keratoplasty

3.  From the first documented successful corneal transplant performed
by Eduard Konrad Zirm in 1906 to contemporary femtosecond
laser assisted surgery, the evolution of keratoplasty has been nothing
short of remarkable.
 The first recorded experiments were performed on rabbits
 The history of today’s corneal grafting dates back to the nineteenth
century when K Himly of Germany suggested replacing an opaque
cornea of one animal with clear cornea of another animal in 1813
 F Reisinger was the first to suggest replacing opaque human
cornea with transparent animal cornea in 1824. He also coined the
term “keratoplasty”
 In 1840, Michael Marcus outlined the first set of basic principles for
keratoplasty.
 The most part, these early attempts at corneal grafting proved to be
unsuccessful
 late 1800s Arthur von Hippel promoting lamellar grafts and his
design of a circular mechanical trephine, a resurgence of interest in
corneal transplantation emerged

4.  Eduard Zirm performed the first documented successful human
corneal transplant in 1906.He effectively performed the
operation for a farmer with bilateral alkali burns ,donor tissue
was obtained from enucleated eye.
 In 1940s, corneal transplant surgery evolved dramatically with
the availability of antibiotics and introduction of steroids in
corneal surgery
 The work of Ramon Castroviejo that had the most profound
influence on modern-day keratoplasty. He refined his techniques
and progressed from use of a square graft to a circular from
traditional overlay sutures to direct appositional suturing
 In modern day evolution of microscope, specular microscopy ,
prospects of eyebanking and better preservation medium has all
lead to refinement of corneal surgeries.

5. Prior to 18th
century
• Dark ages, no work reported on replacing damaged cornea, not much info
about corneal surgeries
18th century
• Early efforts at surgical approaches to correct corneal diseases
19th century
• Concept of replacing damaged cornea by healthy donor cornea was idealised
and performed. There were reports of lamellar as well as PK being performed
20th century
• Early 20th century- first successful PK, further increase in knowledge and skills
• Late 20th century- comeback by lamellar kertoplasty, refinement of techniques
21st century
• Major advancements in form of sutureless keratoplasties, use of iOCT , femto-
assisted surgeries and bio-engineered corneas- more refined techniques.

6.  For most of the past 60 years, penetrating keratoplasty has been
considered the gold standard corneal transplant procedure.
 Corneal surgeons had a monolithic approach to the visual
rehabilitation of the patient with visually significant corneal disease,
not correctible with optical or medical therapy, i.e. penetrating
keratoplasty
 Penetrating keratoplasty is a transplant procedure in which full-
thickness host corneal tissue is replaced with donor corneal tissue.
 Its objectives-
(1) to establish a clear central cornea/visual axis,
(2) to minimize refractive error,
(3) to provide tectonic support,
(4) to alleviate pain, and
(5) to eliminate infection.

7. • Restore the normal
appearance of the eye, which
has limited or no visual
potential
•Purpose is to restore the
altered corneal structure,
improve the patient's visual
function
•option for future optical graft
remains viable.
•eliminate the infectious load
in eyes with keratitis
unresponsive to antimicrobial
therapy
•considered as the last option
when all other treatment
modalities have failed
• Performed to improve
visual acuity
• Any corneal pathology
leading to Vn drop to
6/18 could be treated
here.
OPTICAL THERAPEUTIC
COSMETIC
TECTONIC

8.  PBK
 ABK
 Ectatic disorders
 Stromal corneal dystrophies
 Endothelial dystrophies
 Congenital corneal opacities
 Post infectious keratitis
 Nutritional deficiencies
 Non infectious ulcerative keratitis
 Corneal degenerations
 Chemical injuries
 Trauma
 Re- grafting following allograft failure
 Miscellaneous

