- Email: [email protected]
Epithelial downgrowth after Descemet-stripping automated endothelial keratoplasty
CASE REPORT
Epithelial downgrowth after Descemet-stripping automated endothelial keratoplasty Paul M. Phillips, MD, Mark A. Terry, MD, Stephen C. Kaufman, MD, Edwin S. Chen, MD
A 66-year-old man presented with decreased vision and corneal edema after 2 failed Descemetstripping automated endothelial keratoplasty (DSAEK) graft procedures in the left eye. An uneventful third DSAEK procedure combined with anterior vitrectomy through the previous limbal wound was performed. Postoperative recovery was uneventful. Histopathology of the excised failed graft revealed conjunctival epithelium on the posterior surface of the tissue. At 1 year, the endothelial cell count was 1997 cells/mm2 and the uncorrected visual acuity was 20/20–2. At 18 months, the graft remained clear with no signs of epithelial downgrowth. Clinicians should be aware that epithelial downgrowth can occur following DSAEK surgery. Fortunately, excision of the prior DSAEK graft with removal of the active epithelial membrane appears to have been a successful treament in this patient. J Cataract Refract Surg 2009; 35:193–196 Q 2009 ASCRS and ESCRS
Epithelial downgrowth is a rare but serious consequence following compromise of the ocular integrity by penetrating trauma or intraocular surgery. Historically, epithelial downgrowth was described most commonly after cataract extraction.1 Epithelial downgrowth is also well documented following penetrating keratoplasty (PKP) as well as less invasive ocular
Submitted: June 23, 2008. Final revision submitted: July 24, 2008. Accepted: July 24, 2008. From the Devers Eye Institute (Phillips, Terry, Chen) and Lions Vision Research Laboratory of Oregon (Terry), Portland, Oregon, and the University of Minnesota (Kaufman), Minneapolis, Minnesota, USA. Dr. Terry has a financial interest in the specialized instruments used in this surgery. No other author has a financial or proprietary interest in any material or method mentioned. Supported in part by an unrestricted grant from Research to Prevent Blindness, New York, New York, USA. Bausch & Lomb Surgical, St. Louis, Missouri, USA, manufactured and supplied the specially designed instruments free of charge. Dr. David Wilson and the histology laboratory at the Casey Eye Institute of Oregon Health Sciences University processed the corneal tissue and provided the images used in this report. Corresponding author: Paul Phillips, MD, Devers Eye Institute, 1040 Northwest 22nd Avenue, Portland, Oregon 97210, USA. E-mail: [email protected]. Q 2009 ASCRS and ESCRS Published by Elsevier Inc.
surgeries such as anterior chamber aspiration and glaucoma procedures.2 The pathology leading to epithelial downgrowth is not known but is probably related to poor closure and healing of wounds. Wounds may be compromised by the presence of vitreous, iris, or other debris within incisions, which can lead to leaks or fistulas.3–6 The development of epithelial downgrowth is likely multifactorial, however, and may include a history of multiple operations with or without the presence of significant inflammation, corneal vascularity, and endothelial cell damage. All these conditions may be contributing factors. Endothelial keratoplasty has recently revolutionized the field of corneal surgery. Although Tillet7 published the first successful case of posterior lamellar keratoplasty in 1956, endothelial keratoplasty underwent the most rapid advancement and mainstream acceptance following Melles et al.’s8 description in 1998 of sutureless replacement of the endothelium using only the posterior portion of the donor tissue. Endothelial keratoplasty was described as deep lamellar endothelial keratoplasty by Terry and Ousley9 and subsequently as Descemet-stripping endothelial keratoplasty by Price and Price.10 Endothelial keratoplasty has proven to be less invasive than PKP, yielding a theoretically stronger globe11 and faster visual rehabilitation. Although there have been 3 reports of epithelial ingrowth following endothelial keratoplasty surgery12–14 and 1 report of epithelial downgrowth occurring as an extension of epithelial ingrowth into the graft–host interface,15 0886-3350/09/$dsee front matter doi:10.1016/j.jcrs.2008.07.036
193
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CASE REPORT: EPITHELIAL DOWNGROWTH AFTER DSAEK
Figure 1. A: Preoperative photography showing failed DSAEK graft with stromal edema and poor view of anterior chamber. B: One year after replaced DSAEK graft with anterior vitrectomy, the pupil is no longer peaked.
