|Year : 2016 | Volume
| Issue : 3 | Page : 123-126
A prospective study of incidence and risk factors for secondary glaucoma after penetrating keratoplasty
Aruna Kumari R Gupta1, Roopam Kumar R Gupta2
1 Department of Ophthalmology, C.U. Shah Medical College and Hospital, Surendranagar, Gujarat, India
2 Department of Anatomy, C.U. Shah Medical College and Hospital, Surendranagar, Gujarat, India
|Date of Submission||15-Jul-2015|
|Date of Acceptance||26-Apr-2016|
|Date of Web Publication||19-Sep-2016|
Aruna Kumari R Gupta
Department of Ophthalmology, C.U. Shah Medical College and Hospital, Surendranagar - 363 001, Gujarat
Source of Support: None, Conflict of Interest: None
Aim: To carry out a prospective study to analyze the incidence and risk factors for secondary glaucoma after penetrating keratoplasty (PK). Materials and Methods: Three hundred and eleven consecutive penetrating keratoplasties that were performed between January 1, 2006, and December 31, 2008, with a follow-up of 12 months were prospectively analyzed to determine the factors associated with postoperative glaucoma. Results: Of 311 eyes, secondary glaucoma developed in 57 cases. This yields an incidence of 18.3%. In conditions, such as aphakic bullous keratopathy, the incidence of post-PK glaucoma was 3.0%; in pseudophakic bullous keratopathy 14.0%, and in cases of failed graft 16.0%, while in cases of corneal ulcer and corneal opacity it was 49.0% and 18.0%, respectively. Conclusion: We conclude in our study that the incidence of glaucoma developing post-PK was highest in phakic eyes, which may be due to the formation of posterior synechiae and development of intumescent cataract. Higher incidence of glaucoma developing in infective cases could be due to recipient hot eye and the high incidence in cases of large graft could be attributed to the formation of peripheral anterior synechiae.
Keywords: Graft size, indications, penetrating keratoplasty, phakic status, secondary glaucoma
|How to cite this article:|
Gupta AR, Gupta RR. A prospective study of incidence and risk factors for secondary glaucoma after penetrating keratoplasty. J Clin Ophthalmol Res 2016;4:123-6
|How to cite this URL:|
Gupta AR, Gupta RR. A prospective study of incidence and risk factors for secondary glaucoma after penetrating keratoplasty. J Clin Ophthalmol Res [serial online] 2016 [cited 2021 May 16];4:123-6. Available from: https://www.jcor.in/text.asp?2016/4/3/123/190794
The association between penetrating keratoplasty (PK) and the development of postoperative increase in intraocular pressure (IOP) has been first noted by Irvine and Kaufman. Since then, various authors have reported the incidence of glaucoma following PK to be from 9% to 31% in the early postoperative period ,, and from 18 to 35% in the late postoperative period.,
A variety of factors has been studied for a better understanding of the mechanisms involved in the elevation of IOP following PK. Graft size ,,,, suture technique ,, and iridocorneal compression , have been implicated for postoperative secondary glaucoma. Other factors, especially aphakia , have also been studied.
Timely diagnosis of post-PK glaucoma (PPKG) with initiation of appropriate treatment is mandatory to preserve optimal graft clarity and optic nerve head function. The purpose of this paper was to determine the incidence and risk factors for secondary glaucoma after PK.
| Materials and Methods|| |
Between January 1, 2006, and December 31, 2008, a prospective study was conducted of consecutive PKs performed at our institution. The cases had a follow-up of 12 months. PK was performed following the ethical guidelines for biomedical research on human subjects issued by the Indian Council of Medical Research in 2000. The institutional ethics committee had cleared the project. All the patients had given their informed consent.
Preoperative examination of the recipients included their details, chief complaints, and the presence of any predisposing factors such as ocular surface disorders, trauma, contact lens use, previous history of graft infection, systemic illness, and history of any ocular surgery.
Clinical examination included uncorrected visual acuity, best corrected visual acuity, cycloplegic refraction (not done in infective keratitis cases); slit lamp biomicroscopy to determine any ocular pathology, applanation tonometry (not done in infective keratitis cases). In cases where the recording of IOP was not possible by Goldman applanation tonometry, digital tonometry was done. Dilated fundus examination was done for disc evaluation where media was clear and to rule out any posterior segment pathology.
Investigations included tear film status, gonioscopy, sac syringing, routine blood investigations such as complete blood count, ESR, urine routine and microbiology, blood urea and serum creatinine, fasting blood sugar and fasting urine sugar, serology to screen for infectious diseases such as AIDS (S.HIV), hepatitis (S. HbsAg), and sexually transmitted diseases (S.VDRL). Blood pressure and ultrasonography of the posterior segment was performed to rule out vitreous exudation suggestive of endophthalmitis. The medical records were reviewed for the indication for which PK was done and the IOP measurements in each case were noted.