9.  There are no absolute contraindications for penetrating
keratoplasty except for the absence of light perception
 Relative contraindications-
1. Severe dry eye, neurotrophic states
2. Grade IV chemical burns
3. Anterior staphyloma
4. Severe case of SJS
5. Ocular cicatricial pemphigoid
6. Overall poor ocular surface
7. Stromal vascularization, when involving >2quadrants
8. Inaccurate PR/Retinal detachment
9. Multiple (two or more) graft failures
They can be helped with
keratoprosthesis

10.  1. Lengthy postoperative course
 2. Incidence of allograft rejection (10% to greater than
90%,depending on the indication)
 3. Suture complications: exposure, vascularization,
and infection
 4. Weak graft–host junction: risk of traumatic wound
dehiscence and globe rupture
 5. Unpredictability of corneal tonicity and degree of
ametropia
6. open sky phase
 7. post op glaucoma

11.  First and foremost is to identify the corneal pathology
, and any associated disorder along with it.
 Patient selection– ocular and systemic history:
Age – older patients less likely to undergo allograft
rejection
• Ocular injury
• Infectious keratitis
• Nutritional defeciencies
• Prior ocular surgery
• Prior history of galucoma
• History of collagen vascular disorders
• atopy
Screening

12.  Amblyopia – important to elicit presence of amblyopia
 General history – regarding systemic illness for
anaesthesia clearance.
OCULAR EXAMINATION
 Visual acuity- both UCVA, BCVA ,
-PR for optic nerve function,
-Contact lens corrected Va in
patients of irregular astigmatism
-Stenopic slit Va following full
pupillary dilation to rule out those
cases requiring optical iridectomy

13.  Lids and adenexa – any lid abnormality ~ ectropion,
entropion, lagophthalmos, trichiasis, blepharitis.
 Lacrimal sac and puncta- ROPLAS,
 Corneal surface- tear film abnormality, corneal sensation,
neurotrophic, depth of corneal opacity, size and its
location, stromal vascularisation, ectasia, thinning,
peripheral corneal involvement
 Conjunctiva – scarring, xerosis, symblepheron formation,
limbal ischemia following chemical burn
 Anterior chamber &iris- ciliary flush, keratic precipitates,
anterior synechia and iridocorneal adhesions are signs of
past or present inflammation. Iridocorneal synechiae,
neovascularisation, Peripheral iridectomy , aniridia.
 Pupil - shape, size, number, RAPD.
 Lens status- phakic, aphakic, pseudophakic, phacodonesis
 Fundus - any macular pathology which could be seen in
ABK, PBK
 IOP -

14.  Refraction
 Tear film status
 Keratometry
 Gonioscopy
 USG-B scan
 Pachymetry
 Specular microscopy
 Biometry
 UBM
 Electrophysiological tests

15.  Pre-op preparation=
 infection control- blepharitis, pre-op broad spectrum topical
antibiotic
 IOP lowering – glaucoma control, massage before surgery- either
digitally or with honan ballon.
 lens management- constricted pupil if not planning for triple
procedure, dilated pupil if triple procedure planned.
 donor corneal tissue management – status of patient before
donation, previous history of HSK ,glaucoma, patient on
ventilator for >72hrs, death by cancer, how long has the donor
tissue been in storage media.
 anticipate suprachoroidal hmg- dreadly complication, systemic
parameters should be monitored- manage BP, PR and anxiety of
patient pre-op, stopping anti-coagulant therapy 48hrs before
surgery, entering eye slowly to avoid sudden pressure drop.
 Anaesthesia

16.  Surgical steps-
1. Preparing sterile area
2. Eyelid speculum insertion
3. Scleral ring fixation(optional)
4. Marking host cornea- optical centre
5. Trephination of donor cornea- endothelial side first/up
6. Trephination of host cornea- epithelial side up
7. Open sky phase- placement of VED in AC
8. Placing donor cornea on host bed
9. Suturing the graft with host attaining proper wound
alignment with minimal astigmatism and avoiding
endothelial cell damage
10. Administering medications
11. Tarsorrhaphy in selective cases

17.  Role of scleral fixation rings- It functions as a
potential scaffold to maintain scleral support, exerting
its influence once the eye is opened if scleral rigidity is
insufficient~ paediatric and aphakic cases
 Disadvantage is associated globe distortion and
astigmatism.

