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ORIGINAL PAPER
Graft failure: III. Glaucoma escalation after penetratingkeratoplasty
Emily C. Greenlee Æ Young H. Kwon
Received: 8 February 2007 / Accepted: 25 March 2008 / Published online: 23 April 2008
� Springer Science+Business Media B.V. 2008
Abstract Glaucoma after penetrating keratoplasty
is a frequently observed post-operative complication
and is a risk factor for graft failure. Penetrating
keratoplasty performed for aphakic and pseudophakic
bullous keratopathy and inflammatory conditions are
more likely to cause postoperative glaucoma com-
pared with keratoconus and Fuchs’ endothelial
dystrophy. The intraocular pressure elevation may
occur immediately after surgery or in the early to late
postoperative period. Early postoperative causes of
glaucoma include pre-existing glaucoma, retained
viscoelastic, hyphema, inflammation, pupillary block,
aqueous misdirection, or suprachoroidal hemorrhage.
Late causes include pre-existing glaucoma, angle-
closure glaucoma, ghost cell glaucoma, suprachoroi-
dal hemorrhage, and steroid-induced glaucoma.
Determining the cause of IOP elevation can help
guide therapeutic intervention. Treatments for refrac-
tory glaucoma include topical anti-glaucoma
medications such as beta-adrenergic blockers. Topi-
cal carbonic anhydrase inhibitors, miotic agents,
adrenergic agonists, and prostaglandin analogs should
be used with caution in the post-keratoplasty patient,
because of the possibility of corneal decompensation,
cystoid macular edema, or persistent inflammation.
Various glaucoma surgical treatments have reported
success in post-keratoplasty glaucoma. Trabeculec-
tomy with mitomycin C can be successful in
controlling IOP without the corneal toxicity noted
with 5-fluorouracil. Glaucoma drainage devices have
successfully controlled intraocular pressure in post-
keratoplasty glaucoma; this is, however, associated
with increased risk of graft failure. Placement of the
tube through the pars plana may improve graft
success compared with implantation within the
anterior chamber. In addition, cyclophotocoagulation
remains a useful procedure for eyes that have
refractory glaucoma despite multiple surgical
interventions.
Keywords Glaucoma � Penetrating keratoplasty �Graft failure � Trabeculectomy � Glaucoma
drainage device
Penetrating keratoplasty (PKP) is performed for a
wide spectrum of corneal disorders, including apha-
kic and pseudophakic bullous keratopathy, Fuchs’
endothelial dystrophy, keratoconus, corneal scarring
due to infection or trauma, corneal perforation, or
inherited disorders [1–16]. PKP offers the advantage
of improving vision by replacing affected corneas
with healthy donor tissue. Although it is one of the
most successful organ transplantations performed, it
is associated with significant complications. Numer-
ous adverse consequences have been reported.
E. C. Greenlee � Y. H. Kwon (&)
Department of Ophthalmology and Visual Sciences,
University of Iowa Hospitals and Clinics, 200 Hawkins
Drive, Iowa City, IA 52242-1091, USA
e-mail: young-kwon@uiowa.edu
123
Int Ophthalmol (2008) 28:191–207
DOI 10.1007/s10792-008-9223-5
Complication of PKP include graft rejection or
failure, graft dehiscence, infection, flat anterior
chamber, pupillary block, synechial angle closure,
aqueous misdirection, hyphema, cataract, retinal
detachment, choroidal effusion, suprachoroidal hem-
orrhage, and endophthalmitis [17–27]. One of the
more common complications after PKP is the devel-
opment of glaucoma, which may occur either early or
late postoperatively [28–35]. There are various
mechanisms of glaucoma after PKP. Identification
of the exact cause of intraocular pressure (IOP)
elevation is helpful in proper treatment. Evaluation of
the ocular history, and examination of the drainage
angle is important for determining the etiology of
post-PKP glaucoma. A complete evaluation of post-
PKP glaucoma includes pachymetry, tonometry,
optic nerve examination, and visual field testing.
Pre-operative glaucoma assessment
of the penetrating keratoplasty patient
A prior history of ocular hypertension (OHT) or
glaucoma is often noted during the preoperative
assessment of patients undergoing PKP. This pre-
existing diagnosis should be taken into consideration
during surgical counseling. The possibility of glau-
coma escalation after surgery or likelihood of graft
failure should be discussed preoperatively. Patients
with a prior history of glaucoma are more likely to
have increased IOPs post-operatively and to develop
graft failure compared with those without a glaucoma
history [31, 34, 36–44].
