Indian Journal of Ophthalmology

: 1993  |  Volume : 41  |  Issue : 4  |  Page : 181--184

Post-penetrating keratoplasty glaucoma

G Chandra Sekhar, Prateep Vyas, Rukmini Nagarajan, Anil K Mandal, Satish Gupta 
 VST Centre For Glaucoma Care, L.V. Prasad Eye Institute, Hyderabad, India

Correspondence Address:
G Chandra Sekhar
L.V. Prasad Eye Institute, Road No. 2, Banjara Hills, Hyderabad 500 034


To study the risk factors in the development of glaucoma following penetrating keratoplasty, we retrospectively analysed 190 eyes of 185 consecutive patients who had undergone surgery during 1990. The donor button was larger by 0.2 mm and 0.5 mm in phakia and aphakia/pseudophakia patients, respectively. Over a mean follow-up period of 14.5 months, 52 of the 190 eyes (27.4%) either developed glaucoma de novo or had worsening of preexisting glaucoma. Of these 52 eyes, 38 were managed medically and 14 required surgery. From our study, aphakia (37%), pseudophakia (24%), preexisting glaucoma (81.8%), and regrafting (43.18%) were found to be the significant risk factors in the development of glaucoma following penetrating keratoplasty.

How to cite this article:
Sekhar G C, Vyas P, Nagarajan R, Mandal AK, Gupta S. Post-penetrating keratoplasty glaucoma.Indian J Ophthalmol 1993;41:181-184

How to cite this URL:
Sekhar G C, Vyas P, Nagarajan R, Mandal AK, Gupta S. Post-penetrating keratoplasty glaucoma. Indian J Ophthalmol [serial online] 1993 [cited 2023 Sep 30 ];41:181-184
Available from:

Full Text

Glaucoma following penetrating keratoplasty is a serious clinical problem due to its frequency of occurrence, difficulty in diagnosis and management, risk of graft failure, and irreversible visual loss due to optic nerve damage.

There have been reports detailing the incidence and mechanism of development of glaucoma following penetrating keratoplasty. [1][2][3][4][5] For the management of this condition various surgical and nonsurgical modalities have been described with varying success rates.[6],[7],[8],[9] Though several attempts have been made to define the risk factors in the development of glaucoma, indications for surgery, choice of surgical procedure and its outcome have not been elaborated.[1],[2],[3],[5]

In this retrospective study, we describe our experiences with the incidence, risk factors, and management of post-penetrating keratoplasty glaucoma in a series of 190 eyes (185 patients) which had undergone surgery from January 1, 1990 through December 31, 1990.


We reviewed the charts of 185 consecutive patients (190 eyes) who had undergone penetrating keratoplasty at L.V.Prasad Eye Institute from January 1, 1990 through December 31, 1990, and had had at least 3 months of follow-up. The medical records were reviewed for patient age, sex, diagnosis for which keratoplasty was done, preoperative visual acuity and intraocular pressure measurements along with the use of any antiglaucoma medications or surgeries performed. Intraoperative data recording included: details of the surgical procedure including the type of surgery, whether combined with cataract surgery, intraocular lens removal, intraocular lens exchange, secondary intraocular lens implantation, and anterior vitrectomy.

The criterion for diagnosis of post-penetrating keratoplasty glaucoma was chronically elevated intraocular pressure of greater than 21 mm Hg, as recorded by Goldmann applanation tonometer, wherever possible. In cases where recording of intra�ocular pressure was not possible by Goldmann applanation tonometer, digital tonometry was resorted to and only an unequivocal digital raise of pressure was considered glaucomatous. Patients with acute transient postoperative elevation of intraocular pressure were not considered in this series because elevated intraocular pressure in these patients was attributed to the intraoperative use of viscoelastic substance or conditions such as pupillary block.

