to improper water
tight closure
 Flat cornea
 Hyperopia
 Angle compression leading to raised IOP.
 Eccentric trephination leads to increased astigmatism and
rejection
 Improper trephination leads to endothelial damage d/t
repunching

25.  Iridolenticular damage – avoided by globe hypotony, Ac
maintained with viscoelastics, miotics
 Endothelial damage d/t improper trephination, improper
tissue handling, iris,lens,IOL touch during surgery.
 Intra ocular haemorrage bleeding into AC d/t corneoiridic
scar in post infection, post traumatic case, Iol
explantation in case of PBK, iridodialysis or synechiolysis
at the the angle
 Vitreous loss in case of combined cataract extraction and
keratoplasty

26.  Postoperative complication
 Immediate
 Wound leak leads to shallow AC with low IOP.
 Persistent epithelial defect and filamentary keratitis
 Postoperative inflammation
 Suture related infiltrates suture induced vascularization
 Raised IOP
 Pupillary block
 Anterior synechiae formation
 Choroidal detachment /haemorrhage

28.  Late postoperative complications
 Post PK astigmatism
 Graft infection
 Graft rejection
 Post PK glaucoma
 Retrocorneal membrane formation
 Late wound dehiscence

29. DEEP ANTERIOR LAMELLAR KERATOPLASTY
 DALK – corneal tissue is removed almost to level of
Descemet membrane and replaced with donor
corneal tissue.

30. INDICATIONS
 Degenerative – keratoconus, pellucid marginal. Terriens
, spheroidal salzman nodular, band shaped keratopathy
 Dystrophies( epithelial and stromal)
 Corneal thinning
 Corneal stromal melts
 Infective keratitis upto anterior stromal layer
 Corneal ectasia secondary to lasik

31. CONTRAINDICATIONS
 Absolute:
 Endothelial dysfunction – posterior dystrophies, corneal
edema(pseudophakic and aphakic), ICE syndrome
 Relative:
 Epithelial dysfunction- limbal stem cell deficiency, chronic
surface disease
 The big-bubble technique is contraindicated if there is
 a pre-existing break in the Descemet’s membrane (post
hydrops) or
 there are deep scars (however small) involving the
Descemet’s membrane

32. ADVANTAGE
 Non penetrating surgery –less risk of Intraocular
complications
 Selective removal of pathology
 More rapid visual rehabilitation
 Early removal of suture, Less need of suture and wound
induced astigmatism
 Minimal requirement of donor tissue
 Reduced incidence of graft rejection retains normal recipient
endothelial layer
 Preservation of globe integrity

33. DISADVANTAGE
 Irregular or significant regular astigimatism
 Irregular interface
 Ocular surface disease leads to persistent epithelial
defect
 Stromal opacification
 Interface debris
 DALK is technically demanding and time consuming.

34. S/P DALK FOR KERATOCONUS IN 7YR CHILD

35. S/P DALK 1 WEEK POSTOP

36. COMPLICATION
 Intraoperative
 Irregular lamellar bed
 Perforation of posterior stroma/DM
 Graft host malposition/edge irregularities
 Interface debris

37.  Post operative complication
 Pseudoanterior chambers
 Persistent epithelial defect
 Infection – suture related , inferface infection.
postkeratoplasty atopic sclerokeratitis
lid adnexal abnormalities
poor ocular surface
 Recurrence of HSV, corneal dystrophy
 Graft rejection less common
 Graft vascularization of lamellar bed in SJS, trachoma,
chemical burns

40. POSTERIOR LAMELLAR/ ENDOTHELIAL
KERATOPLASTY(DLEK/DSEK/DSAEK)
 Replacement of diseased posterior corneal layers &
endothelium with donor corneal tissue while the
host anterior corneal stroma is retained

41. INDICATIONS:
 Fuch’s endothelial dystrophy
 Pseudophakic/aphakic bullous keratopathy
 Failed graft
 Iridocorneal endothelial syndrome
 Argon laser iridotomy induced bullous keratopathy
 Congenital hereditary endothelial dystrophy
 Posteriod polymorphous corneal dystrophy

42. CONTRAINDICATIONS
 Corneal ectasia
 Stromal dystrophies
 Stromal scarring or opacification – infection,
interstitial keratitis
 Anterior corneal dystrophies

43. ADVANTAGE
 Rapid vision rehabilitation
 Preservation of ocular surface
 Less incidence of astigmatism
 Stronger wound
 Reduced graft rejection
 Smaller incision with preservation of globe integrity