In addition to identifying patients with pre-existing
glaucoma, surgeons should attempt to anticipate
those who may be at risk of developing glaucoma
postoperatively. Certain corneal diagnoses, such as
aphakic and pseudophakic bullous keratopathy, are
more likely to cause postoperative glaucoma [26,
45–48]. Other diagnoses, such as Fuchs’ endothelial
dystrophy and keratoconus, are less likely to result in
secondary glaucoma [26, 28, 49–51]. Preoperative
discussion should include the possibility of postop-
erative glaucoma based on corneal diagnosis.
Pachymetry
Corneal pachymetry, in addition to providing impor-
tant information regarding the status of the cornea,
aids in the evaluation of potential glaucoma. A large
meta-analysis of the corneal thickness literature from
1968 to 1999 reported a normal averaged central
corneal thickness (CCT) of 0.534 mm ± 11.6% (i.e.,
0.473–0.597 mm) for Caucasian patients. Collagen
disorders (e.g. keratoconus) and endothelial-based
corneal disorders (e.g. Fuchs’ endothelial dystrophy)
resulted in a decrease and increase in the corneal
thickness respectively. Increases in corneal thickness
beyond the normal range were noted after cataract
surgery and PKP [52].
The concept of corneal thickness affecting IOP
measurements was initially reported in 1971 [53, 54].
Numerous studies have demonstrated that deviations
from normal corneal thickness affect applanation
tonometry readings, with thicker (but non-edematous)
corneas resulting in overestimation of IOP [55–60].
The proposed mechanism for this is that it takes
greater force to applanate against a thicker-than-
normal cornea. Conversely, a thinner cornea results in
underestimation of IOP, because of the ease of
applanating. Increased corneal thickness due to
edema, however, may lead to underestimation of
the IOP [57, 61–66]. The IOP measurement of failing
grafts may be falsely low due to corneal edema
(Fig. 1). Interestingly, patients with a history of OHT
Fig. 1 Thick cornea in a failing graft. The slit beam shows
increased thickness in a failing corneal graft
192 Int Ophthalmol (2008) 28:191–207
123
have been shown to have thicker corneas [55, 56, 60,
67–71], while those with normal tension glaucoma
(NTG) to have thinner corneas [55, 67, 72–74].
Race has also been studied in regard to average
CCT. Blacks have been noted to have thinner corneas
than whites, and this may lead to an underestimation of
IOP and potential delay in glaucoma diagnosis in this
population [74–83]. A study by Aghaian et al. noted
that Caucasians had a CCT of 550.4 lm, Hispanics
548.1 lm, and African-Americans 521.0 lm in a US
tertiary care glaucoma clinic. There has also been a
suggestion that differences in CCT may exist among
different Asian populations. The same study noted
thinner CCT in Japanese patients (531.7 lm) com-
pared with Chinese (555.6 lm) and Filipinos
(550.6 lm) [74]. Despite numerous studies, there is
no single standard nomogram of corneal pachymetry
and IOP adjustment, because of multiple factors
involved including patient race, diagnosis, corneal
diagnosis, and tonometry method.
Tonometry
Various tonometers have been used to measure the
IOP on pathologic corneas. Goldmann applanation
remains the preferred method if adequate mires can
be observed. Several methods of Goldmann appla-
nation have been described for those with high
astigmatism. One method is to obtain two mea-
surements taken 90� apart and to average them.
Another method involves placing the axis of the
biprism tip along the negative axis of the astigma-
tism [84].
The Goldmann applanation may be unreliable in
post-keratoplasty corneas because of the irregularity
of mires. The validity the MacKay–Marg tonometer
on scarred corneas and after PKP was first noted in
the 1970s [85, 86]. The MacKay–Marg tonometer
allows the effect of corneal rigidity to be transferred
to a sleeve surrounding a central plunger which
measures the IOP. The MacKay–Marg tonometry
principle is also used for the handheld Tono-Pen
(Mentor, Norwell, MA, USA). When the Tono-pen
was compared with the MacKay–Marg tonometer,
there was no significant difference in IOP measure-
ment in normal corneas and in corneas after PKP
and epikeratophakia [87]. However, Geyer et al.
found the Tono-pen to overestimate compared with
the Goldmann tonometry readings in both normal
and post-keratoplasty eyes, especially in the lower
IOP range (\9 mmHg) [88]. Another electronic
portable tonometer similar to the Tono-pen is the
ProTon tonometer. Jain et al. reported the ProTon
tonometer to have higher accuracy than Schiotz
tonometry in normal corneas, and Goldmann appla-
nation to have higher accuracy then either method in
scarred or post-keratoplasty corneas [89]. Another
study found the ProTon tonometer to be reliable in
both normal and post-PKP eyes compared with
Goldmann applanation tonometry [90]. Browning
et al. found a higher mean IOP with the ocular
blood flow (OBF) pneumotonometer compared with
the Goldmann applanation or Tono-pen XL in eyes
after PKP or with a diagnosis of keratoconus or
Fuchs’ endothelial dystrophy [91]. Another study
demonstrated no significant difference among the
OBF tonometry, Tono-pen, and Goldmann applana-
tion in post-PKP eyes
Noncontact tonometers have the benefits of not
requiring anesthetic or sterilization. Two tonometers
which have been studied in post-PKP eyes are the
Xpert and TGDc-01 tonometer. The TGDc-01 also has
the benefit of the measurement being taken through the
eyelid. Unfortunately, these tonometers have not been
found to be very reliable. A study by Lisle and Ehlers
noted a wide variation in IOP measurements with the
Xpert non-contact tonometer compared with Gold-
mann applanation in post-keratoplasty eyes [92].