The follow-up information recorded included visual acuity, status of the corneal graft, status of anterior chamber, and the intraocular pressure as measured by Goldmann applanation tonometer. Disc evaluation was performed in cases where media was clear and permitted a view of the disc. Visual field analysis could not be done in any patient and therefore, intraocular pressure was the only criterion for assessing the progress or control of glaucoma. In all the patients the first line of management was medical therapy to the maximum tolerated level. When medical therapy failed to control intraocular pressure, surgery was resorted to. Cyclocryotherapy was performed on 12 eyes, trabeculectomy on one phakic eye, and seton (Molteno) surgery on another eye. The status of the graft (clear, rejected, or failed), intraocular pressure, and visual outcome were also reviewed.


This study included 190 eyes of 185 patients (136 men, 49 women) in whom a total of 232 penetrating keratoplasties were performed from January 1, 1990 through December 31, 1990. Of these 185 patients, 5 had undergone bilateral surgery. The follow-up period ranged from 3 to 28 months with a mean follow-up of 14.5 months. Most of the eyes (114 eyes) had over 1 year of follow-up. Of the 232 penetrating kerato�plasties performed, 104 were on phakic and the remaining were on aphakic or pseudophakic eyes. In 127 eyes penetrating keratoplasty alone was done, while in 105 eyes penetrating keratoplasty was combined with other procedures [Table 1].

It is apparent from the results that the risk of developing glaucoma was minimum when penetrating keratoplasty alone was performed (13%), and when penetrating keratoplasty was combined with other procedures, the risk of developing glaucoma increased upto 50% [Table 1].

We observed that in conditions such as aphakic bullous keratopathy (ABK), pseudophakic bullous keratopathy (PBK), and vascularised corneal scar the incidence of post-penetrating keratoplasty glaucoma was 30 to 42%, while in keratoconus and corneal dystrophies it was 6 and 16%, respectively [Table 2]. The incidence of post-penetrating keratoplasty glaucoma was 10.7% in phakic eyes, while in the aphakic and pseudophakic eyes, it was 36.5% and 24%, respectively [Table 3]. Additionally, the incidence of post-penetrating keratoplasty glaucoma increased with repeat grafts. As seen in [Table 4], glaucoma occurred in 19 (43.18%) of the total 44 regrafts. Preexisting glaucoma was noted in 11 eyes, with glaucoma worsening in 9 postoperatively.

A total of 38 eyes were treated medically of which 33 remained controlled. In the remaining 5 eyes the intraocular pressure could not be controlled despite which surgery was not advised because of glaucoma�tous optic atrophy, opaque graft, or patients being asymptomatic and refusing further surgery. Fourteen patients underwent surgery wherein cyclocryotherapy was performed in 12 eyes and one eye each had undergone trabeculectomy and Molteno implant. Both procedures were successful in controlling the intraocu�lar pressure. Of the 12 cyclocryo treated eyes, 3 eyes required two sittings of cyclocryotherapy. In 11 eyes the intraocular pressure remained controlled till the last follow-up and one eye became phthisical.

As regards the visual outcome, patients treated medically had better visual prognosis (20/400 or better in 24/38) as compared to surgical group (20/400 or better in 2/14). Twenty-six eyes had poor vision of which 16 were attributable to opaque graft (9 failure, 7 rejection). Of the remaining 10 eyes with clear graft,poor vision was secondary to glaucomatous optic atrophy in 6 and nonglaucoma-related posterior segment pathology in 4.


Post-penetrating keratoplasty glaucoma is defined as an elevated intraocular pressure following penetrating keratoplasty, with or without optic nerve damage and visual field changes. In some patients the condition becomes chronic and is a serious clinical problem for diagnosis and management.