44. DISADVANTAGE
 Significant stromal haze, subepithelial fibrosis requiring
second procedure
 Increased incidence of primary graft failure during
surgical learning curve
 Post operative donor dislocation
 Pupillary block d/t air bubble

45. POST DSEK

46. COMPLICATIONS

47.  Intraoperative complications
 Poor microkeratome dissection of donor tissue in DSEK
 Inability to strip host DM & endothelium in DMEK
Retained DM.
 Excessive manipulation of donor tissue leading to cell
loss and possible primary graft failure
 Tearing of donor tissue
 Interface debris or blood
 Choroidal hemorrhage (lower than PK)
 Inversion of donor lenticule

48.  Postoperative complication
 Pupillary block glaucoma (Urrets-Zavalia syndrome)
 Dislocation/discontinuation of lenticle
 Primary graft failure
 Epithelial ingrowth
 Interface opacification, Infection at interface
 Graft rejection (lower than PK)
 Reduced endothelial count
 CME

53. DSEK DSAEK
Manual dissection- Increased donar
tissue perforation
Automated dissection – less risk of
perforation
Do not yield smooth anterior surface of
donor posterior lamella
Yields good post donor lamella of
superior optical quality
More time consuming and visual
recovery is slow
Less time consuming and visual
recovery is rapid
Adhesion is better because of greater
thickness& irregular anterior surface
Adhesion is not easy because of thin
and smooth anterior surface
Donor lenticule dislocation is less more

54. CORNEAL GRAFT FAILURE
 Corneal graft is considered failed
 if it fails to retain optical clarity,
 if there is no impact on therapeutic attempts,
 if there is severe astigmatism that could not be optically
corrected -resulting in regraft

55. CAUSES OF GRAFT FAILURE
 Allograft rejection 29.2%
 Post pk glaucoma 16.9%
 Infection excluding endophthalmitis 15.4%
 Surface problem 12.7%
 Primary graft failure 6.6%
 Endothelial decompensation 3.8%
 Endophthalmitis 2.7%
 Recurrence of host disease 2.0%
 Severe astigmatism 0.6%

56. GRAFT FAILURE (2 TO 45%)
 It should be differentiated from graft rejection
 Significant edema of donor tissue in Non-inflamed eye
present in 1st postoperative day and does not resolve
by 2-4 weeks d/t usually not followed by period of
clear cornea

57.  Prolonged death or prolonged preservation > 7days
 Poor endothelial function
 Elderly donor > 70 years
 Iatrogenic damage to donor tissue during PKP
 Defective preservation media or Intraocular fluids
RISK FACTORS

58. MECHANISM
 Hyposecretion of aqueous after PK result in corneal
edema d/t decreased supply of metabolites to
endothelium
 Increased positive pressure increases the chance
of contact between endothelium and other
intraocular structure– so preoperative hypotony with
digital massage or IV mannitol is mandatory.

59.  Primary and secondary failure
 Primary
 Eye with well apposed grafts after surgery but with
persistent corneal edema
 d/t inadequate endothelial function, traumatic pre or
intra operative technique
 To prevent PGF, donor cornea should have atleast
200 cells/mm2 for better chance of graft survivial

60.  Secondary graft failure
 Donor endothelial tissue is detached from recipient
stromal cornea preventing the cornea from clearing
 Causes- residual fluid or viscoelastic in the interface or
retained DM and graft rejection
 Management –unresponsive to hypertonic saline or
steriods.
 1.Observation for atleast 3 weeks prior to regraft
 2. Regraft

62. GRAFT REJECTION
 Specific immunologically mediated that may be
irreversible/reversible in which corneal graft is clear
for at least 2 weeks, suddenly succumbs to graft
edema in conjunction with anterior segment
inflammation sign

63. CHARACTERISTICS
 Immune mediated resulting in decompensation of
transplanted cornea
 3 or more weeks
 Inflammatory process limited to graft
 Starts at graft margin nearest to proximal blood vessels
 Movement of inflammatory reaction towards centre to
involve the entire graft
 Increase in corneal thickness( edema) in previously
clear compact graft

64. PATHOLOGY
 Cell mediated by CD4+ and CD8+ cells
 Delayed Hypersensitivity reaction
 Inflammation induce vessels, lymphatics growth into
cornea and attracts APC into central cornea
 MHC antigen expression on corneal cells are
upregulated
 Recognition of foreign Histocompatiblity antigens leads
to immune cascade afferent immune response

65. Donar antigen processed by host APC
(afferent rejection cascade)
Presented to host immune sytem in
conjunction with HLA II & IL 1
Host mounts immune response
against foreign antigen
(efferent rejection cascade)
Activated Thcells release IL2,
IFN macrophages
Lymphokines cytokines
migration inhibition factor