Another study compared Goldmann applanation to
the TGDc-01 digital tonometer and reported that only
53.5% of post-keratoplasty eyes showed an absolute
difference between the two tonometers of B3 mmHg
[93].
Gonioscopy
The eye examination should also include gonioscopy
in patients suspected of developing postoperative
glaucoma. Whenever possible, the configuration of
the drainage angle should be documented preopera-
tively for subsequent comparison. The gonioscopy
may be difficult, because of corneal edema and tissue
alterations at the graft–host junction. Gonioscopy
may allow the examiner to determine the etiology
of glaucoma. Differentiating pupillary block from
synechial angle closure, or open from closed-angle
glaucoma, will guide appropriate therapeutic
intervention.
Int Ophthalmol (2008) 28:191–207 193
123
Visual field testing/optic nerve examination
Preoperative visual field testing and optic nerve
examination with photographs can document the
development or progression of glaucoma after sur-
gery. Computerized optic nerve head analysis may be
of further benefit. However, the optic nerve exami-
nation or analysis can be difficult due to pre- and
post-operative corneal pathology.
Effect of pre-existing glaucoma on the success
of penetrating keratoplasty
A pre-existing history of glaucoma has long been
recognized as a risk factor for graft failure [31, 34,
36–44, 50, 94]. Glaucoma may precipitate corneal
decompensation and resulting graft failure (Fig. 2).
Results of the Collaborative Corneal Transplantation
Studies Research Group showed a three-year graft
failure rate of 47% with a history of glaucoma
compared with 30% without glaucoma [36]. The
Australian Corneal Graft Registry attributed glau-
coma as a cause of graft failure in 11% [31]. Both
studies included high-risk patients which may
account for the high failure rate. In a study which
excluded high-risk patients, Reinhard et al. reported a
three-year graft failure rate of 29% in those with
glaucoma compared with 11% without glaucoma
(Table 1). Interestingly, no difference was noted
between the groups in terms of immune reactions.
Half of the graft failures in the glaucoma group was
attributable to glaucoma [34].
In a study of re-graft patients by Aldave, rejection
episodes occurred earlier in glaucoma patients
(18 months) than in non-glaucoma patients
(32 months) regardless of glaucoma treatment. Glau-
coma surgical treatment was associated with earlier
rejection compared with medically treated glaucoma
or without a history of glaucoma. The grafts failed
12 months earlier in the glaucoma group [95]. A
study by Price et al. reported preoperative glaucoma
medication use as a risk factor for graft failure [96].
The use of topical medications was reported as a risk
factor for graft failure, because of increased rejection,
endothelial decompensation, and ocular surface dis-
ease [97].
Corneal graft failure because of glaucoma has been
attributed to IOP effect on the corneal endothelium,
either through an immune mechanism or direct
pressure-induced endothelial damage. Endothelial
damage has been documented in various types of
glaucoma. For example, attacks of acute angle-closure
glaucoma have been shown to alter the corneal
endothelium [95–99]. The endothelial damage has
Fig. 2 Graft failure secondary to glaucoma. The corneal graft
has a poor corneal light reflex. It is hazy, indicating the onset of
graft failure
Table 1 Graft failure rate with glaucoma
Three-year graft failure rate
with glaucoma (%)
Three-year graft failure rate
without glaucoma (%)
High risk
for failure
Collaborative Corneal Transplantation Studies
Research Group (CCTSRG) [36]
47 30 Yes
Australian Corneal Graft Registry (ACGR) [31]a 40.7–43.4 15.3 Yes
Reinhard [34] 29 11 No
a Patients with a history of IOP raised in past but not at time of graft were combined with those whose IOP was raised at grafting. For
those with a history of IOP raised in past but not at time of graft, the graft failure rate was 40.7%. For those with IOP raised at time of
grafting, the failure rate was 43.4%
194 Int Ophthalmol (2008) 28:191–207
123
also been reported in open-angle glaucomas [69,
100–102].