In a recently reported series the incidence of post�penetrating keratoplasty glaucoma was found to be 18% [5]sub and the important risk factors suggested were aphakia and preexisting glaucoma. Data from the Australian Corneal Graft Registry has shown the incidence of elevated intraocular pressure (>25 mm Hg) following penetrating keratoplasty as 7%. [10] The various risk factors described for the development of glaucoma were aphakia, pseudophakia, and failed graft. In these groups the incidence of post-penetrating keratoplasty glaucoma was reported to be as high as 50%. [1]

In the present series, 52 of 190 eyes developed high intraocular pressure following post-penetrating keratoplasty, giving an overall incidence of 27.4%. This high incidence in our study is due to the quality of sample which includes a large number (91/190) of eyes belonging to the high-risk category for development of post-penetrating keratoplasty glaucoma such as aphakia, pseudophakia, repeat graft, and vascularised scar. We found the incidence of post-penetrating keratoplasty glaucoma in these eyes to vary from 30 to 41% as compared to keratoconus and corneal dystrophy in which the incidence of glaucoma varied from 6 to 16%. Furthermore, in eyes with vascularised corneal scar the incidence of post-penetrating keratoplasty glaucoma was considerably high (30.7%). This, to some extent, is due to some of these eyes having had sector iridectomy for improvement of vision which would distort the pupil and contribute to progressive angle closure, secondary to the adhesion of the floppy iris to the graft/host junction.

Our results further show that aphakic and pseudo�phakic eyes are at much higher risk of developing glaucoma as compared to phakic eyes [Table 3]. This observation is consistent with other earlier reports. [1],[2],[3],[5]

The risk of developing glaucoma significantly increases in those patients where penetrating kerato�plasty is combined with other procedures such as cataract surgery, anterior vitrectomy, intraocular lens removal, exchange of intraocular lens, and repeat penetrating keratoplasty [Table 1][Table 4]. The increased risk of developing glaucoma in these eyes is probably because of increased postoperative inflammation leading to peripheral anterior synaechiae and trabecular meshwork collapse or damage.

Various described methods to control intraocular pressure in post-penetrating keratoplasty glaucoma are trabeculectomy, [11] seton surgery [6],[8].[9] ciliary body destructive procedures, [12] and argon laser trabecu�loplasty. [13] However, chances for control of intra�ocular pressure by trabeculectomy in these eyes is poor. There have been a few reports of successful manage�ment of post-penetrating keratoplasty glaucoma with seton devices such as Molteno implant or anterior chamber tube shunt to encircling band (ACTSEB). [6],[8],[9]

Conventional surgical treatment in these cases involves ciliary body destruction either by cyclo�cryotherapy, YAG laser, or argon laser cyclophoto�coagulation either trans pupillary or by endolaser. [12],[5] Argon laser trabeculoplasty has been tried without much success in these cases. [13] The adjunctive use of antimetabolites such as 5-fluorouracil in trabeculec�tomy is also not recommended because of toxicity of this drug on the graft epithelium. [14] Mitomycin C used in conjunction with trabeculectomy has many advantages and may prove to be an effective surgical procedure in the management of post-penetrating keratoplasty glaucoma; however, one should be cognizant of the associated risk of graft rejection and graft failure. [8]

In our study, of 52 cases 14 required surgical intervention and the rest were managed by medical therapy. Of 38 medically treated eyes, 33 remained controlled on follow-up, while 5 did show high intraocular pressure during follow-up but surgical inter�vention was not advised since all these patients had previously lost their vision due to glaucomatous disc damage, graft failure, or posterior segment pathology. All these patients were either asymptomatic or refused further surgery to control intraocular pressure.

Our approach for all phakic eyes has been to consider trabeculectomy as a first procedure because these eyes have undisturbed angle structure and do not have vitreous in anterior chamber, and so may do well after trabeculectomy. In this series, trabeculec�tomy was performed on one patient wherein the intraocular pressure remained controlled till the last follow-up. One patient had Molteno implant surgery with a 4-month follow-up wherein the intraocular pressure remained under control. In the remaining 12 patients cyclocryotherapy was performed. Of these 12 patients, 3 patients required two sittings of cycloc�ryotherapy. In 11 patients the intraocular pressure remained under control till the last follow-up and one eye became phthisical. Cyclocryotherapy is not considered as a procedure of choice because of the high risk of phthisis, vision loss secondary to clouding of cornea, and progression of cataract. [15]

In our series, 50% (26 eyes) of post-penetrating keratoplasty glaucoma eyes had a visual acuity of 20/ 400 or less despite prompt management. In 6 of these, the cause for poor vision could be directly attributed to glaucoma due to glaucomatous optic atrophy with clear graft. Likewise, the development of glaucoma could have been a contributing factor in 9 eyes with failed graft.