18. Marking of host cornea
Optical axis is marked so that the donor
cornea could be centered over it,
marking done by simply putting
trephine with gentle pressure which is
more prominent on dry surface- its
followed by 8to12 prong radial markers
for suture placement
Trephination of donor cornea
Donor cornea should always be 0.25
mm larger than the host corneal
button removed because the size gets
reduced while trephination even when
same sized trephines are used. Donor
cornea is trephined with the
endothelial side facing up using a
sharp disposable blade in a guillotine
punch block apparatus
Trephination of recipient cornea
Sizing of the host trephine depends on
several factors, including host corneal size,
pathology, and risk of rejection. the graft
may be slightly decentered to encompass
for pathology, larger size grafts could also
be required if the disease progresses upto
corneal periphery(thinning)- large grafts
are more liable to undergo rejection.
Preparing recipient bed
After trephination the wound is entered
with sharp scoissors troutman or vannas
scissors. It gives more control in forming
posterior wound ledge. VED is also
injected while trephination via limbal
paracentesis site to give cushion effect,
prevent abrupt AC entry. Cut should be at
90 ° to corneal surface~minimise
astigmatism
ESSENTIAL STEPS

19.  Pre- requisite-
 At first viscoelastic is filled in AC, provide balanced
orientation for suture placement, & prevent
endothelial damage
 Donor cornea button grasped with non toothed
forceps at epithelium- stromal junction preventing
contact with endothelium.
 Tissue transferred on recipient bed and slightly
rotated to get spherical reflex on intraoperative
keratometer~ helps in reducing astigmatism.

20. Step1- placement of four interrupted radial (10-0 ) cardinal sutures
First suture placed at
12 o’ clock :donor tissue
grasped with fine
toothed, double-pronged
forceps(Pollack forceps
)at the epithelial–
stromal junction then
needle inserted at donor
tissue opposing the
wound. Suture depth
~90%. Tying done in 3-1-
1 or 2-1-1 fashion
Next suture placed at 6
O’ clock : most critical-
(tissue alignment and
astigmatism)
placed such that equal
amount of tissue
distributed at either side.
After tying AC should be
reformed.
The 3 o’clock suture is
placed and tied, followed
by the 9 o’clock suture.
Once again, tissue
alignment should be
checked and any aberrant
cardinal sutures replaced.
a diamond-shaped pattern
of corneal striae will
appear in the donor
cornea

21. Suturing should provide
Stable wound, physiological wound closure with symmetric spacing of sutures no optical aberration,
provide constant tension throughout suture life, no inflammation
Knots buried either on donor or recipient side(keep away from limbus) while keeping the AC formed
Alignment of these sutures should be bowmans layer of graft to bowmans layer of host
Wounds checked with cellulose sponge for leakage, any leakage found is closed with
another 10/0 NYLON suture, stubborn ones closed with ‘X’ suture
Step- 2 : Complete suturing
Eight to 12 additional radial interrupted 10/0 nylon sutures
are placed snugly to ensure adequate tissue apposition, but
not tightly

22. Interrupted sutures
only,(IS)
•Standard
•Allow complete or
partial removal of suture
at one sector
•An avg of 16 interrupted
sutures are enough to gain
watertight closure
Indicated in-
•Vascularisation of
cornea
•Multiple previous
rejections
•Inflammatory
conditions
•Ulceration
•Paediatric keratoplasty
Single Continuous
suture (SCS)
• one irregular bit can
impair the integrity of
the closure and once
passed cannot be
removed without
removing the entire
suture
• Ease of placement
,suture removal , and
the potential for suture
adjustment intra and
postoperatively to
reduce astigmatism.
Combined interrupted
and continuous sutures
(CCIS)
• This technique allows
Earlier removal of
interrupted sutures for
astigmatism control.
• Not to be used if there is
vascularization or
infectious keratitis
Double continuous
sutures(DCS)
• added safety of a second
suture
• First cont suture-80%
depth next at 50-60%
depth
• Deeper one can be
removed early to gain
control over
astigmatism
• More expertise required