Glaucoma treatments, both medical and surgical,
have been associated with graft failure. Topical
medications increase inflammatory cells in conjunc-
tival and limbal tissue [103, 104], which may
predispose to immunologic graft rejection. In addi-
tion, preservatives, such as benzalkonium chloride,
can induce an inflammatory reaction [105, 106].
Medications, for example beta-blockers and carbonic
anhydrase inhibitors, can facilitate endothelial failure
[107–109]. The likelihood of graft rejection may also
be increased by cholinergic agents which may disrupt
the blood–aqueous barrier and cause inflammation,
thereby increasing the likelihood of graft rejection
[110].
Intraocular surgery has been shown to decrease
endothelial cell counts [111, 112]. Antimetabolites
often used in trabeculectomy can be toxic to the
corneal endothelium [113]. Mitomycin C has been
shown to be less toxic to the corneal epithelium
compared with 5-fluorouracil [114, 115]. There is
also a transient breakdown of the blood–aqueous
barrier after trabeculectomy [116] or glaucoma
drainage devices (GDD) [117], which can predispose
the cornea to graft rejection. GDDs may cause
endothelial damage when tubes are placed in direct
contact with the corneal endothelium [118]. It has
also been proposed that the tube may permit retro-
grade flow of inflammatory cells into the anterior
chamber which may affect the corneal endothelium
[119].
In summary, the effects of glaucoma on corneal
grafts are numerous. A pre-existing history of glau-
coma is a significant risk factor for graft failure, as is
the preoperative use of glaucoma medications. It may
also precipitate corneal decompensation through
effects on the endothelium. Corneal endothelial
damage may occur from either the glaucoma itself
or its treatment. Glaucoma medications and surgery,
especially GDDs have been reported to cause endo-
thelial compromise.
Glaucoma associated with penetrating
keratoplasty
The incidence of secondary glaucoma after PKP has
been reported to range from 10% to 53% [21, 26, 28,
35, 45, 47, 49, 50, 120–124]. In the early postoper-
ative period, the incidence has been reported to be
from 9% to 31% [21, 46, 125] and in the late
postoperative period from 18% to 35% [30, 46, 47,
49, 122, 125]. The concept of increased IOP after
PKP was first described in 1969 by Irvin and
Kaufman [94].
Preoperative considerations
Patients with glaucoma are more likely to develop
glaucoma progression after PKP [21, 26, 47, 49, 122,
126]. Numerous studies have reported a higher
likelihood of developing glaucoma in aphakic
(ABK) or pseudophakic bullous keratopathy (PBK)
patients after PKP [26, 45, 47, 48]. Schanzlin et al.
found no difference between ABK and PBK in the
development of secondary glaucoma [124]. Polack
[50] and Goldberg [49] found preoperative glaucoma
to account for the glaucoma in aphakic eyes postop-
eratively. Foulks, however, found aphakia to be an
independent risk factor after controlling for preoper-
ative glaucoma [47]. Aside from ABK and PBK,
Franca et al. found herpes simplex keratitis and
trauma to be associated with increased risk for the
development of secondary glaucoma [45]. Similarly,
Kirkness noted trauma and inflammation to be risk
factors for the development of glaucoma in addition
to ABK and PBK [122]. Another risk factor is older
age [21, 30, 47, 49, 94, 122, 125]. Sihota reported
preoperative diagnosis of adherent leukoma as
another risk factor for secondary glaucoma [35]. On
the other hand, keratoconus or Fuchs’ endothelial
dystrophy diagnoses are less likely to develop
glaucoma after PKP [26, 28, 49–51]. Table 2 cate-
gorizes glaucoma risk by corneal diagnosis.
Table 2 Glaucoma risk by preoperative corneal diagnosis
Glaucoma risk
High Low
Aphakic/pseudophakic bullous
keratopathy
Keratoconus
Herpes simplex keratitis Fuchs’ endothelial dystrophy
Trauma
Older age
Adherent leukoma
Int Ophthalmol (2008) 28:191–207 195
123
Intraoperative considerations
Variations in PKP surgical technique have been
implicated in secondary glaucoma. Seitz et al. found
no detectable difference in IOP between mechanical
versus excimer laser trephination in keratoconus or
Fuchs’ endothelial dystrophy patients [127]. Suturing
technique of the donor button may be associated with
increased IOP. Olson and Kaufman proposed a
mathematical model which described compression of
the trabecular meshwork/Schlemm’s canal because of
tight suturing, long bites, larger trephine sizes, smaller
recipient diameter, and increased peripheral corneal
thickness [128]. Zimmerman et al. suggested mechan-
ical collapse of the trabecular meshwork in aphakic
transplants occurred because of loss of the posterior
fixation of the ciliary body-lens support structure and
loss of the anterior support of Descemet’s membrane.
