COMPLICATIONS AND

MANAGEMENT OF PKP
SIR HAROLD RIDLEY

• First IOL implant

• 1949
EDUARD ZIRM

• First human Keratoplasty

• 1905
• 45 yr old pt (lime injury)
• Donor – 11 yr old boy
The evolution of PKP can be divided into five periods:-

1) Inspiration (1789-1824)
2) Trials and Frustration (1825- 1872)
3) Conviction (1873-1905)
4) Achievement (1906-1965)
5) Refinement and Innovation (1966-present)
 Indications

The indications for PK have continued to change since 1940

Regrafts was the M.C Indication

1. Pseudophakic bullous keratopathy

2. Keratoconus
3. Corneal scars
4. Corneal dystrophies ( endothelial)
5. Regrafts
6. Aphakic bullous keratopathy
 Greater success

• Immune previlege
• Proper surgical technique
• Prevention and early recognition
• Management
• Technology

 In uncomplicated or “low risk” grafts, the survival rate as high as

95% at 5 years
 In contrast, “high-risk” recipients, the failure rate can easily exceed
35% at 3 years
 “Immune privileged”
• absence of vascularity hinders delivery of immune elements
• absence of directly draining lymphatics prevents high-volume
delivery of antigens and APCs to T-cell reservoirs such as lymph nodes
• Blood aqueous barrier non-pigmented epithelial cells of the CB
• The expression of CD95 (Fas) ligand can induce apoptosis of
stimulated Fas+ T cells (infiltrating lymphocytes)
• ACAID Antigens placed in the anterior chamber can cause selective
suppression of the systemic immune response
• The low expression of MHC II antigens limits the targets of the
immune response
• Relative paucity of antigen presenting cells (APCs) in the central cornea

Advances in corneal preservation techniques, antibiotics;

newer surgical methods and technology have improved success rate
Anterior chamber–associated immune deviation
(ACAID)

Antigens released into the aqueous humor are recognized by

These APCs dendritic cells
exit via TM andofenter
the iris
theand ciliary
venous body
circulation into the
spleen, bypassing the lymphatic system

Immune response directly communicates with spleen that results in

induction of CD4 Tregs (regulatory cells) and suppressor CD8 cells
down-regulates delayed-type cellular immunity

Induces a systemic suppression of future potentially damaging

response to infection or inflammation
Effector blockade takes 1 week protecting the eye from the
to develop collateral damage
It is a type of immune previlege which suppresses host’s
defence mechanisms by inhibiting delayed type of cell
mediated immunity, thereby preventing potential damage
to sensitive ocular tissue
COMPLICATIONS

Intra operative

Post operative
SURGICAL STEPS
• Pre operative preparations
• Insertion of lid speculum
• Placement of scleral fixation ring
• Marking of host cornea
• Trephination of donor cornea
• Trephination of host cornea
• Placement of visco in anterior chember
• Placement of donor corneal tissue in host bed
• Placement of cardinal sutures
• Complete suturing
• Suture readjustment
 Pre op preparation

Infection control
• Most common source of endophthalmitis is patient
periocular flora.
• Management and elimination of blepharitis
• Lashes should be covered
• Single application of one drop of 5% povidone iodine

Endophthalmitis
 IOP control

• Optimal control of glaucoma pre op

• Complete lid and EOM akinesia
• Digital massage or honan ball at 30 mm hg for 30 min
 Lens management

PHAKIC pt COMBINED Sx

2% pilocarpine 2.5 % phenylephrine

constricts the pupil Dilates the pupil

protects the crystalline lens Cataract extraction

 Donor corneal tissue management

 Epithelial defects
 Infiltrates
 Foreign bodies
 Scars
 Other pathologies

60 minutes of warming time

 To anticipate suprachoroidal haemorrhage

• Most feared ophthalmic intraoperative complication

• INCIDENCE ranges from 0.45% to 1.08%.
• The risk appears to be much higher in eyes that have undergone
previous surgery
• Risk factors: older age, glaucoma, previous vitrectomy, tachycardia,
systemic hypertension, arteriosclerosis, anticoagulant therapy

