This document summarizes various early and delayed postoperative complications that can occur following penetrating keratoplasty (corneal transplant surgery) and their management. Early complications discussed include suture-related problems, wound leaks, epithelial defects, inflammation, iris incarceration, graft failure, glaucoma, and infections. Delayed complications mentioned are graft rejection, infectious crystalline keratopathy, corneal membranes, cataract formation, and recurrence of the original corneal disease. Treatment approaches for each complication are also provided.

1. POSTOPERATIVE
COMPLICATIONS AND
MANAGEMENT OF
PENETRATING KERATOPLASTY
Dr.Vanshaj
Dr.Richa

2. EARLY DELAYED
 Suture related problem
 Wound Leaks and Wound Displacement
 Iris incarceration
 Wound dehicence
 Descemet membrane detachment
 Filamentry keratitis
 Epithelial defect
 Primary graft failure
 Graft rejection
 Hyphema
 High IOP& pupillary block glaucoma
 Low IOP
 Microbial keratitis
 Endophthalmitis
 HSV keratits
 Graft rejection
 Infectious crystalline keratopthy
 Urretz-Zavalia syndrome
 Cataract
 Corneal membranes
 Hurrican keratopathy
 Astigmatism
 Glaucoma
 Recurrence of recipient original
disorder
 Disease transmission by donor
cornea
 VR problems

3. EARLY
COMPLICATIONS:
 Within 4 weeks

4. SUTURE RELATED PROBLEMS:
Suture
related
problems
features treatment
Exposed
knots
FB Sensation.
Gaint
papillary
conjunctivit.s
Nidus for
infection.
Vascula-
rization.
Rotation
/replace
suture with
knots burried
Broken suture remove

5. Tight suture Persistent
epithelial
defect
Nidus for
infection
remove
Loose suture Exposed
failure to
epithelization
remove
Entanged
suture knots
Can loosen,
Become
exposed
or act as a
nidus

6. Suture
abscess
Poor
prognostic
factor for graft
Can lead to –
• wound
dehiscence
• graft failure
secondary
to infection
• corneal
scarring
•endophtha-
lmitis
Debride
suture roof,
suture & send
for
microbiologic
al
examination
Broad
spectrum
antibiotics
Immune
infiltrate
Immunol-
ogical
reaction to
suture
material/ talc
from surgical
gloves
Topical
steroid and or
ciclosporin
Vascularizati-
on

7. Wound Leaks and Wound
Displacement:
 Shallow AC with low IOP on POD 1 –
WOUND LEAK
 Shallow/flat AC may occur due to pupillary
block or choroidal detachment.
 Siedels test
 Prolonged wound leak:
I. persistent fistula
II. Secondry glaucoma
III. peripheral anterior synechia
IV. Significant endothelial loss
V. Epithelial ingrowth

8.  CAUSES:
Broken,loose,misplaced suture
Suture track leak - full thickness suture
Suture between thin or necrotic tissue
Excessive gap between suture
Unequal thickness between graft and host

9. MANAGEMENT:
Anterior
chamber flat
Wound suture
leak or iris
prolapse
Surgical repair
immediately
Anterior
chamber formed
Wound leak
Pressure
bandage,BCL,
acetazolamide

10. If wound does not seal in 24 hours
RESUTURE

11. EPITHELIAL DEFECTS:
 Re- epithelization & maintenance of intact
epithelium is essential for postoperative wound
healing & survival of graft.
 Average time for complete epithelization is 4-6 days.
 Removal of the histocompatibility antigen on the
donor epithelial cells would decrease the incidence
of allograft rejection. Stulting et al. Showed that
there is no decrease in likelihood of rejection by
doing that.

12. RISK FACTORS FOR EPITHELIAL
DEFECTS:
 Ocular surface disorder
 Lid abnormalities
 Infection & inflammation
– HSV
 Iatrogenic
 Epitheliotoxic drugs
 Damaged donor epithelium
 Basement membrane
disorder
 Intrinsic epithelial disorder
 Trauma
 Poor nutrition
 Metabolic diseases

13. EPITHELIAL DEFECTS-
MANAGEMENT:
 Prevent and treat risk factor.
 Using nonpreserved artificial tears and limiting medication
toxicity to the epithelium are essential.
 Pressure patching -decreasing eyelid motion over the
healing surface.
 I f healing not complete in 1 week -BCLCollagen shields.
 Autologous serum.
 Amniotic membrane transplantation.
 I f healing not complete in 2 week-Temporary permanent
tarsorrhaphy.
 BotulinumA toxin injected into the levator muscle to
produce a protective ptosis.
 Keratoepithelioplasty.