Zimmerman demonstrated that full-thickness sutures
approximating Descemet’s membrane were not asso-
ciated with changes in outflow facility, while mid-
stromal bites decreased the outflow by 37% [129]. The
size of the donor button in relation to the recipient bed
was also proposed as a cause of increased IOP [128,
130, 131]. Larger donor buttons relative to recipient
host beds have been associated with better postoper-
ative IOP control [132, 133], although another study
did not support this finding [134].
Studies on combined cataract and PKP procedures
have reported no increased risk of elevated IOP
postoperatively [26, 135, 136]. Franca et al. did not
observe a difference in postoperative IOP elevations
in those undergoing combined procedures versus
PKP alone [45].
Postoperative considerations
Increased IOP can occur early or late in the postop-
erative period [51, 137]. Causes of IOP elevations
postoperatively include damage to the trabecular
meshwork, loss of angle support, angle closure,
inflammation, retained viscoelastic, and steroid
response [46, 51, 120, 138]. Chien et al. reported an
early postoperative IOP elevation ([30 mmHg) in
12% (18/155 patients) overall, and in 21% (10/48
patients) with a history of glaucoma [30].
The various causes of IOP elevation after PKP can
be divided into the time periods in which the IOP
elevation occurs. Early elevations occur immediately
postoperatively to days after surgery. Late elevations
occur weeks to months after PKP. Both the early and
late classifications can further be subdivided into
open-angle and closed-angle mechanisms.
Causes of early postoperative IOP elevation include
pre-existing glaucoma, inflammation, retained visco-
elastic, hyphema, tight suturing with long bites, larger
recipient bed with same size donor button, mechanical
angle collapse in aphakia, pupillary block, aqueous
misdirection, and suprachoroidal hemorrhage. Late
postoperative glaucoma may be caused by pre-exist-
ing glaucoma, chronic open-angle glaucoma from
aphakic transplants, peripheral anterior synechiae
(PAS) formation, steroid-induced glaucoma, aqueous
misdirection, ghost cell glaucoma, and suprachoroidal
hemorrhage (Table 3).
Preoperative counseling alerts patients to the risk
of their developing glaucoma after PKP. Intraopera-
tive measures may then be taken to prevent IOP
elevations by altering the surgical technique and
selection of larger donor corneas relative to host beds.
Postoperatively, the etiology of the pressure elevation
should be determined from the examination so that
appropriate measures may be taken to manage the
IOP elevation. Retained viscoelastic can be removed
in the early postoperative period. Hyphema may be
managed with topical steroids and cycloplegics.
Gonioscopy is important in the diagnosis of pupillary
block. Laser iridotomy may be difficult through an
Table 3 Causes of post-PKP glaucoma
Early Late
Open-angle Closed-angle Open-angle Closed-angle
Pre-existing glaucoma Pre-existing glaucoma Pre-existing glaucoma Pre-existing glaucoma
Inflammation Pupillary block Persistent inflammation Peripheral anterior synechiae
Retained viscoelastic Aqueous misdirection Steroid-induced Aqueous misdirection
Hyphema Suprachoroidal hemorrhage Ghost cell glaucoma Suprachoroidal hemorrhage
196 Int Ophthalmol (2008) 28:191–207
123
edematous cornea but may be placed in an area of
clearer visualization. One of the causes of post-
keratoplasty glaucoma is PAS which would not be
alleviated with peripheral iridotomy if the entire
angle is closed. One proposed mechanism of PAS
formation is a floppy, atrophic iris which can be
prevented by suturing the iris or iridoplasty [139].
Aqueous misdirection and ghost cell glaucoma
should be controlled with topical or oral glaucoma
medications and cycloplegia, and if necessary, pars
plana vitrectomy. In the case of suprachoroidal
hemorrhage, IOP should be managed with topical or
oral glaucoma medications with choroidal drainage
once the hemorrhage has liquefied, typically within
3–5 days post hemorrhage. Topical steroid use can
control inflammation which can help reduce the
possibility of graft rejection. Care must be taken to
recognize the development of steroid-induced glau-
coma which may occur after several weeks of topical
steroid use [140–142]. Stronger topical steroids, for
example prednisolone acetate, may be replaced by
medications which have less chance of increasing
IOP, such as fluorometholone, loteprednol, rimexo-
lone, or cyclosporin A [143–146].
It is important to control the IOP promptly because
the longer the IOP remains elevated, the more
endothelial damage is likely to occur. Sustained IOP
elevations may cause permanent endothelial and optic
nerve damage, and can result in graft failure. Endo-
thelial cell loss has been documented after acute
angle-closure glaucoma [99, 147–152] and open-angle
glaucomas [151, 152]. The longer the duration of IOP
elevation during an acute angle closure glaucoma, the
more the endothelial cell loss reported [147].