24.  TORQUE vs ANTI-TORQUE SUTURE
Radial overlay
suture
And anti- torque
intrastromal
suture.
Non significant
astigmatism
Radial underlay (intra
stromal) suture and
torquing
Overlay suture.
This rotates
The graft and causes
significant
astigmatism
Whatever technique is used, final astigmatism cannot be
predicted until all sutures are out. Visual acuity often
improves once all sutures are out because of a decrease in
irregular astigmatism

25.  Sub conjunctival gentamicin(20mg)+ dexamethasone
(4mg) + sunconj cefazoline 25mg/ topical 4th gen FQ ,
alongwith timolol 0.25% gel and topical NSAIDS for
pain control ,
 Selective tarsorrhaphy can be done if surface healing
problems are anticipated- neurotrophic condition, pre
op lid abnormality

26. Immediate post-op/ first 24 hrs
 Pressure patching- for first 24 hrs
 Oral FQs in high risk cases(penetrating trauma,
combined procedures, pre existing ext eye infection)
 Prophylactic anti- glaucoma medication: vitrectomy,
synechiolysis, ant segment reconstruction along with
PK- oral CAI.
 NSAIDS and mydriatics, peribulbar long acting
anaesthetic : to alleviate pain
 Systemic steroids- in high risk cases1mg/kg for 5-7 days

27.  Early post-op care(first 7 days)-
 reestablishing the corneal epithelium, controlling inflammation,
preventing infection, treating any operative complication
 Vn, EOM, lid and pupil assessment f/b wound assessment-
 Epithelium status, leakage, suture status(tight, loose, broken,
exposed knots,infilterate), AC rkn, IOP measurement- tonopen
 Siedel’s test performed
~ wound leak found with siedel’s positive- BCL applied, if persists
for >3 days- resuture
~ Extreme anterior chamber shallowing or iris incarceration in the
wound—requires immediate surgical management
~ Topical antibiotic: Fluoroquinolone eyedrops 4 times daily until
epithelium is healed—usually within 7-14 days
~ Fluorometholone acetate 0.1% or Prednisolone acetate 1 % are
generally used 4 to 6 times daily initially or on hourly basis on
severe inflammation. Gradual and slow tapering of steroids
~IOP , lens staus monitored carefully in following visits
~ FLAT AC
High IOP- pupillary block- treat- mydriatics, YAG-PI.
Low IOP ,with positive siedel’s- wound leak

28. 1-12 week
 Prevention of rejection, infection, and cystoid macular
edema along with manipulation of corneal
astigmatism
 Educating patients – RSVP
 1 week following the surgery is the time of greatest
recognition of early endophthalmitis

31. Intraoperative complications
• Scleral perforation
• Trephination disarrays
• AC hmg
• Expulsive choroidal hmg
Post operative complications
• Wound leaks, displacement
• Persistent epithelial defect
• Filamentary keratitis
• Suture related- exposure, infection, infilterate, abscess, kaye dots
• Elevated IOP- glaucoma
• Anterior synechia formation
• Choroidal detachment
• Pupillary block
• Post-op infection
• Primary graft failure

32.  Scleral perforation- fixation sutures passed to secure scleral
rings for scleral support could cause scleral perforation.
Cryotherapy should be done if such situation occurs.
Round needles for passing fixation sutures
 Trephination disarrays
 Retained DM- improper removal of donor cornea with
corneal scissors, graft placed over such surface~ endothelial
loss and eventually graft becomes hazy. Such instance
occur in edematous host corne or corneas with interstitial
keratitis which have thickened DM.
Improper graft size- smaller
graft~tighter suture~
HYPEROPIA and TM
collapse
Eccentric trephination-
Higher post-op
astigmatism
Damaging donor corneal
button~ endothelial loss
By dropping the tissue,
incomplete trephination and
then pulling/tugging edges