PREVENTIVE MEASURES:

to stop anticoagulant therapy

Control of BP and anxiety
Pre op IOP reduction
General anaesthesia in high risk patients
To shorten the operating time
 Intra operative

Insertion of lid speculum

Pressure against the eye

Globe distortion

Irregular trephination
Poor suture alignment

Increased astigmatism
 Placement of scleral fixation ring
FLEIRINGA RING
o Children
o Aphakics LOW SCLERAL RIGIDITY
o Pseudophakics
o Vitrectomised eye

Scleral perforation
Retinal hole
RD
Damage to ciliary body
Haemorrhage at angle
 Marking of host cornea

Decentered grafts

High astigmatism

Oversized grafts ( >8.5mm)

Increased risk of rejection

 Trephination of donor cornea

• Done before host trephination

• Trephined with the endothelial

side facing up

• Prevent the damage to the endothelium

• To obtain round donor button with perpendicular edges

• Submerge donor tissue in storage medium while preparing

host bed
 Trephination of host cornea

 Optimum visco through paracentesis to provide cushioning effect

 Minimal pressure with the trephine and to avoid the abrupt entry in
to the anterior chamber suprachoroidal haemorrhage

 To visualise scissors at all times with maintained upward pressure

iris damage

 Optimal trimming of the tags

wound leakage and apposition problems

 Tissue disparity between the host corneal bed and donor cornea
major cause of astigmatism
 Retained DM

• Inadervently placed corneal scissors

anterior to Descemet membrane

• Oedematous corneas
Interstitial keratitis

• decreased visual acuity from fibrosis and opacification of the

retained Descemet membrane,
and accelerated endothelial cell loss from direct trauma

• Creation of false or double anterior chamber

Removal of retained DM
Yag laser
 Iris or lens damage
 Most likely in thinned and perforated corneas

 Iridodialysis can occur

 Prevented by placement of visco in anterior chamber

 Repair of irido dialysis by 10-0 polypropylene or nylon suture

 Placement of donor corneal tissue in host bed
Grasped with the fine toothed forceps at the junction of epithelium
and stroma

To rest on visco material

To avoid any contact of the endothelium with instruments or

surfaces

Most spherical reflex obtained with an intra operative keratometer

 Suturing related
Interrupted
Continuous

ADVANTAGES
INDICATIONS ADVANTAGES
INDICATIONS
• Cornea of uneven thickness • Cornea of even thickness
•• Technically less difficult
Vascularisation in host corneal •• Uniform wound healing
No vascularisation
• Selective
bed suture removal in case of •• Incites less inflammation
No inflammation
•children and uneven wound healing
Inflammatory conditions • Even distribution of tension around
(infective) the wound
•• Multiple failed grafts
Individual suture bites can be
•adjusted
Therapeutic grafts
DISADVANTAGES
• Paediatric grafts
DISADVANTAGES • Cannot be selectively removed
• Stimulates more inflammation,
• vascularisation ( more knots)
 Torn PC / Vitreous loss
• During combined procedures

• Placement of IOL in sulcus in small tears without VD

• Anterior automated vitrectomy

Role of peripheral iridectomy

 Anterior chamber haemorrhage

• In highly vascularized corneas, neovascular vessels of the iris

• Usually minimal

• Stops after the wound is closed and IOP is restored

• Severe haemorrhage may occur during iol explantation as it

may rip off the iris

• May cause iridodialysis

 Management

Cautery
Compression with visco
Tamponade with weck cell sponges
(soaked in epinephrine or thrombin)
Suturing the donor in place

Takes time to clear once it seeps into vitreous

 Expulsive Suprachoroidal Hemorrhage

• most devastating complication

• Incidence ranges from 0.45% to 1.08%
• occurs during the open-sky phase of the procedure, it
typically results in the expulsion of intraocular contents
Pathophysiology

Sudden decompression
Raised episcleral venous pressure (Valsalva maneuvers)