66.  Anterior chamber associated immune deviation
 Corneal lymph angiogenesis and ham-
angiogenesis
 Lymphocytotoxic antibodies directed against HLA 1
 Donor derived Langerhans cells also mediate
rejection

67. CLASSIFICATION
 Epithelial rejection
 Chronic stromal rejection
 Hyperacute stromal rejection
 Chronic focal rejection/endothelial rejection

68. EPITHELIAL REJECTION (10 – 14%)
 Quiet, asymptomatic subsides in 6to 10 days
 Linear pattern from graft host junction at the site of
vascularization with gradual progression towards
center
 Elevated undulating line with positive FS and rose
Bengal stain
 A/w persistent epithelial defect or epithelial ring
presentation

69. Epithelial downgrowth-
Scalloped leading edge advancing
from periphery towards central
cornea DD from endothelial
rejection line

70. CHRONIC STROMAL REJECTION (2.4 – 15%)
 Low grade rejection- risk of development of other
severe Rejection
 Subepithelial infiltrate - Krachmer spots for 6
weeks to 21 months
 0.2 to 1 mm in diameter either in or immediately
below bowman’s layer

73. HYPERACUTE STROMAL REJECTION
 Occurs simultaneously with / immediately following
endothelial rejection
 Sudden onset of peripheral full thickness stromal haze in
previously clear graft adjacent to area of vascularization
with rapid progression to center in 24 to 48 hrs
 An abscess like picture without hypopyon in early stage
 Ciliary congestion a/w epithelial defect

74. CHARACTERISTICS
 Migrates away from vascularized part of graft
 Growth of vessels into stroma
 Mimics corneal abscess in heavily vascularized cornea
 Haze may invade adjacent host cornea proximity to
vascularization
 Complicated by persistent epithelial defect leading to
stromal necrosis, descemetocele and perforation

77. CHRONIC FOCAL REJECTION/
ENDOTHELIAL REJECTION (2 – 40%)
 Most common, severe form which leads to graft failure d/t
significant loss of endothelial cells
 Onset within month

78. RISK FACTORS
 Direct correlation with degree of vascularization
 Young individual with active immune system
 Large size /eccentric graft
 No of quadrants of anterior synechiae
 Preoperative glaucoma
 Previous corneal transplant

79.  Reversible – responds to corticosteroids, reduction
in edema , restoration of clarity, resolution of
inflammation
 Irreversible- endothelial decompensation – graft
failure

80. SIGNS AND SYMPTOMS
 Redness, photophobia, irritation, halos around of light and
dimension of vision
 Conjuctival hyperemia, Ac reaction
 KPs – Diffuse scattered/ lined up in a chain like fashion
forming pathognomonic endothelial rejection line of
khodadoust.
 Graft edema, Stromal edema & DM folds

83. MANAGEMENT
 Prevention
 Treatment
Early detection and aggressive therapy

84. PREVENTION
 Preoperative measures to minimize antigenic difference by
steroids prophylaxis
 Intraoperative – meticulous surgical technique, avoiding
decentration of recipient bed trephination, optimal suturing,
good graft host apposition
 Followup, timely suture management- decreases suture
related vascularization and rejection

85. TREATMENT
 Corticosteroids – prednisolone acetate / prednisolone
sodium phosphate 1%
 Preoperatively- 4times/ 1 week
 Post operatively- hrly 3days, 2hrsly 15 days,
4 times for 3 months then tapered 1drop for every 2
months
For acute rejection hourly steroids
Systemic steroid either by oral (60 to 80 mg) or
intravenous route (500mg in 150ml of IV fluid)

86.  Cytotoxic agents
 Azathioprine
 Cyclosporin – topical 1% in artificial tears.
 Immunoregulatory agent
 Tacrolimus
 Rapamycin
 Mycophenolate mofetil

87. CORNEAL GRAFT INFECTION
 Predisposing factor
 Suture related problem
 Persistent epithelial defect
 Recurrence of HSV keratitis
 Ocular surface disorder

88.  Graft failure
 Use of soft contact lens
 Lid abnormalities
 Donor tissue contamination
 Incomplete excision of infected tissue

89. CLINICAL FEATURES
 Peripheral keratitis, ulceration in suture related
 Central or paracentral keratitis, ulceration in epithelial
defect
 Stromal infiltrate, Ac inflammation
 Inferior part is affected – tear film insufficiency/ exposure
keratitis
 Herpetic keratitis – dendritic keratitis / non healing epithelial
defect
 Infectious crystalline keratopathy