33. Iris–lens damage-
• full thickness
trephination
• occurs in thinned out
,perforated cornea
• can be prevented by
filling AC with VED
beforehand via
paracentesis
• Significant iris damage
during trephination
should be repaired
Capsular damage
• If anterior capsule
damaged- must deal
immediately,
appropriate response
would be to convert into
triple procedure, hence
biometry should be
done pre-operatively in
all.
• Prevented by pupillary
constriction pre-
operatively
• Posterior capsule could
be torned in triple
procedure, sig. vitreous
loss, PI could be done.
• Failure to adequately
remove the vitreous can
lead to vitreous wick,
cystoid macular edema,
poor wound closure,
and an increased risk of
postoperative
endophthalmitis.

34.  Expulsive choroidal hemorrhage-
 non technical complication
 Associated risk factors- advanced age, myopia, glaucoma, inflammation,
infection, hypotonia or previous trauma(perforation), Valsalva maneuvers
during keratoplasty
 may lead to blindness because of the extrusion of intraocular contents
 Pre-op reduction of IOP, gentle trephination, prevents sudden fall in IOP-
preventive
 During open- sky phase , if choroidal hmg occurs, visible as dark brown
shadows in front of red reflex
 Recognition, early attempt to fix it, redirect hmg posteriorly to restore anterior
anatomy.
 If occurs immediately or shortly after entering the eye – sclerotomy is done~
probably infero-temporally
 If it occurs during open- sky phase-occlude the wound with thumb and
posterior sclerotomy is done.
 If intraocular contents have been
 extruded, it may be best to perform an evisceration primarily
 rather than require further surgery

35.  Wound leakage and displacement-
 Persistent wound leakage could
cause fistula, PAS, glaucoma,
endophthalmitis
 prevention
Flat AC,
Low IOP
SIEDEL’s test
+ positive
- negative
Wound leak
Immediate
Surgical
repair
Pupillary block or
Choroidal detachment
AC
AC formed Siedel’s + Pressure patching or BCL
application, aqueous suppressants
If leakage persists >48hrs –
surgical method of repair
needed
Good tissue
apposition
Symmetrical
tissue
distribution
Proper
suture
placement

36. Persistent epithelial defect
• Causes: previously- ocular surface disease, dec corneal
sensations, anterior blepharitis, longer donor storage time
• If such conditions prevails- treat
Lid abnormality first f/b limbal stem cell transplantation
then PK.
 A watch on indications like HSK- which is notorious for
recurrence~ preventable by long term prophylactic oral
acyclovir.
 Possibility of active herpetic infection may be considered
even though patient didn’t have it previously
 Hurricane shaped epithellial keratopathy- antibiotic-steroid
combination causing toxicity. Whorling spiral appearance
from periphery towards centre

37. Filamentary keratitis-
• Early post-op period
• Develop at graft host margin immediately surrounding the
suture tract
• Management
Minimal symptoms
• Hypotonic tear substitutes, help dissolve mucus strands
Severe symptoms
• Filaments could be removed with forceps
• Additive hypotonic tear solutions
• Mucolytics like acetyl cystine could also be added
• Many patients can be prescribed with BCL- but in such condiion close monitoring
nedded , as infectious keratitis might develop