Rupture of a long or short posterior ciliary arteries

 Suprachoroidal Hemorrhage

• poor visual prognosis

• prompt recognition
Immediate and initial step

Tamponade the eye with digital pressure

Attempt to restore intraocular pressure

Prevent the expulsion of intraocular contents
once blood clots

Closure of the wound with either

the recipient or donor cornea
 Post operative

Early Late
Wound leaks and diplacements
PED
Filamentary keratitis
Suture related
Raised IOP
Synechia formation
Post op inflammation
Pupillary block
CD
Hyphema
Fixed dilated pupil
Post op infection
Primary donor failure
Wound leaks

Low IOP
Flat/shallow AC
Positive seidel test
 Wound leak

• Immediate • Pressure
surgical repair patch
• BCL
• AGM
Formed
Flat AC
AC

Broken/
Wound
loose dehiscence
suture
• BCL • Surgical
repair
 Persistent epithelial defects

Intact epithelium

• Improved visual acuity

• Graft transparancy
• Graft survival
• Protection of graft against infection and melting
 Risk factors

Surface disorders Host Donor

• Alkali burn • Decreased corneal • Handling of donor tissue

• SJS sensation • Type of storage media
• OCP • Blepharitis • Donor medical history
• Neurotrophic • Increased recipient age • Longer storage time
keratopathy • LSCD
• Dry eye
 PED
Treated aggressively as it heals slowly after 1week
The risks of stromal scarring and ulceration increase significantly with defects
present longer than 3 weeks
Rx
• Permanent or temporary tarsorraphy
• BCL
• Collagen shield
• AMT
• Nonpreserved artificial tears
• Antibiotics with minimal epithelial toxicity
• To minimize topical steroids or change to oral steroids

Rule out active herpes virus infection when an epithelial defect does not
respond to treatment.
 Filamentary keratitis
• Abnormal collection of mucus and epithelial cells on the
corneal surface
• often develop at the graft–host margin immediately
surrounding a suture track
• cause foreign body sensation and redness
• carefully removed with forceps if severe
• Stain poorly with fluroscein and brilliantly with rose bengal.

 Artificial tears
 Topical acetylcysteine
 BCL
 Punctal occlusion
 Suture-Related Complications

Indications of suture removal:

• Loose suture
• Tight suture
• Exposed knot
• Stromal vascularisation
• Healed graft
• Suture infiltrate/ abscess
 Suture-Related Complications

Complications of loose sutures/

exposed knots :
• Pain, FB sensation
• GPC
• Vascularisation
• Dellen
• Infection
• Delayed wound healing
• Graft failure
Complications of tight suture:
• Epithelial healing problems
• Cheese wiring
• Flat graft
• Astigmatism
Rx Exposed knot

o Suture rotation at slitlamp

o Topical antibiotics with watchful observation

o Lubricants

o SR as the wound healing permits.

Any suture that is broken or loose or associated with stromal

vascularisation across the wound should be removed immediately
 Suture related infection
Risk factors : Accumulation of mucus & debris
Exposed suture
Use of soft CL
Use of topical steroids

Suture abscess
 Corneal scarring
 Wound dehiscence
 Corneal perforation
 Endophthalmitis
 Graft failure
 Suture abscess

Defn: Infiltrate in donor or recipient cornea which is in direct contact

with the suture material.
Common organisms
S. Epidermidis
S. Aureus
S. Pnemoniae Risk factors
Loose or broken suture
Recent SR
Corticosteroid use
PED
Soft CL
KCS
Previous herpes simplex keratitis
 Immune infiltrates
An immunological reaction to the suture material itself or to the talc
from the surgical gloves.

Rx
Intensified topical corticosteroid regimen

Oral steroids if epithelium is not intact

 Infiltrates
IMMUNE INFECTIOUS

• Multiple • Solitary

• Host side of G-H interface • Graft or host side of

interface

• No epi defect • Epi defect present

• No AC reaction • AC reaction present

Intensive corticosteroids regimen

 Rx

• Removal and culture of the affected suture

• Broad spectrum fortified antibiotics until sensitivities are known

• Discontinuation of topical corticosteroids

• Systemic steroids to prevent rejection.