14. POSTOPERATIVE INFLAMMATION:
 Topical corticosteroids.
 May lead to the formation of intraocular fibrin due to
breakdown of the blood–aqueous barrier.
I. Pupillary block,glaucoma
II. Direct damage to endothelium.
 IntraocularTPA (25µg)

15. IRIS INCARCERATION:
 Causes:
I. Collapse of AC
II. Inflamed eyesswollen & flaccid iris
III. Poorly placed suture
 Closes AC angle at site incarceration
I. Glaucoma
II. Graft failure
 Large adhesion at graft host junction localised graft
edema & vascularization.
 Manages by-
I. Argon laser iridoplasty
II. viscoelastic substance is injected into the anterior chamber
and the iris is swept out of the wound with an iris or
cyclodialysis spatula introduced through another area of the
wound or through a separate limbal incision.

16. WOUND DEHISCENCE:
 Can occur immediately/several years later.
 Causes:
I. Trauma
II. Infectious keratitis
III. Suture failure
IV. Spontaneous wound separation
 Resuture immediately

17. DESCEMET MEMBRANE
DETACHMENT:
 Intracameral air / C3F8,SF6 or viscoelastic
 Transcorneal suturing
 Corneal transplantation

18. FILAMENTRY KERATITIS:
 Filaments consist of abnormal collections of
mucus and epithelial cells on the corneal
surface.
 Usually predominate in the early
postoperative period.
 Develop at the graft–host margin.
 Foreign body sensation and redness.
 Hypotonic artificial tears,topical
acetylcysteine,removed with a forceps,BCL.

19. PRIMARY GRAFT FAILURE:
 Gross corneal edema in grafts with large broad
folds immediately after keratoplasty.
 Not followed by period of clear cornea.
 Factors:
I. Prolonged death-enucleation time
II. Poor donor endothelial count
III. Aphakic and psuedophakic donor
IV. Elderly donor
V. Inadequate preservation
VI. Surgical trauma
VII. HSV infection

20. PRIMARY GRAFT
FAILURE:MANAGEMENT
 irreversible edema unresponsive to
hypertonic saline/steroids.
 Hyposecretion of aqueous humor, which may
occur after penetrating keratoplasty, may
result in corneal edema due to a decreased
supply of metabolites to the endothelium.
 Observe for 3-4 weeks for signs of clearing.
 no improvement- repeat PKP.

21. HYPHEMA:
 Incidence increase with intaoperative
manipulatons like extensive
synechiolysis,iridoplasty,iridotomy.
 Clears spontaneously without treatment.
 IOP high- treat aggressively.
 Beta-blockers + Brimonidine/acetazolamide
 Prolonged persistence-clot irrigation and
aspiration.

22. HIGH IOP & PUPILLARY BLOCK
GLAUCOMA:
 Due to:
I. Residual viscoelastics in
AC
II. Uveitis
III. Hyphema
IV. Crowding ofAC angle
V. Pupillary block-it occurs
due to posterior
synechiae.
VI. Forward movement of
lens iris diaphragm.

23. HIGH IOP MANAGEMENT:
 Topical glaucoma medicaton-
I. b-adrenergic antagonists
II. Adrenergic agonists
III. Alpha -2 adrenergic agonists
IV. Carbonic anhydrase inhibitor-acetazolamide
V. Hyperosmotic agents
VI. Peripheral iridotomy,surgical iridectomy.

24. LOW IOP:
 Causes :
I. Wound leak
II. Iridocyclitis: cilliary shock
III. Cyclodialysis
IV. Choroidal detachment
V. Retinal detachment

25. HSV KERATITIS:
 Can incite graft rejection.
 Patterns:
I. Dendritic
II. Geographic
 Stromal -graft edema,KPs.
 Propensity to occur in graft host
junction,absence of khadadaoust line.
 Topical acyclovir 5 times a day for 2weeks post-
op.
 Oral acyclovir 400mg BD/valacyclovir 500 mg BD
for 1 year.

26. Rose bengal staining of geographical ulcer caysed by HSV
after PKP:

27. MICROBIAL KERATITIS:
 Incidence higher in developing countries.
 ½ occur within 1st 6 months of surgery.
 Either infection within graft/ along suture tracts at
graft host junction
Inflammatory Reaction
Initiation of Graft Rejection
Graft Failure Graft Melting Endophthalmitis
 Corneal scrapings – Gram’s stain/KOH/Culture & Sensitivity.
 Therapy modified based on lab report.
 Initial therapy – Fluoroquinolone or combination of Cefazolin 5% e/d and
Tobramycin 1.3% e/d

28. DELAYED
COMPLICATIONS:
 From months to years

29. GRAFT REJECTION:
 Viable donor cells possessing class 2 and 1 antigen &
major histocompatibility antigen comes in contact
between recepient lymphocytic population,genrates
immune response.
Graft clear for atleast 2 weeks
graft edema + inflammatory signs

30. Graft rejection Clinical features
epithelial Elevated,undualating
line(stains).
Starts near a vessel at GHJ.
Subepithelial infitrates Confined to the graft
02-0.5mm,white
Randomly distributed
Beneath bowmans layer.
stromal Peripheral full thickness
Of corneal haze
endothelial increased corneal thickness
Khodadoust line
(line of pigmented KPs