38. Suture related complications-
Suture exposure
• Careful placement of
suture and with
appropriate tension-
no exposure
• Loose suture cause-
won’t get
epithelialized,
• cause local
inflammation,
stromal
vascularisation ~
rejection ,
• mucus debris
collection~filaments
, giant papillary
conjunctivitis,
• ulcer, dellen
formation etc.
• Rx
• Suture rotation tried
with close watch over
vascularisation and
infection
Suture related
infection
• Mucus and debris
collection due to
exposure becomes
nidus of infection
• Access to stroma
might lead to suture
abscess, BCL , topical
steroids~accentuate
process.
• Rx-
• Removal and culture
of suture, topical
steroids at halt,
systemic could be
started. Fortified
antibiotics
Suture related
immune infilterates
• Cause of
immunological rkn
to suture material, or
powder of gloves.
• Character
• Multiple
• Usually occurs on the
host side of the graft–
host interface
• No overlying
epithelial defect
• Rx
• Intensified
corticosteroid , if
epithelium not
intact, oral steroids
(0.5-1 mg/kg/d)
• f/b slow tapering
Kaye dots
• development of
discrete white dots in
the donor corneal
epithelium in a 1–2-
mm region central to
the graft sutures has
been described by
Kaye*
• correspond to
epithelial cells in
various stages of
degenerationno
epithelial defect-
patient
asymptomatic
• Not associated with
any immune
response, nor a sign
of rejection. Self
limiting.
*Kaye DB. Epithelial response in penetrating keratoplasty. Am J Ophthalmol.

39. Post PK glaucoma-
• Association b/w PK and post- PK glaucoma was first
described by- Irvine and Kaufman *
• Zimmerman et al postulated the effect of trabecular
meshwork collapse on post-op glaucoma.**
• Any sustained raise in IOP- lead to endothelial cell
loss , which in turn gets detrimental for graft survival
• CAUSES-
• Other causes- retained VED, ant synechiae, pupillary
block
• Rx- topical beta blocker, topical α 2 agonist and/or oral
CA inhibitor
Tight suturing
Long suture bites
Larger trephine sizes
Same sized donor host trephination
Inc. recepient peripheral corneal thickness
Irido-corneal angle compression
* Irvine AR, Kaufman HE. Intraocular pressure following penetrating keratoplasty. Am J
Ophthalmol. 1969;68(5):835–844.
** Zimmerman TJ, et al. Transplant size and elevated intraocular pressure postoperatively.
Arch Ophthalmol. 1978;96:2231.

40. Post operative inflammation
• If uncontrolled, fibrin formation due to breakage of
blood- aqueous barrier
• Fibrin serve as scaffold for formation of membranes~
leads to : pupillary block, 2° glaucoma, ultimately
endothelial cell damage
• Hourly topical steroids with mydriatics , non
responsive- periocular or systemic steroids advocated
• Intraocular TPA (last resort)- 25µg – onset of action-
20 min, complete lysis within 3hrs*
• Hmg is a risk
Snyder RW, Sherman MD, Allinson RW. Intracameral tissue plasminogen activator for
treatment of excessive fibrin response after penetrating keratoplasty. Am J Ophthalmol.
1990;109(4):483–484.

41. Anterior synechia formation-
• Any kind of contact with endothelial cell could lead to
endothelial cell loss~ compromising graft clarity due to
edema and in long run becomes leading cause for graft
failure.
• Synechia formation leads to 2 ° glaucoma, mechanical
traction also – both eventually cause endothelial cell loss.
• Risk factors- larger grafts , aphakic, pseudophakic eyes,
presence of flaccid iris, operating in an inflammed eye
• Management- complete synechiolysis, in larger grafts PI
should be done intaoperatively

42. Pupillary block-
• Medical mmt- mydriatics and cycloplegics to dialate
pupil, β blockers, CA inhibitors to lower IOP.steroids
to control inflammation, PI to prevent ant synechiae
formation.
Flat / shallow AC, with
Closed wound
IOP measurement
Pupillary
block
Choroidal detachment