Patients who had a previous history of glaucoma were excluded from the study. All PK were performed by standard surgical technique under local anesthesia except in children where general anesthesia was used. Donor button oversized by 0.5 mm was used, except in cases of keratoconus, where the graft of the same size as the recipient was used. Anterior vitrectomy was performed when required. Donor cornea was sutured to recipient cornea with interrupted 10.0 nylon monofilament sutures with adjustable suture technique. All cases received amikacin (25 mg), cefazolin (100 mg), and dexamethasone (4 mg) subconjunctivally at the end of the operation. In cases of infective keratitis, dexamethasone was not given. Intraoperative data recording included the details of the surgical procedure, type of surgery, i.e., whether combined with cataract extraction, intraocular lens removal, secondary intraocular lens implantation, and anterior vitrectomy. Postoperatively, the eyes were patched, and topical steroid was administered once the epithelium was intact over the transplant, except in cases of infective keratitis. Topical steroid (prednisolone) was instilled in the operated eye four times a day initially, and the frequency was increased or decreased depending on the degree of inflammation. Topical antibiotics (ofloxacin or gatifloxacin) were given four times in the initial period. At the end of 1 month following surgery, most of the patients were shifted to weaker antibiotic steroids combination (tobramycin and fluorometholone) four times a day. This dosage of medication was tapered during the postoperative period to once after 1 year. In eyes where inflammatory signs persisted, topical steroids were continued longer at higher dosage. If there was sign of graft rejection, then intensive topical steroids were given. Cycloplegic (cyclopentolate 1%) was given twice daily till iritis subsided and was discontinued after 1 week. Topical antibiotics and antifungals were continued till there was no suspicion of infection. Topical antiglaucoma medication (timolol 0.5%) twice daily and lubricants (carboxymethyl cellulose) four times were given during the initial period.
The patients were evaluated on every follow-up in the same manner as the preoperative assessment including the condition of the corneal graft was also noted. The raised IOP was controlled either medically or surgically. Medical treatment included oral acetazolamide 250 mg four times and liquid glycerol 30 cc twice a day and topical antiglaucoma drops were given. Patients not responding to full medical treatment were treated surgically. Surgical methods included filtration procedure and/or by cyclocryotherapy as per the case. The patients were evaluated on the 1st day, at the end of 1st week, 1st month, third and 6 months and then after 1 year postoperatively. Statistical analysis was done using paired and unpaired t-test.
| Results|| |
Three hundred and eleven PKs were performed between the study period on observing the demographic details mean age of the patients was 43.04 ± 17.67 (range 6 years to 78 years). Maximum number of patients was in 41–50 years group (24.0%). In this study, the male recipients were more (64.0%) than female recipients (36.0%). Right eyes were operated more (59.0%) than the left eyes (41.0%).
Of the 311 eyes, secondary glaucoma developed in 57 cases. This yields an incidence of 18.3%. Average preoperative IOP was 15.11 mm Hg (range 12.2–20.6). The IOP (mm Hg) measured on postoperative days averaged 23.58 after 1st week, 25.20 after 1st month, 26.77 after 3rd month, 23.52 after 6 months, and 23.12 after 1 year. Maximum increase was seen at 3 months (P = 0.001). Mean IOP was 24.59 ± 7.87 mm Hg (range 22.4–50.6 mm Hg).
The study of the medical records of these 57 patients showed that in conditions of keratoconus the incidence of PPKG was 0%, aphakic bullous keratopathy (ABK) 3%; in pseudophakic bullous keratopathy 14%, failed graft 16.0%, corneal opacity 18.0%, and in cases of corneal ulcer 49.0%. Among corneal ulcer cases the incidence was 26.0% in cases of bacterial keratitis and 23.0% in cases of fungal keratitis.
The records of the phakic status of these 57 patients showed that 25 patients (44.0%) were phakic, 17 patients (30.0%) were aphakic, and 15 patients (26.0%) were pseudophakic.
We studied the incidence of PPKG with respect to the graft size and found that with 7 mm graft size the incidence was 8%, with 7.5 mm graft size it was 26.0%, with 8 mm graft size 8%, 8.5 mm graft size 12.0%, 9 mm graft size 12.0%, 9.5 mm graft size 13.0%, 10 mm graft size 13.0%, 10.5 mm graft size 3.0%, and with 11 mm graft size 5%.
| Discussion|| |
The definition of PPKG is an elevated IOP (>21 mm Hg) following PK, with or without optic nerve damage and visual field changes. The etiology of PPKG is multifactorial such as distortion of the angle with collapse of the trabecular meshwork, suturing technique, and peripheral anterior synechiae (PAS). Other factors that contribute to postoperative glaucoma are preexisting glaucoma, use of viscoelastic substances, steroid-induced glaucoma, and the presence of ocular inflammation in the pre- or post-operative period.,, The leading cause for late PPKG, however, is synechial angle closure, PAS formation preoperatively or as a consequence of a preceding intraocular surgery ,, and floppy atrophic iris. The purpose of our study was to determine the incidence and risk factors for secondary glaucoma after PK at our center.