 Kaye dots
• discrete white punctate opacities in the donor corneal
epithelium anterior to suture line of corneal graft
• Not associated with erosions or fluorescein staining
• not associated with rejection or infection
• Disappear over 30 days

Dots correspond to epithelial

cells in various stages of
degeneration
 Hyphema
 Incidence increases if extensive synechiolysis, iridoplasty, or
iridectomy has been performed
 Usually clears spontaneously
 Risk for the development of posterior synechia, peripheral anterior
synechia, or corneal blood staining increases with time.

Medical
• IOP lowering agents
• Mydriatics- prevent PAS
• Topical corticosteroids

Surgical: uncontrollably elevated IOP

 Formation of anterior synechia
SEQULAE Risk factors
• Secondary angle closure  Larger grafts
glaucoma
 Aphakic patients
• Damage to endothelial cells

 Pseudo phakic patients

• Increased risk of graft
rejection
 Presence of flaccid iris
(secondary to surgery/trauma)
Treatment
Use of mydriatics or miotics : break synechiae

Small and non progressive progressive > 50% of AC angle

Observation Argon laser surgery Sx

to the basal iris
Pupillary block

Flat or shallow AC
Securely closed wound confirmed by seidel test

Pupillary block choroidal detachment

Raised IOP Low IOP
 RX
Medical
Mydriatics and cycloplegics
IOP lowering agents
Corticosteroids

If no response

Surgical
Peripheral iridectomy
+/-
Pars plana vitrectomy
Choroidal detachments
• usually due to uveal effusion in the early postoperative period
• due to the sudden change in pressure gradient between the
choroid and the suprachoroidal space.
• self-limiting
• wound leak must be ruled out
Long standing ones may lead to-

o Anterior synechia
o ACG
o Pupillary block
o CME

Persistent CD with compromised AC angle

Surgical drainage with reformation of AC

 Elevated intraocular pressure
DISTORTION OF ANGLE STRUCTURES:

1. Compression of AC angle
2. Collapse of the TM

• Tight sutures
• Long suture bites
• Larger Grafts
• Same size donor host
trephination Iridocorneal angle crowding
• Increased recipient peripheral
corneal thickness IOP
 2. TM collapse

o Loss of anterior support Interruption of DM by PKP

incision
o Loss of posterior support loss of support by lens and
zonules
Aphakia
Vitrectomy
Combined cataract

TM collapse &
decreased outflow
 Elevated intraocular pressure
Acute elevation of intraocular pressure after PKP with or
without optic nerve and visual field changes.
Causes:
• Distortion of AC angle
• Preexisting glaucoma
• Uveitis / Post op inflammation
• PAS
• Pupillary block (DSEK)
• Hyphaema
• Retention of visco
• Steroid induced
• Aqueous misdirection
 Rx
post op
topical B blocker
Oral carbonic anhydrase inhibitor
Topical apraclonidine 0.5%
Systemic osmotic agents Short term basis

Sx
• glaucoma filtration sx
• AC shunt implantation
• Cyclocryotherapy
• Laser cyclophotocoagulation
Infections After Penetrating
Keratoplasty
 Infectious crystalline keratopathy
• a noninflammatory, intrastromal bacterial colonization of a corneal
graft
• associated with long-term topical steroid therapy
Gray-white, midstromal branching, needle-like opacities in anterior
or mid-stroma

RISK FACTORS:
PKP
LASIK
Contact lens wear
Lamellar keratoplasty
Corneal relaxation incisions
 ICK
• The lesion is indolent, progressive, and occurs beneath an intact epithelium in the absence
of clinically evident stromal inflammation

• Most common - Streptococcus viridans

Others: S. Pneumoniae,
Coagulase-negative Staphylococcus,
Peptostreptococcus, Haemophilus species,
Mycobacterium species, Pseudomonas
Candida species

• The lesions themselves are not due to crystal deposition

• Light microscopy generally demonstrates the causative organism in aggregates within the
interlamellar or intralamellar spaces of the stroma without inflammatory cells.
 Path: presence of biofilm secreted by the organism

scant inflammatory response

tenacious and difficult to eradicate

Treatment: Discontinue or taper steroid

Fortified topical antibiotic drops given in an intensive dosing regimen.
S. viridans topical penicillin G 333 000 units/mL,
cefazolin 33–50 mg/mL,
vancomycin 33–50 mg/mL.