Medical treatments for post-keratoplasty
glaucoma
The medical management of secondary glaucoma
after PKP requires diligence and a thorough discus-
sion with the patient about potential side-effects. A
beta-adrenergic blocker, such as timolol, acts as an
aqueous suppressant and is effective in cases of angle
closure. Timolol has been shown to be effective in
post-PKP aphakic transplants with secondary angle
closure in a small series of patients [138]. Timolol
has also been reported to cause corneal epithelial
toxicity [153, 154]. Adrenergic agonists, such as
epinephrine, have been used to reduce IOP. However,
they have been associated with cystoid macular
edema in aphakic and pseudophakic patients and,
therefore, should be used with caution in these
patients [155–157].
Medications to avoid, or use with caution, in post-
PKP patients include miotics and topical carbonic
anhydrase inhibitors. Miotic agents, for example
pilocarpine, facilitate the outflow of aqueous to
reduce the IOP; they are, therefore, not effective in
angle closure. They are frequently avoided in PKP
patients because of the breakdown of the blood–
aqueous barrier, which may exacerbate graft rejection
[158]. Dorzolamide, a topical carbonic anhydrase
inhibitor, has been documented to cause irreversible
corneal decompensation in patients with decreased
endothelial function. Topical carbonic anhydrase
inhibitors should be avoided in patients who have
increased risk of graft rejection [109, 110]. Prosta-
glandin analogs increase uveoscleral outflow and are
frequently avoided in patients with active inflamma-
tion or a history of herpes simplex keratitis, because
they can induce recurrent inflammation [159–161]
and herpetic re-activation [162–168]. Furthermore,
the preservative (benzalkonium chloride) used in
many topical glaucoma medications can cause toxic
effect to the corneal epithelium [169–172]. Systemic
carbonic anhydrase inhibitors, for example acetazol-
amide, while helpful in the short-term treatment of
glaucoma, are usually poorly tolerated in the long-
term because of multiple systemic side-effects,
including malaise, fatigue, anorexia, weight loss,
depression, nausea, gastrointestinal upset, loss of
libido, paresthesias, poor taste, and metabolic acido-
sis [173–175].
Surgical treatments for post-keratoplasty
glaucoma
Argon laser trabeculoplasty
Argon laser trabeculoplasty (ALT) is effective in
open-angle glaucoma patients; however, it is not very
useful in angle closure or angle recession. There have
been mixed reports on the effect of ALT in aphakic
glaucoma [176–181]. After ALT, the success rate is
50% at 5 years [182]. Van Meter et al. has reported
success in a small series of patients with ALT with
Int Ophthalmol (2008) 28:191–207 197
123
the average IOP reduction of 9.1 mmHg in post-PK
glaucoma patients [177].
Trabeculectomy
Once medical or laser treatments have failed, trabec-
ulectomy may be considered for refractory secondary
glaucoma. Trabeculectomy without antimetabolites is
less likely to be successful in patients at high risk of
failure [47, 183, 184]. One study reported success
with trabeculectomy in only 9% without medications,
and 42% with medications [183]. A small study of
post-keratoplasty glaucoma patients by Foulks noted
four of five patients with successful IOP control with
trabeculectomy; however, three of these had compli-
cations, including graft failure [47]. Insler et al.
examined another small series of patients undergoing
combined trabeculectomy and PKP. Three out of
seven had controlled IOP with surgery alone whereas
the remaining patients were controlled with addi-
tional medications. Complications included graft
failure and retinal detachment in two patients [184].
The probability of graft survival was 62% after
45 months in 29 patients undergoing trabeculectomy
after PKP with the mean follow-up period of
7.8 months after PKP [111].
The use of antimetabolites, for example 5-fluoro-
uracil and mitomycin C, increases the probability
of trabeculectomy success by inhibiting fibroblast
proliferation. Post-operative subconjunctival 5-fluo-
rouracil has been used in high-risk glaucoma such as
aphakic glaucoma; however, this was associated with
a high rate of corneal epithelial toxicity [185].
Mitomycin C enhances trabeculectomy success and
is not associated with significant corneal epithelial
toxicity [114, 115, 186, 187]. Ayyala et al. reported a
77% success rate after trabeculectomy in post-PKP
glaucoma [188]. Figueiredo et al. reported a 67%
success rate [189]. Chowers et al. found a success rate
of 91% in a small series of patients undergoing either
combined mitomycin C trabeculectomy/PKP or tra-
beculectomy after PKP [190]. Another study by
WuDunn revealed an 85% probability of graft
survival at one year and 60% at two years, and
55% probability of IOP control at one year and 50%
at two years [191]. In a study by Ishioka et al.,
trabeculectomy with mitomycin C led to better results
than without mitomycin C for post-PKP glaucoma.