In the present series, the incidence of PPKG was 18.3%. Other studies reported the incidence of PPKG to be 18%, 21.5% by França et al., and 27.4% by Sekhar et al. In another study by Karadag et al. IOP increased in the early postoperative period in 5.5% of cases and chronically elevated IOP was reported in 16.6% of cases.
This study shows that the incidence of glaucoma after PK differ significantly based on the indication for PK (from a low of 0% for keratoconus to a high of 49.0% after Infectious keratitis). Our observation of higher incidence of secondary glaucoma in infectious keratitis cases may be due to preoperative and postoperative inflammation and the development of PAS as also reported by Kirkness and Moshegov. Other studies also reported the rate of chronic glaucoma after PK differed significantly based on the indication from a low of 0–12% for keratoconus to a high of 75% after infectious keratitis.,, When the incidence of glaucoma was studied based on microbiology, i.e., bacterial or fungal there was no significant difference in incidence of glaucoma in our study. Studies by Goldberg et al. Simmons et al., Kirkness and Moshegov  and Polack, also reported a low incidence of secondary glaucoma after PK in keratoconus similar to our findings. Goldberg et al. reported increased IOP in cases of ABK. In some studies, bullous keratopathy, graft rejection, history of glaucoma, and trauma were reported to be high-risk factors for IOP elevation following PK.,, Wagoner et al. reported that eyes with corneal edema were significantly more likely to develop glaucoma than those with stromal scarring dissimilar to our findings.
The study of association of glaucoma with phakic status found that out of 57 patients 25 patients (44.0%) were phakic, 17 patients (30.0%) were aphakic, and 15 patients (26.0%) were pseudophakic. In this study, the incidence of glaucoma was more in phakic eyes whereas other studies reported aphakic eyes , at much higher risk of developing glaucoma. The proposed mechanism of glaucoma in aphakic cases was more manipulation of eye structures leading to more inflammation by Goldberg et al., Karesh et al., and Zimmerman et al., angle distortion by Olson and Kaufman, and mechanical collapse of the trabecular meshwork by Zimmerman et al. Some studies reported that aphakic and pseudophakic eyes in the presence of PAS had a greater tendency to develop PPKG when compared to phakic eyes,,,, while other studies found no difference between aphakic and pseudophakic eyes but reported a higher incidence of PPKG in pseudophakic and aphakic eyes as compared to phakic eyes. As the incidence in our study was more in phakic cases, we propose that the formation of posterior synechiae and development of intumescent cataract leads to the higher incidence of secondary glaucoma in phakic eyes.
In our study, 5 phakic eyes of corneal abscess were rendered aphakic, 3 corneal opacity cases phakic to pseudophakic, 2 failed graft cases phakic to aphakic, and 1 descematocoel case phakic to pseudophakic. We did not find any statistically significant increase in IOP in cases where combined surgery was done similar to other studies,,, while many studies reported an increase in the relative risk associated with PPKG following combined surgical procedure with PK.,
The relationship between donor button size and host bed size has also been the subject of several studies.,, On comparing the graft size with the outcome, we observed that with graft size of 8 mm and above there was increased incidence of secondary glaucoma which may be due to the formation of PAS at the host-graft junction. A donor button 0.5 mm larger than the host bed has been shown to be associated with a lower incidence of postoperative glaucoma , but in our study this was not assessed as we used donor button oversized by 0.5 mm in all cases except in cases of keratoconus, where the graft of same size as the recipient was used. In our study, incidence of glaucoma in cases with difference in suturing technique was not studied. Studies by Pramanik et al., Erdurmus et al. and Fan et al. found IOP elevation related to steroid use following PK, but in our study, we did not observe any steroid responders so this factor was not evaluated.
| Conclusion|| |
PPKG glaucoma continues to be a clinical problem that can be sight threatening in its ultimate outcome. However, recognition of the risk factors, controlling the inflammatory response judiciously, and more frequent monitoring of IOP may yield better results. We conclude in our study that the incidence of glaucoma developing post-PK was highest in phakic eyes, which may be due to the formation of posterior synechiae and development of intumescent cataract. Higher incidence of glaucoma developing in infective cases could be due to recipient hot eye and the high incidence in cases of large graft could be attributed to formation of PAS.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Irvine AR, Kaufman HE. Intraolar pressure following penetrating keratoplasty. Am J Ophthalmol 1969;68:835-44.
Goldberg DB, Schanzlin DJ, Brown SI. Incidence of increased intraocular pressure after keratoplasty. Am J Ophthalmol 1981;92:372-7.