we believe this is the first case of DSAEK primary graft failure with epithelial downgrowth occurring in a patient after 2 DSAEK procedures. The unique feature of our case is that the histopathology demonstrated conjunctival epithelium extending over the donor endothelium as the etiology of the graft failure. CASE REPORT A 64-year-old man with Fuchs dystrophy and a history of cataract surgery in the left eye 5 years earlier presented to an outside corneal surgeon (not one of the authors) with slowly progressive corneal edema. On November 17, 2005, uneventful DSAEK was performed in the left eye. On postoperative day 1, a partial dislocation was noted and air was reinjected. The graft reattached but did not clear. After what appeared to be a primary graft failure, repeat DSAEK was performed on February 14, 2006. Again, the surgery was uneventful and the graft was well positioned but remained edematous and did not clear. The patient was referred to our center for a second opinion and subsequent surgical rehabilitation. On presentation, 6 months after the first DSAEK, the patient complained of pain, light sensitivity, and redness with decreased visual acuity. On examination, the best spectacle-corrected visual acuity was 20/400. Central corneal thickness was 806 mm and the intraocular pressure (IOP), 15 mm Hg. Slitlamp examination demonstrated complete stromal edema without keratic precipitates or anterior chamber inflammation. The pupil was noted to be peaked toward the temporal wound, and vitreous strands were noted
attached to the posterior wound margin (Figure 1, A). There were no signs of epithelial downgrowth, with no membranes, cysts, or scalloped margins noted on any area of the posterior surface of the cornea. The patient was offered the options PKP or a third DSAEK and after a thorough discussion of the risks and benefits of each option, he decided to proceed with another DSAEK surgery. Surgery was performed on June 27, 2006, and included a limited anterior vitrectomy, which cleared the anterior chamber of vitreous and rounded the pupil. The failed DSAEK graft was removed by opening the graft–host interface at the temporal edge using sharp and blunt dissection with a crescent blade and a spatula. Once the interface was opened, the blunt spatula easily separated the horizontal donor–recipient interface and then broke the sealed edges of the graft. The tissue was removed, fixed in formalin, and sent to pathology. The remainder of the surgery followed our standard DSAEK technique, including peripheral stromal scraping. On the first postoperative day, the graft was adherent and thin. The uncorrected visual acuity (UCVA) was 20/100. At the 1-week examination, the UCVA was 20/80 and the IOP was 15 mm Hg. The histopathology report of the removed failed graft described multilayered surface conjunctival epithelial cells with occasional goblet cells extending over the surgical margin of the specimen and onto the posterior surface. These findings were consistent with epithelial downgrowth (Figure 2) originating from the conjunctiva. Despite the findings of epithelial downgrowth, the patient continued to improve postoperatively, with no signs of recurrence. Postoperatively, what was thought to be a small
Figure 2. Histopathology of the removed DSAEK graft demonstrating multilayered surface conjunctival epithelial cells with occasional goblet cells (arrows) extending over the surgical margin of the specimen and onto the posterior surface, consistent with epithelial downgrowth.
J CATARACT REFRACT SURG - VOL 35, JANUARY 2009
CASE REPORT: EPITHELIAL DOWNGROWTH AFTER DSAEK
epithelial inclusion cyst was noted peripheral to the donor graft on the endothelial surface of the host. However, with a follow-up of more than 18 months, the cyst has not enlarged and the patient’s graft has remained clear. The UCVA is 20/20-2 and the endothelial cell count, 1997 cells/mm2 (Figure 1, B).
