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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: [email protected]

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

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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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