Karesh JW, Nirankari VS. Factors associated with glaucoma after penetrating keratoplasty. Am J Ophthalmol 1983;96:160-4.
Chien AM, Schmidt CM, Cohen EJ, Rajpal RK, Sperber LT, Rapuano CJ, et al.
Glaucoma in the immediate postoperative period after penetrating keratoplasty. Am J Ophthalmol 1993;115:711-4.
Foulks GN. Glaucoma associated with penetrating keratoplasty. Ophthalmology 1987;94:871-4.
Olson RJ, Kaufman HE. A mathematical description of causative factors and prevention of elevated intraocular pressure after keratoplasty. Invest Ophthalmol Vis Sci 1977;16:1085-92.
Zimmerman T, Olson R, Waltman S, Kaufman H. Transplant size and elevated intraocular pressure. Postkeratoplasty. Arch Ophthalmol 1978;96:2231-3.
Olson RJ. Aphakic keratoplasty. Determining donor tissue size to avoid elevated intraocular pressure. Arch Ophthalmol 1978;96:2274-6.
Bourne WM, Davison JA, O'Fallon WM. The effects of oversize donor buttons on postoperative intraocular pressure and corneal curvature in aphakic penetrating keratoplasty. Ophthalmology 1982;89:242-6.
Foulks GN, Perry HD, Dohlman CH. Oversize corneal donor grafts in penetrating keratoplasty. Ophthalmology 1979;86:490-4.
Zimmerman TJ, Krupin T, Grodzki W, Waltman SR. The effect of suture depth on outflow facility in penetrating keratoplasty. Arch Ophthalmol 1978;96:505-6.
Wilson SE, Kaufman HE. Graft failure after penetrating keratoplasty. Surv Ophthalmol 1990;34:325-56.
França ET, Arcieri ES, Arcieri RS, Rocha FJ. A study of glaucoma after penetrating keratoplasty. Cornea 2002;21:284-8.
Redbrake C, Arend O. Corneal transplantation and glaucoma. Ophthalmologe 2000;97:552-6.
Coleman AL. Glaucoma. Lancet 1999;354:1803-10.
Lass JH, Pavan-Langston D. Timolol therapy in secondary angle-closure glaucoma post penetrating keratoplasty. Ophthalmology 1979;86:51-9.
Kirkness CM, Ficker LA. Risk factors for the development of postkeratoplasty glaucoma. Cornea 1992;11:427-32.
Simmons RB, Stern RA, Teekhasaenee C, Kenyon KR. Elevated intraocular pressure following penetrating keratoplasty. Trans Am Ophthalmol Soc 1989;87:79-91.
Kirkness CM, Moshegov C. Post-keratoplasty glaucoma. Eye (Lond) 1988;2 Suppl: S19-26.
Cohen EJ, Kenyon KR, Dohlman CH. Iridoplasty for prevention of post-keratoplasty angle closure and glaucoma. Ophthalmic Surg 1982;13:994-6.
Sekhar GC, Vyas P, Nagarajan R, Mandal AK, Gupta S. Post-penetrating keratoplasty glaucoma. Indian J Ophthalmol 1993;41:181-4.
Karadag O, Kugu S, Erdogan G, Kandemir B, Eraslan Ozdil S, Dogan OK. Incidence of and risk factors for increased intraocular pressure after penetrating keratoplasty. Cornea 2010;29:278-82.
Polack FM. Glaucoma in keratoplasty. Cornea
Wagoner MD, Ba-Abbad R, Al-Mohaimeed M, Al-Swailem S, Zimmerman MB; King Khaled Eye Specialist Hospital Corneal Transplant Study Group. Postoperative complications after primary adult optical penetrating keratoplasty: Prevalence and impact on graft survival. Cornea 2009;28:385-94.
Seitz B, Langenbucher A, Nguyen NX, Küchle M, Naumann GO. Long-term follow-up of intraocular pressure after penetrating keratoplasty for keratoconus and Fuchs' dystrophy: mparison of mechanical and excimer laser trephination. Cornea 2002;21:368-73.
Pramanik S, Musch DC, Sutphin JE, Farjo AA. Extended long-term outcomes of penetrating keratoplasty for keratoconus. Ophthalmology 2006;113:1633-8.
Erdurmus M, Cohen EJ, Yildiz EH, Hammersmith KM, Laibson PR, Varssano D, et al.
Steroid-induced intraocular pressure elevation or glaucoma after penetrating keratoplasty in patients with keratoconus or Fuchs dystrophy. Cornea 2009;28:759-64.
Fan JC, Chow K, Patel DV, McGhee CN. Corticosteroid-induced intraocular pressure elevation in keratoconus is common following uncomplicated penetrating keratoplasty. Eye (Lond) 2009;23:2056-62.