91. INFECTIOUS CRYSTALLINE KERATOPATHY
• Noninflammatory, intrastromal bacterial colonization of a
corneal graft
• α-hemolytic streptococci of the viridans
• Bacteria are thought to gain access to the corneal stroma via
epithelial ingrowth into a suture track or by direct access
through an epithelial defect.
• A pauci-inflammatory response is characteristic, and corneal
thinning and necrosis are not seen

93.  Corneal scraping –gram staining & KOH
 Blood agar chocolate agar and sabauraud’s agar
 Confocal microscopy
CAUSATIVE ORGANISM
INVESTIGATION
 Gram positive- Coagulase negative staph aureus
 Aspergillus
 Strep pneumoniae, viridians
 Pseudomonas aeruginosa- gram negative

94. MANAGEMENT
 Intensive topical fortified antibiotics(cefazolin,
ceftazidime, vancomycin, gentamycin)
 Acylovir 3% for herpetic infection

95. POST PK GLAUCOMA
 Elevated pressure >21 mg after keratoplasty with or
without visual field loss/ optic nerve head damage
 Risk factors:
 Preexisting glaucoma
 Adherent leucoma
 ICE syndrome
 Aphakic / pseudophakic bullous keratopathy
 Ac inflammation
 Perforated corneal ulcer

96.  Early onset:
 Preexisting glaucoma
 Inflammation
 Hyphema
 Viscoelastic induced
 Wound leak and angle closure
 Pupillary block d/t air bubble

97.  Intermediate onset
 Inflammation
 Vitreous in AC
 Graft rejection
 Steroid induced
 Ghost cells

98.  Late onset
 PAOG
 Epithelial ingrowth
 Steroid induced
 Rejection/inflammation sequelae
 Pupillary block
 Malignant glaucoma
 Synechial closure

99. INVESTIGATION
 If corneal surface is intact- goldmann applanation
tonometer
 If corneal surface is irregular- pneumatic applanation
tonometer, tonopen, dynamic contour tonometer
 Gonioscopy
 Anterior segment OCT- when anterior segment not visible.
 Posterior segment evaluation

100. MANAGEMENT
 Medical
 Timolol 0.5%, betaxolol 0.5%
 Brimonidine 0.1%
 Lantanaprost, bimatoprost, travoprost
 Acetazolamide, methazolamide
 Topical use of dorzolamide and brinzolamide not
recommended as they block CA enzyme in corneal
endothelium – graft decompensation

101.  Surgical
 Laser trabeculoplasty argon, NdYag
 Glaucoma drainage devices
 Cyclodestructive procedure- cryotherpathy
cyclophotocoagulation
 Trabeculectomy

102. POST PK ASTIGMATISM
 Most common complication in successful graft
 4 to 5D
 Risk factor
 Preoperative astigmatism
 Vascularized severe corneoiridic scar
 Peripheral thinning, keratoconus, scleral ectasia
 Pellucid marginal degeneration,
 Aphakic bullous keratopathy

103.  Trephination technique
 Anterior trephination- ballooning –large tissue- ovalization
 Trephination tilt
 Graft size, placement, host graft apposition
 Small graft- higher astigmatism
 Large graft- lesser astigmatism
 Eccentric placement
 Disparity in shape of donor and recipient cornea
 Disparity in tissue thickness at graft host junction

104.  Suture related
 Suture technique, placement, depth, length, timing of suture
removal
 Interrupted suture or combined suture is associated
irregular astigmatism than continuous suture
 Proper placement of cardinal suture to avoid unequal tissue
distribution
 Tight or loose suture or breakage or chesse wiring
 Infectious abscesses and immune infiltrate
 Toxic suture infiltrate
 Kaye dots
 Vascularization

105.  Increased IOP in early post op period
 Impaired wound healing
 Epithelial irregularities

106. Suture related Immune
infiltrate
Infectious suture infiltrate
multiple solitary
Occurs on host side Occur on graft or host side
No epithelial defect Epithelial defect

107. KAYE DOTS
 Discrete white dots in the donor corneal epithelium in a 1–
2-mm region central to the graft sutures.
 Not associated with erosions or fluorescein staining,
rejection or infection, not altered or caused by drug
therapy,
 onset is at 6.5 weeks postoperatively
 Histologically, the dots correspond to epithelial cells in
various stages of degeneration.
 After suture removal, the dots typically shift centrally and
gradually disappear over a period of 30 days

110. MANAGEMENT
 Low astigmatism- glasses, RGP contact lens
 High astigmatism-
 Wound recession keratotomy
 incision
 Suture enhancement
 Wedge resection
 Laser ablation
 Surface ablation
 regraft

111. THANK YOU!!