• The use of Nd:YAG laser to disrupt the protective glycocalyx matrix

surrounding the organisms causing ICK
 Microbial keratitis
PREDOMINATING :
Streptococcus pneumoniae(27%)
Staphylococcus aureus (20%)
Gram-negative organisms (20%)
and fungal organisms (13%). Microbial
keratitis

Immediate Late
post op post op
Recurrence

Contaminated Intra op Acquired

donor button contamination infection
Predisposing risk factors:
• Suture-related problems Broken suture or
loose suture material
• epithelial defects recent removal of sutures
• bandage contact lens wear
• history of herpetic keratitis
• corticosteroid use
• ocular surface disorders
• eyelid and ocular adnexal abnormalities
Management
• Scrapings for cultures and smears
• Contact lens removed and placed on a separate culture plate
• Cultures of the donor rim at the time of Sx
• Once culture results are available, antibiotic therapy can be
tailored to the individual organisms
• Topical corticosteroids should be stopped
• Antibiotics should be tapered gradually
• Prognosis for graft survival is relatively poor
 Endophthalmitis

Usually within 72 hrs of surgery

Risk factors Cause Clinical

Contaminated donor
button / instruments / Signs of inflammation
irrigating solutions
75% bacterial
with or without
Prologed storage S epidermidis hypopyon
Pt own flora
VD 20% fungal Diminished or poor red
Drug allergy C. albicans reflex
Sec to SR /keratitis
 Vanco 1 mg in 0.1
Seidel test ml
B scan Ceftazidime 2.25
mg in 0.1 ml

Aqueous sampling Amphotericin B

Vitreous aspiration 0.005 mg in 0.1 ml
VITRECTOMY
 Herpetic Keratitis After Keratoplasty

Recurrent herpetic dendritic keratitis

Increases risk of graft failure

• 10–25% of patients during the first year

• 9–21.6% during 2 to 5 years (use of steroids)

Manifestations : early recurrences occur at the periphery in the host–

donor interface
• dendritic ulceration within the graft
• geographic ulceration
• herpetic stromal infiltration of the graft

Role of oral acyclovir

Newly acquired :
• Surgical trauma
• Suture removal Endogenous reactivation
• topical corticosteroid use
• immune reactions
• possibility of virus transmission through the donor cornea
 GRAFT FAILURE

GRAFT REJECTION
 Graft failure
Defn: Irreversible loss of graft corneal transparency

PRIMARY GR. FAILURE SECONDARY GR. FAILURE

Irreversible graft oedema in Irreversible graft oedema in late post

immediate post op period op period

• Poor donor tissue • Irreversible rejection

• Improper tissue preservation • Infection
• Faulty surgical technique • Trauma
• Improper tissue preservation
• Surgical trauma to endothelium
`
 Graft rejection

Graft rejection is an immunologically mediated reversible loss of

graft transparency in a graft which remained clear for at least
10–14 days following PKP

• The incidence is greatest in the first year-and-a-half following

surgery but can occur up to 20 years or more after surgery.
• INCIDENCE of graft rejection:
12% good prognostic keratoplasty
40% in complicated cases
 MECHANISM OF CORNEAL GRAFT REJECTION

• Primarily a delayed type cell-mediated response controlled by the

CD4 T cells
• Inflammatory stimuli tend to attract APCs into the central corneal stroma
• MHC antigen expression on corneal cells is up-regulated by local
production of pro inflammatory cytokines
• The recognition of HLA antigens leads to the initiation of this immune
cascade (afferent immune response arm), which results in host
sensitization.
• Donor class I antigens : cytotoxic T cells (CD8) and
Donor class II antigens: helper T (Th or Thelper) cells (CD4)