DISCUSSION Although epithelial downgrowth into the anterior chamber after DSAEK might be considered rare, we have presented a case that was discovered in a patient after 2 failed DSAEK grafts. Epithelial ingrowth into the interface between the donor and recipient stroma has been described.12–15 In one of the reports, the epithelium was noted to extend outside the graft–host interface,15 leading to its designation as epithelial downgrowth. However, epithelial downgrowth with the epithelium invading the anterior chamber and growing over the host endothelium has not been reported following DSAEK. The presence of graft failure in the setting of epithelial downgrowth and the presence of goblet cells, indicating the conjunctival origin of the invasive cells, are unique to this case. In 2 previous case reports,14,15 epithelial ingrowth did not lead to graft failure, as corneal edema was not present in either case. In our case, the donor graft had failed before DSAEK was repeated. What is unclear, however, is whether the epithelial downgrowth led to or was the result of the first or second graft failure in this patient. The possible causes of epithelial downgrowth in this case include those inherent in intraocular surgery, including possible implantation of epithelium at the time of surgery; inadequate tissue closure, leading to subclinical wound leakage; corneoscleral suture tracks; damaged or unhealthy endothelium; multiple surgical procedures; and inflammation. It is important to note that a repeat DSAEK, including a thorough vitrectomy with careful wound closure, appears to have been a successful treatment in this case, without having to resort to a full-thickness PKP. This patient had several risk factors, including multiple surgeries and, possibly more important, the presence of vitreous within the surgical wound. The formed vitreous probably acted as a scaffold for the migration of conjunctival epithelium from the conjunctival tissue adjacent to a compromised wound. Given the nature of DSAEK surgery, poor endothelial function may have also played a role. Most risk factors should theoretically be minimized by DSAEK compared with standard PKP, and it is therefore tempting to dismiss this incident of epithelial downgrowth as a ‘‘chance’’ occurrence related to the history of multiple intraocular surgeries, the presence of vitreous in the wound, or the incidental
195
implantation of epithelial cells at the time of surgery rather than to the DSAEK procedure specifically. However, previous studies have implicated pathological or damaged endothelium in epithelial migration through loss of contact inhibition.16 If unhealthy endothelium does play a role in allowing intraocular epithelium to thrive and migrate, the endothelial damage that occurs during DSAEK procedures must be considered. Although the epithelial downgrowth may have been a result of multiple previous surgeries in our patient, it is probably most important to address the more modifiable risk factors. In this case, the presence of vitreous in the posterior wound could have easily been avoided and a prophylactic anterior vitrectomy should always be performed in any case where the posterior capsule integrity is in question and vitreous in the anterior chamber is suspected. Wound construction and approximation with sutures should be a priority, and excessive postoperative inflammation should be avoided. Finally, an attempt to avoid excessive endothelial cell damage, which might provide an easy path to the overgrowth of epithelial cells, should always be made. REFERENCES 1. Maumenee AE, Shannon CR. Epithelial invasion of the anterior chamber. Am J Ophthalmol 1956; 41:929–942 2. Chen SH. Pineda R II. Epithelial and fibrous downgrowth: mechanisms of disease. Ophthalmol Clin North Am 2002; 15(1):41–48 3. Maumenee AE. Treatment of epithelial downgrowth and intraocular fistula following cataract extraction. Trans Am Ophthalmol Soc 1964; 62:153–163; discussion 163–166. Available at: http:// www.pubmedcentral.nih.gov/picrender.fcgi?artidZ1310154& blobtypeZpdf. Accessed August 8, 2008 4. Stark WJ, Michels RG, Maumenee AE, Cupples H. Surgical management of epithelial ingrowth. Am J Ophthalmol 1978; 85:772–780 5. Weiner MJ, Trentacoste J, Pon DM, Albert DM. Epithelial downgrowth: a 30-year clinicopathological review. Br J Ophthalmol 1989; 73:6–11 6. Blodi FC. Failures of the cataract extractions and their pathologic explanation. J Iowa State Med Soc 1954; 44:514–516 7. Tillett CW. Posterior lamellar