31.  Prednisolone acetate 1percent or dexamethasone
sodium phosphate 0.1 percent eye drops 4 times a
day,with tapering over 1 month.
 Dexamethasone eoint at night time.
 Endothelial rejection- treated more aggresively.
 Sub-tenon injection of methylprednisolone.
 Tab. Prednisolone 1mg/kg/day tapered over 1-2
weeks. Or Intravenous methylprednisolone(500mg).
 Systemic azathioprine-has potential side effects
 Cyclosporine- metabolite of fungus topocladium
inflatum

32. INFECTIOUS CRYSTALLINE
KERATOPATHY:
 Chronic, progressive
corneal infection.
 Anterior lamella of graft
involved-most
commonly by
streptococcus viridans.
 No clinically evident
stromal inflammation.
 Crystalline branching
opacities in anterior &
mid stroma

33. URRETS-ZAVALIA SYNDROME:
 Permanent fixed dilated pupil after penetrating
keratoplasty/DALK in patients with keratoconus.
 Iris atrophy
 Secondary glaucoma
 Mydriasis unresponsive to miotics.
 Unknown etiology (severe iris ischaemia – possible
mechanism).
 Management –
I. Reduce IOP
II. Avoid Atropine pre-operatively
III. Peripherally painted Contact Lens for photophobia, glare

34. CORNEAL MEMBRANES:
 Epithelial ingrowth (conjunctival/corneal) – through
gap at host-graft junction.
I. cryotherapy with air in the AC to insulate the
intraocular contents.
II. Sugical extiparation.
III. Removal of abnormal tissue with fistula & replaced
with graft.
IV. Prevention of medically uncontrollable glaucoma
& pain using a seton.
 Fibrous ingrowth (retrocorneal membrane) –
gray/white fibrous membranes between DM and
endothelium-repeat PKP.

35. HURRICAN (WHORL)/ VORTEX
KERATOPATHY:
 due to an antibiotic–
steroid combination
containing neomycin,
polymyxin,
dexamethasone, and
benzalkonium chloride.
 whorling spiral
extending from the
peripheral border of
the graft inward.

36. CATARACT:
 Incidence varies from 25-80%
 Due to –
I. Poor surgical technique
II. Altered lens metabolism
III. Toxic drugs– corticosteroids,
anticholinesterase

37. ASTIGMATISM:
 Average – 4-5 D
 Higher in eyes with –
I. Scarring due to corneal ulcer
II. Keratoconus
III. Eccentric graft
IV. Mal-aligned graft
V. Faulty suturing techniques
VI. Improper placement of
second suture
VII. Unequal depth
VIII. Non-radial sutures
IX. Tight sutures
X. Unequal distribution of
tension in continuous suture
 Surgical precaution to
minimize Astigmatism:
I. Central and sharp trephination
II. Use of a sharp trephine
III. Symmetric suture placement
(especially 2nd suture)
IV. Avoid tight suture placement
V. Suture adjustment (for
continuous suture) or selective
suture removal (for
interrupted sutures)

38. GLAUCOMA:
 Most commonly due to PAS and epithelial downgrowth
& then due to steroid induce.
 2 unique mechanisms –
I. Collapse of trabecular meshwork
II. Compression of AC angle
 Larger Donor Grafts – associated with deeper AC lower
incidence of post-op progressive angle closure and lower
post-op IOPs.
 Avoid prostaglandins.
 LaserTrabeculoplasty.
 Trabeculectomy with MMC Surgery.

39. RECURRENCE OF ORIGINAL
RECIPIENT DISORDER:
 Due to migration of recipient keratocytes into graft stroma.
 Occurs frequently in –
I. Granular – 100% at 4 years*
II. Macular – 5.2%
III. Lattice – 48%
IV. Reiss Buckler’s dystrophy
V. Central crystalline dystrophy
VI. Posterior Polymorphous dystrophy
 Repeat graft
 Superficial keratectomy/ Excimer laser Phototherapeutic
keratectomy – for superficial lesions.

40. ENDOPTHALMITIS:
 This may occur as a early complication or as late
complication.
 Pain ,decreased visual
acuity,hyperemia,chemosis.
 Tap from anterior chamber,VitreousTap.
 Intensive topical, intravitreal and systemic
antibiotics.
 As a late complication it might associated
with suture removal,vitreous incarceration in
keratoplasty wound.

41. VITREORETINAL PROBLEMS:
 Retinal Detachment:
 Rare
 Incidence increases with complicated procedure, especially after
vitreous manipulation.
 Macular Edema:
 Common cause of non improvement of vision despite clear graft.
 Predispositions –
I. Aphakic bullous keratopathy
II. Pseudophakic bullous keratopathy
III. Trauma
IV. Any previous intraocular surgery
 Non steroidal antiinfflamory drugs.

42.  PHOTOTOXIC MACULAR DAMAGE:
 Microscope light induced.
 Free radical produced due to interaction of light and
oxygen causes injury to retinal cell mitochondria.
 Symptoms- central and paracentral scotoma,decrease
visual activity.
 Signs-macular edema followed by gradual pigmentation.

43. THANK YOU