• Immune mediated complex cascade of cellular events

decompensation of the graft tissue

 Risk factors for the allograft rejection
• Young pts <40 yrs , two fold risk
• Vascularisation stromal > 2 quadrants
• Regrafts, prior rejection Sensitized host
• Bilateral grafts
• Eccentric grafts Closer to limbus
• Large grafts
• Anterior synechiae
Direct contact with host vasculature
• Inflammation at the time of Sx
• Glaucoma
Non-immunological mechanisms
• Aphakia
• Previous intraocular surgery Chronic inflammation
• Ocular surface diseases eg SJS, OCP
• H/o blood transfusions
• ABO incompatibitily Acc. to studies
 Cacade of events ( Reflex arc)

DONOR ANTIGENS :
HLA I: Corneal epithelium, keratocytes and endothelium
HLA II: Antigen presenting cells (APC)

AFFERENT ARM ( Host sensitization) : recognition of the foreign

HLA antigens on the cells of the corneal allografts by the hosts
antigen presenting cells (APC)

EFFERENT ARM (Host mounted response) :

Activated Th cells release inflammatory mediators (IL-2, IFN-
gamma), cytokines, lymphokines stimulates T and B
cells
B cells produce antibodies
Complement activation
 Epithelial

Sub Graft
Stromal
epithelial rejection

Endothelial
 Diagnosis

70% 30%
Patients’ symptoms clinical diagnosis

• redness vascular dilatation

• decreased vision vascular transudation
cellular infiltration
tissue oedema
circumcorneal flushEarliest
AC flare sign

cellular infiltrates
graft oedema
Epithelial rejection
Appearance of elevated rejection line that stains with
fluorescein or rose bengal.
 Sub epithelial rejection
White infiltrates 0.2-0.5 mm in diameter randomly distributed
immediately below the bowman membrane in donor tissue.
 Stromal rejection
Sudden onset peripheral full thickness haze in a previously
clear graft associated with circumcorneal rejection.
In association with endothelial rejection.
 Endothelial rejection

Diffuse KPs Khodadaust line

 DDs
 Herpes simplex keratouveitis

 Recurrent HZO

 Epithelial downgrowth (confused with endothelial rejection line)

 Low grade corneal infection

Rx
Corticosteroids
Topical 1 hrly
Peri ocular
Systemic (pulse therapy)

Systemic and Topical cyclosporine / tacrolimus

RETROCORNEAL MEMBRANES

Epithelial downgrowth
Fibrous ingrowth
 Epithelial downgrowth
• Entrance of epithelium into AC through an incompletely healed wound
• Cataract extraction remains the most frequent cause
Pathogenesis:
Delayed closure or dehiscence of the surgical wound, often with a
fistula or inadvertent bleb and incarceration of tissue in the surgical
margin
• pain, photophobia, and blurred vision

 faint gray line with scalloped, rolled edges on the posterior surface of
the cornea or iris and represents the leading edge of the epithelial
invasion

 This leading edge can be stable over months to years or rapidly

progressive over days to weeks
 rapid central advancement

Diagnosis : clinical suspicion

• Argon laser photocoagulation- The involved areas turn white
when the laser energy is applied as opposed to an inapparent burn
to the normal iris
• Specular microscopy
• Confocal microscopy - The endothelium underlying the
epithelium is either absent or has undergone epithelial metaplasia
• glaucoma is the most common
presenting sign and a common
pathway for eventual enucleation

• Early diagnosis and complete

removal of the epithelial
membrane are paramount

• complete excision and closure of

any fistula decreases the need for
enucleation
 Fibrous ingrowth
Fibrous proliferation and invasion of the tissues surrounding the
surgical site
• distinct from epithelial downgrowth, less likely to result in
enucleation
Pathogenesis:
Subepithelial connective tissue and corneal stromal fibroblasts
participate in normal traumatic and surgical wound healing, and an
exuberant response leading to fibrous ingrowth
• Translucent membrane , frayed or irregular,
the stroma of the membrane may be vascular
• No ancillary diagnostic tests to confirm
POST OP ASTIGMATISM
Results primarily from deformation of cornea by surgery
• Final success rate
• Average 4 to 6 diopters
Severe astigmatism :
• decreased visual acuity, anisometropia, aniseikonia, image
distortion, and monocular diplopia, rendering an otherwise
successful operation ineffective.
• The astigmatism can be irregular with associated higher-order
aberrations
• Spectacles or contact lenses therefore do not improve visual acuity
in 10–20% of post keratoplasty cases
 Factors contributing