Trabeculectomy with mitomycin C successfully
controlled IOP in 73.0% compared with 25.0% in
trabeculectomy without antimetabolite. The graft was
clear in 69.2% of the mitomycin C group compared
with 37.5% in the group without mitomycin C during
a mean follow-up period of 22.3 months [192].
Adverse prognostic factors for glaucoma control with
trabeculectomy after PKP were multiple grafts and
synechial angle closure [183]. Table 4 summarizes
the success of mitomycin C trabeculectomy in post-
PKP glaucoma over time.
In summary, trabeculectomy seems to successfully
control IOP in post-PKP patients although there still
is the possibility of graft failure. Intraoperative
antimetabolites improve the success rate of IOP
control. Mitomycin C is better tolerated than 5-
fluorouracil as an adjunct antimetabolite because of
its lower corneal epithelial toxicity.
Glaucoma drainage devices (GDD)
GDD can be successfully implanted to facilitate the
outflow of aqueous (Fig. 3a, b). Glaucoma drainage
devices may be associated with a greater incidence of
graft failure than trabeculectomy [117, 118, 188–191,
193–198]. Zalloum et al. reported a 50% higher graft
failure rate in patients with Molteno implants and
PKP compared with no graft failure in patients
with trabeculectomy with PKP [198]. Uncontrolled
secondary glaucoma occasionally requires the
implantation of a GDD because of failed prior
treatments or scarred conjunctiva. The graft failure
rate of GDD has been reported to be in the range
10–51% [117–119, 188, 193, 195, 199, 200]. Kirk-
ness reported a 68% probability of controlling IOP
and maintaining graft survival after GDD implanta-
tion at 26 months [119]. Suggested causes of graft
failure are direct contact of the tube with the corneal
Table 4 Success of mitomycin C trabeculectomy in post-PKP
glaucoma
Mitomycin C
trabeculectomy
IOP success rate (%)
Mean follow-up
(months)
Figueiredo [189] 67 9
Chowers [190] 91 15
Ayyala [188] 77 17
Ishioka [192] 73 22
WuDunn [191] 50 24
198 Int Ophthalmol (2008) 28:191–207
123
endothelium [193, 195, 201] or retrograde flow of
inflammatory cells into the anterior chamber [119].
Another proposed mechanism is mechanical trauma
during implantation or micromotion during eye
movement and blinking which results in endothelial
damage [202].
A study by Sherwood et al. evaluated the Molteno
and Shocket implant in post-PKP patients. Ninety-six
percent of patients had an IOP of 18 mmHg or less
with a mean follow-up period of 22 months, and graft
failure from tube-corneal touch was reported in 42%
of patients at 22 months [200]. Another study
examining the effectiveness of Molteno implants for
post-PKP glaucoma found graft rejection in five of
seventeen patients undergoing double-plate Molteno
implantation. Of these five patients, four had GDD
within the anterior chamber and one in the vitreous
cavity [117]. Alvarenga et al. reported graft success
in 58.5% and 25.8% at one and two years, respec-
tively, with GDD. In addition, IOP control was
reported in 74.0% and 63.1% of patients at one and
two years, respectively. The study included GDD
implantation before, after, or simultaneously with
PKP and found the presence of a GDD as an
independent risk factor for graft failure [203].
Studies of GDD implantation and PKP have
reported successful control of IOP between 51%
and 96% with a follow-up of 13–74 months [46, 117,
119, 193, 195, 200, 201, 204–206]. In the same
studies, graft success rates have been reported to be
between 26% and 80% with a follow-up of
13–38 months [117, 119, 193, 195, 200, 201,
207–209]. Several studies have reported their results
regarding timing of surgery and likelihood of graft
survival. Both Beebe and Rapuano reported higher
graft failure rates when GDD surgery was performed
after PKP [193, 195]. Beebe et al. reported a graft
failure rate of 51% after PK and GDD implantation in
the anterior chamber over 6 to 58 months [193].
Rapuano et al. observed a 44% graft rejection rate in
eyes with GDD after PKP compared with 29% for
simultaneous surgery and 31% for GDD placement
before PKP [195]. In contrast, Kwon et al. reported
the tube-first group to be 3.8 and 4.7 times more
likely to experience graft failure than the simulta-
neous and PK-first groups, respectively. The study
also found the Ahmed implant to be 3.3 times more
likely to be associated with graft failure than the
Baerveldt. The IOP success rate was 82% with a graft
survival rate of 55% at three years [201]. A study
investigating the success of simultaneous PKP and
Ahmed implant was performed by Al-Torbak in
patients with corneal opacities and glaucoma. The
cumulative probability of graft success was 92% and
50% while the probability of IOP control was 92%
and 86% at one and three years, respectively. Graft
failure occurred in 10 of 25 cases, most of which
were due to immune rejection and tube endothelial
touch. [205]. Another study by Coleman et al.
reported a graft success rate of 62% at 20 months
with simultaneous PKP and Ahmed implant [208].