43.  Choroidal detachment and hmg
 These are smooth, rounded elevations restricted by the vortex
veins and the optic nerve.
 They can extend forward to the scleral spur, resulting in shallow
AC
 MECHANISM-choroidal effusion due to sudden drop in pressure
gradient b/w choroid and suprachoroidal space, more fluid
getting collected in suprchoroidal space, and increased uveo-
scleral outflow, ciliary detachment if present- aqueous
shutdown. ~ hence flat AC.
 Inflammation could also cause choroidal effusion mainly due to
variation in capillary permeability.
 If AC angle is compromised for more than 48 to 72 hours and the
choroidal detachment is persistent, surgical drainage with
reformation of the anterior chamber is recommended.
 Symptoms- sudden onset pain and decreased vision.
 Risk factors include advanced age, atherosclerotic vascular
disease, hypertension, and glaucoma.

44.  Fixed dilated pupil:
 its seen post operatively in patients with keratoconus-
occuring as a syndrome of –
 Drugs like atropine, scopolamine, phenylephrine have been
found as culprits
 It may be due to ischemic atrophy of the sphincter pupillae
muscle secondary to iris strangulation during dilation.
 Recovery in 1-18 weeks, in mean time IOP lowering drugs
given .
1. Iris atrophy
2. Pigmentation on lens capsule &
corneal endothelium
3. Sec. glaucoma with post synechiae.

45. Post operative infection-
 Graft infection usually manifests within 24 to 48 hours with
ciliary injection, graft edema, mucopurulent discharge, and
occasionally an infiltrate.
 Risk factors- persistent epithelial defects, contact lens
usage, loose or broken sutures, corticosteroid therapy, and
keratoconjunctivitis sicca, positive donor corneal rim
culture. Eyes receiving corneas with positive rim cultures
have a 12- to 22-fold increased incidence of
endophthalmitis*
 The current recommendation is for donor tissue to be
brought to room temperature for 1 hour immediately before
use. Since std. antibiotics at 4 degrees celcius in storage
media cannot reliably sterilize an inoculum of sensitive
bacteria.**
*Leveille AS, McMullan FD, Cavanagh HD. Endophthalmitis following penetrating keratoplasty.
Ophthalmology. 1983;90:38–39
**Baum J, Barza M, Kane A. Efficacy of penicillin G, cefazolin, and gentamicin in M-K medium at 4°C.
Arch Ophthalmol. 1978;96:1262– 1264..

46.  ENDOPHTHALMITIS-

47.  In one sense it is failure of the graft to achieve the
stated aim for performing the procedure, more so
often it means a graft loosing its clarity, but in TPK
even if clarity is compromised while no appearance of
re-infection occus~ its successful PK.
 cornea requires approximately 1000 cells/mm2 to
remain clear and compact
primary graft failure
• Occurs in 1st post op week
• A graft which never clears remaining
thickened postoperatively, is termed a
primary failure
Secondary graft failure
• Beyond 1st post op week
• occurs in a graft that has functioned in the
immediate postoperative period
• commonest cause is an immune mediated
process termed allogenic graft rejection
• Not all episodes of allogenic graft rejection
progress to secondary graft failure. Some
resolve with endothelial function returnin.g

48.  ALLOGENIC GRAFT REJECTION-
 Allogenic graft rejection refers to a cell-mediated immune
reaction directed against the corneal allograft. It is directed
against Major Histocompatability Complex (MHC)
alloantigens present on donor cells.
 Since 3 anatomical layers are introduced rejection could be
targeted to any one of these or in combination.
 Epithelium- 15months ~ commonest type.
 Stroma- replaced over yrs
 Endothelium – life long

49. Careful case selection
Identifying high risk cases
Usage of corticosteroid
Tissue matching
Antiviral prophylaxis where
h/o HSV +nt
prevention 1)Previous graft rejection
2)PK folllowing herpes
keratitis
3)Large graft diameter
4)Age<40 yrs
5)Inflammed eye,
traumatised
eye~perforation
6)Eyes previously known to
be having glaucoma
7) Recepient corneal
neovascularisation> 2
quadrants
High risk
cases