keratoplasty. Am J Ophthalmol 1956; 41:530–533 8. Melles GRJ, Eggink FAGJ, Lander F, Pels E, Rietveld FJR, Beekhuis WH, Binder PS. A surgical technique for posterior lamellar keratoplasty. Cornea 1998; 17:618–626 9. Terry MA, Ousley PJ. Deep lamellar endothelial keratoplasty in the first United States patients; early clinical results. Cornea 2001; 20:239–243; errata, 353 10. Price FW Jr, Price MO. Descemet’s stripping with endothelial keratoplasty in 50 eyes: a refractive neutral corneal transplant. J Refract Surg 2005; 21:339–345 11. Barry JS, Spiteri A, Habib NE. Traumatic wound dehiscence of old extracapsular cataract extraction incision after endothelial keratoplasty [letter]. Cornea 2008; 27:127;127; reply by PK Nagra, KH Hammersmith, EJ Cohen, CJ Rapuano and MA Terry, 127–128
J CATARACT REFRACT SURG - VOL 35, JANUARY 2009
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CASE REPORT: EPITHELIAL DOWNGROWTH AFTER DSAEK
12. Culbertson WW. Descemet stripping endothelial keratoplasty. Int Ophthalmol Clin 2006; 46(3):155–168 13. Suh LH, Yoo SH, Deobhakta A, Donaldson KE, Alfonso AC, Culbertson WW, O’Brien TP. Complications of Descemet’s stripping with automated endothelial keratoplasty; survey of 118 eyes at one Institute. In press, Ophthalmology 2008 14. Koenig SB, Covert DJ. Epithelial ingrowth after Descemetstripping automated endothelial keratoplasty. Cornea 2008; 27:727–729 15. Walker BM, Hindman HB, Ebrahimi KB, Green WR, Eberhart CG, Garcia I, Jun AS. Epithelial downgrowth following Descemet’s-stripping automated endothelial keratoplasty [letter]. Arch Ophthalmol 2008; 126:278–280
16. Cameron JD, Flaxman BA, Yanoff M. In vitro studies of corneal wound healing: epithelial-endothelial interactions. Invest Ophthalmol 1974; 13:575–579. Available at: http://www.iovs. org/cgi/reprint/13/8/575. Accessed August 8, 2008
J CATARACT REFRACT SURG - VOL 35, JANUARY 2009
First author: Paul M. Phillips, MD Devers Eye Institute, Portland, Oregon
Epithelial downgrowth after Descemet-stripping automated endothelial keratoplasty Paul M. Phillips, MD, Mark A. Terry, MD, Stephen C. Kaufman, MD, Edwin S. Chen, MD
A 66-year-old man presented with decreased vision and corneal edema after 2 failed Descemetstripping automated endothelial keratoplasty (DSAEK) graft procedures in the left eye. An uneventful third DSAEK procedure combined with anterior vitrectomy through the previous limbal wound was performed. Postoperative recovery was uneventful. Histopathology of the excised failed graft revealed conjunctival epithelium on the posterior surface of the tissue. At 1 year, the endothelial cell count was 1997 cells/mm2 and the uncorrected visual acuity was 20/20–2. At 18 months, the graft remained clear with no signs of epithelial downgrowth. Clinicians should be aware that epithelial downgrowth can occur following DSAEK surgery. Fortunately, excision of the prior DSAEK graft with removal of the active epithelial membrane appears to have been a successful treament in this patient. J Cataract Refract Surg 2009; 35:193–196 Q 2009 ASCRS and ESCRS
Epithelial downgrowth is a rare but serious consequence following compromise of the ocular integrity by penetrating trauma or intraocular surgery. Historically, epithelial downgrowth was described most commonly after cataract extraction.1 Epithelial downgrowth is also well documented following penetrating keratoplasty (PKP) as well as less invasive ocular
Submitted: June 23, 2008. Final revision submitted: July 24, 2008. Accepted: July 24, 2008. From the Devers Eye Institute (Phillips, Terry, Chen) and Lions Vision Research Laboratory of Oregon (Terry), Portland, Oregon, and the University of Minnesota (Kaufman), Minneapolis, Minnesota, USA. Dr. Terry has a financial interest in the specialized instruments used in this surgery. No other author has a financial or proprietary interest in any material or method mentioned. Supported in part by an unrestricted grant from Research to Prevent Blindness, New York, New York, USA. Bausch & Lomb Surgical, St. Louis, Missouri, USA, manufactured and supplied the specially designed instruments free of charge. Dr. David Wilson and the histology laboratory at the Casey Eye Institute of Oregon Health Sciences University processed the corneal tissue and provided the images used in this report. Corresponding author: Paul Phillips, MD, Devers Eye Institute, 1040 Northwest 22nd Avenue, Portland, Oregon 97210, USA. E-mail: [email protected]. Q 2009 ASCRS and ESCRS Published by Elsevier Inc.