Fig. 3 (a) Glaucoma drainage device after penetrating kera-
tolasty. Secondary glaucoma is treated with implantation of a
glaucoma drainage device. The beveled tip of the tube is seen
in the superotemporal quadrant. (b) Glaucoma drainage device
tube as seen by gonioscopy. If the tube is not well-visualized
through the graft-host junction, it may be seen by gonioscopy.
This tube is seen through the mirror of a goniolens
Int Ophthalmol (2008) 28:191–207 199
123
Table 5 summarizes the IOP success rate and graft
failure rate of various GDDs over time (Table 6).
Given the possible mechanism of graft failure
because of direct corneal endothelial trauma from the
tube, studies have been performed to evaluate the
difference in graft survival with the tube placed in the
posterior segment. Arroyave et al. reported a signif-
icantly higher corneal graft survival (83%) in GDD
implantation within the vitreous cavity compared
with the anterior chamber (48%) after one year. There
was no significant difference in IOP control between
the two groups [206]. Sidoti et al. reported 12 and
24-month IOP control success rates of 85% and 62%
and graft survival rate of 64% and 41%, respectively,
in patients undergoing PKP and pars plana GDD
insertion [210].
In summary, GDDs have been shown to effec-
tively control IOP in refractory post-PKP glaucoma.
The procedure is generally associated with a higher
rate of graft failure than trabeculectomy, but may be
warranted when trabeculectomy fails or cannot be
performed. There are conflicting results regarding the
optimum timing of surgery. Some studies report a
higher likelihood of survival with GDD implantation
prior to PKP while others report the reverse. Others
report good results with combined surgery. One way
of improving graft survival seems to be placing of the
tube in the vitreous cavity rather than in the anterior
chamber. However, this requires additional surgery
(i.e. vitrectomy).
Cyclodestructive procedures
When medical or surgical intervention fails to control
post-keratoplasty glaucoma, cyclodestructive proce-
dures may be performed for IOP control. Prior to the
advent of cyclophotocoagulation (CPC), cyclocryo-
therapy was the procedure performed in uncontrolled
post-PKP glaucoma. West et al. and Binder et al.
reported good IOP control with cyclocryotherapy
[211, 212]. Kirkness, however, reported poor control
of IOP and significant complications, such as dis-
comfort, corneal decompensation, inflammation, and
phthisis [119].
The development of CPC provided a more easily
tolerated procedure with less discomfort and inflam-
mation than cyclocryotherapy. Studies in post-PKP
glaucoma with CPC have reported good results in the
treatment of refractory glaucoma [194, 196, 197, 213,
214]. Beiran et al. reported the probability of suc-
cessful IOP control (\21 mmHg) after CPC with or
without medication was 70% at one year and 63% at
five years. The probability of graft survival was 79%
at one year and 56% at five years [215]. Ocakoglu
et al. reported 97% of eyes with an IOP \22 mmHg
at six months and 72% of eyes at twelve months with
or without medications in patients undergoing CPC
for refractory post-PKP glaucoma [216]. Another
study reported IOPs of 6 to 21 mmHg were achieved
Table 5 Glaucoma
drainage device for post-
PKP glaucoma
a Graft failure rate was
31% in tube shunt before
PKP, 29% in combination
surgery, and 44% in tube
shunt after PKP
GDD IOP success
rate (%)
Mean follow-up
(months)
GDD Graft failure
rate (%)
McDonnell [117] 71 13 Molteno 41
Coleman [208] 52 20 Ahmed 38
Sherwood [200] 96 22 Molteno, Shocket 42
Rapuano [195]a 96 23 Molteno 29–44
Alvarenga [203] 63 24 Ahmed, Baerveldt, Molteno 74
Beebe [193] 86 25 Molteno, Shocket 51
Kirkness [119] 80 26 Shocket 20
Kwon [201] 82 36 Ahmed, Baerveldt 45
Al-Torbak [205] 86 36 Ahmed 50
Table 6 Cyclophotocoagulation for post-PKP glaucoma
CPC IOP
success
rate (%)
Mean
follow-
up (months)
Graft
failure
rate (%)
Ocakoglu [216]a 72 12 0
Beiran [215] 63 60 44
a No patient with clear graft developed graft failure. Two of 32
eyes with prior corneal edema before treatment cleared after
treatment
200 Int Ophthalmol (2008) 28:191–207
123
in 79% of patients undergoing CPC for refractory
post-PKP glaucoma with the need for re-treatment in
57% with a minimum of six months follow-up [217].
In summary, CPC can be successful in controlling
secondary PKP glaucoma. It is a useful adjunct to
treatment for refractory glaucoma.
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