Post-penetrating keratoplasty glaucoma continues to be a clinical problem that can be sight threatening in its ultimate outcome. However, recognition of the risk factors such as preexisting glaucoma, pseudophakia, and aphakia, and more frequent monitoring of intra�ocular pressure, may yield better results. With newer surgical modalities such as seton implant and mitomycin C-augmented trabeculectomy giving new hope for these patients, it is for prospective studies to investigate into the benefits and relative risks before such modalities become established in the management of post-penetrating keratoplasty glaucoma.


1Goldberg DB, Schanzlin DJ, and Brown SI. Incidence of increased intraocular pressure after keratoplasty. Am J Ophthalmol. 92:372-377, 1981.
2Karash JW and Nirankari VS. Factors associated with glaucoma after penetrating keratoplasty. Am J Oph�thalmol. 96:160-164, 1983.
3Warring GO (III), Stulting D, and Street D. Penetrating Keratoplasty for Pseudophakic corneal edema with ex�change of intra ocular lens. Arch Ophthalmol. 105:58-62, 1987.
4Olsori RJ and Kaufman HE. A Mathematical description of causative factors and prevention of elevated intraocu�lar pressure after keratoplasty. Invest Ophthalmol Vis Sci. 16:1085-1092, 1977.
5Foulks GN. Glaucoma associated with penetrating kera�toplasty. Ophthalmology. 94:871-874, 1987.
6Beebe WE, Starita RJ, Fellmen RL, Lynn JR, and Gelender H. The use of Molteno implant anterior chamber tube shunt to encircling band for the treatment of glaucoma in keratoplasty patient. Ophthalmology. 97:1414-1422, 1990.
7Busin M, Arffa RC, Mc Donald MB, and Kaufman HE. Glaucoma following penetrating keratoplasty in Intra ocular lens removal during penetrating keratoplasty. Ophthalmology. 94:505-509, 1987.
8Mc Donnell PJ, Robin JB, and Schanzlin DJ. Control of glaucoma in eyes after penetrating keratoplasty. Ophthalmology. 95:364-369, 1988.
9Kirkness CM. Penetrating keratoplasty, glaucoma and silicone drainage tubing. Dev Ophthalmol. 14:161-165, 1987.
10Williams KA, Rodar D, Esterman A, et al. Factors predictive of corneal graft survival. Report from Australian Corneal Graft Registry. Ophthalmology. 99:403-414, 1992.
11Gilvarry AME, Kirkness CM, Steele ADMcG, Rice NSC, and Flicker LA. The management of post penetrating keratoplasty glaucoma by trabeculectomy. Eye. 3:713�718, 1989.
12Binder PS, Abel R Jr., and Kaufman HE. Cyclocryo ther�apy for glaucoma after penetrating keratoplasty. Am J Ophthalmol. 79:489-492, 1978.
13Van meter WS, Allen RC, Waring GO III, and Stulting D.Laser trabeculoplasty for glaucoma in aphakic and pseudophakic eyes after penetrating keratoplasty. Arch Ophthalmol. 106:185-188, 1988.
14Skuta GL, Beeson CC, and Higginbotham EJ et al. Intra operative Mitomycin versus post operative 5-Fluoroura�cil in high risk galucoma filtering surgery. Ophthalmol�ogy. 99:438-444, 1992.
15Gross Cyclodestructive procedure for glaucoma. In Focal Point. Section 3, 1992.