PRE-OPERATIVE FACTORS:
Ectatic conditions: Keratoconus and
Pellucid marginal degeneration

 often requires large and inferiorly displaced grafts.

 peripheral thinning in ectasia, if not excised, may influence the
astigmatic outcome

Corneal thinning, scarring

Corneal neovascularization and
Aphakia
INTRA-OPERATIVE FACTORS
Graft Diameter- 7-8.5 mm are usually used; with the
• donor button usually oversized by 0.2mm to 0.5mm
• Graft size influences astigmatism

Preferred in Ectatic disorders

• Smaller central grafts

will fail to excise the
peripheral pathology
• reduce post op myopia
Trephination - uneven, irregular, or oval trephination
• Small degrees of tilting of the trephine or decentration on the
Teflon block will produce an oval cut

cause a disparity between the

major and minor axes of the graft

Tissue alignment - Discrepancy in donor and host tissue sizing

Tissue deficiency Tissue excess

Decrease the chord length Increases the chord length

steepening in that meridian flattening in that meridian
Suture techniques:
• No single technique has been
proven superior
• Radial suture placement is of
critical importance
• As a guide, use 8- or 12-point
inked radial marker
• Suture tension, depth and
length
• The 6 o'clock cardinal suture
is the most critical in terms
of final tissue alignment and
astigmatism
POST-OPERATIVE FACTORS
• wound healing
• overriding of the graft host junction
• timing of suture removal
• Postoperative trauma, on-going surface inflammation
• other surgical procedures such as cataract surgery or
filtration procedures will also impact astigmatism
 Techniques to reduce post keratoplasty astigmatism

• Spectacle or CL wear

• Selective SR

• Relaxing incisions

• Compression sutures

• Wedge resection

• Laser correction; LASIK/PRK

• Corneal topography provides the most useful and complete
information regarding corneal shape.
• Topographical pattern post PK symmetric bow-tie
asymmetric bow-tie
round pattern, and
irregular patterns
• tolerate up to 4 D astigmatism
• sutures can be left in until they break or until they begin to
cause a problem (i.e. vascularization with graft rejection,
loose suture, etc.)
• Selective suture removal at 3–6 months
• Surgical intervention (RI, AK) should be delayed until
refractive stability is observed for a minimum of 2 months
following complete suture removal
 Relaxing Incisions
• Placed at the Graft-host junction or
in the graft “astigmatic keratotomy”
• Arcuate incisions or transverse
• 90% depth, 180 degree apart or follow topography
• Usually the incision length is 45 - 90 degrees,
centred on the steep axis
• Coupling effect : flattening in the steep axis and a
corresponding steepening of the flat axis 90 degree away
• The coupling ratio is usually 1:1
A pattern of post-keratoplasty astigmatism.
Note that the flat axis is not
uniformly orthogonal to the steep axis
Astigmatic Keratotomy
• graft in the 6-7 mm zone
• In decentered grafts: 0.5 to 1mm inside the G-H junction
• Femtosecond laser: more precise incision of corneal tissue in
depth, length, and curvature
Compression Sutures
• Used in combination with relaxing incisions
• High levels of astigmatism
• placed along the flat axis; ninety degrees away from the
relaxing incisions.
LASIK
• Optimal time: 12 post-PKP
• High pressure applied by the suction ring

risk of corneal dehiscence

epithelial ingrowth
bleeding
• most surgeons prefer PRK over LASIK
• MMC should be used to prevent subepithelial fibrosis
following PRK in post-PK eyes
 Recent advances

Femtosecond Laser-assisted Penetrating Keratoplasty

• increased biomechanical wound stability

• with a seven-fold increase in resistance to leakage
• possibly less astigmatism
• provide greater surface area for rapid healing
• The first femtosecond laser platform to accomplish the full-
thickness corneal cuts for PKP was the Intralase
• Femto-DALK
TOP HAT MUSHROOM

TRADITIONAL

ANVIL ZIG ZAG

THANK YOU