surgeries such as anterior chamber aspiration and glaucoma procedures.2 The pathology leading to epithelial downgrowth is not known but is probably related to poor closure and healing of wounds. Wounds may be compromised by the presence of vitreous, iris, or other debris within incisions, which can lead to leaks or fistulas.3–6 The development of epithelial downgrowth is likely multifactorial, however, and may include a history of multiple operations with or without the presence of significant inflammation, corneal vascularity, and endothelial cell damage. All these conditions may be contributing factors. Endothelial keratoplasty has recently revolutionized the field of corneal surgery. Although Tillet7 published the first successful case of posterior lamellar keratoplasty in 1956, endothelial keratoplasty underwent the most rapid advancement and mainstream acceptance following Melles et al.’s8 description in 1998 of sutureless replacement of the endothelium using only the posterior portion of the donor tissue. Endothelial keratoplasty was described as deep lamellar endothelial keratoplasty by Terry and Ousley9 and subsequently as Descemet-stripping endothelial keratoplasty by Price and Price.10 Endothelial keratoplasty has proven to be less invasive than PKP, yielding a theoretically stronger globe11 and faster visual rehabilitation. Although there have been 3 reports of epithelial ingrowth following endothelial keratoplasty surgery12–14 and 1 report of epithelial downgrowth occurring as an extension of epithelial ingrowth into the graft–host interface,15 0886-3350/09/$dsee front matter doi:10.1016/j.jcrs.2008.07.036
193
194
CASE REPORT: EPITHELIAL DOWNGROWTH AFTER DSAEK
Figure 1. A: Preoperative photography showing failed DSAEK graft with stromal edema and poor view of anterior chamber. B: One year after replaced DSAEK graft with anterior vitrectomy, the pupil is no longer peaked.
we believe this is the first case of DSAEK primary graft failure with epithelial downgrowth occurring in a patient after 2 DSAEK procedures. The unique feature of our case is that the histopathology demonstrated conjunctival epithelium extending over the donor endothelium as the etiology of the graft failure. CASE REPORT A 64-year-old man with Fuchs dystrophy and a history of cataract surgery in the left eye 5 years earlier presented to an outside corneal surgeon (not one of the authors) with slowly progressive corneal edema. On November 17, 2005, uneventful DSAEK was performed in the left eye. On postoperative day 1, a partial dislocation was noted and air was reinjected. The graft reattached but did not clear. After what appeared to be a primary graft failure, repeat DSAEK was performed on February 14, 2006. Again, the surgery was uneventful and the graft was well positioned but remained edematous and did not clear. The patient was referred to our center for a second opinion and subsequent surgical rehabilitation. On presentation, 6 months after the first DSAEK, the patient complained of pain, light sensitivity, and redness with decreased visual acuity. On examination, the best spectacle-corrected visual acuity was 20/400. Central corneal thickness was 806 mm and the intraocular pressure (IOP), 15 mm Hg. Slitlamp examination demonstrated complete stromal edema without keratic precipitates or anterior chamber inflammation. The pupil was noted to be peaked toward the temporal wound, and vitreous strands were noted
attached to the posterior wound margin (Figure 1, A). There were no signs of epithelial downgrowth, with no membranes, cysts, or scalloped margins noted on any area of the posterior surface of the cornea. The patient was offered the options PKP or a third DSAEK and after a thorough discussion of the risks and benefits of each option, he decided to proceed with another DSAEK surgery. Surgery was performed on June 27, 2006, and included a limited anterior vitrectomy, which cleared the anterior chamber of vitreous and rounded the pupil. The failed DSAEK graft was removed by opening the graft–host interface at the temporal edge using sharp and blunt dissection with a crescent blade and a spatula. Once the interface was opened, the blunt spatula easily separated the horizontal donor–recipient interface and then broke the sealed edges of the graft. The tissue was removed, fixed in formalin, and sent to pathology. The remainder of the surgery followed our standard DSAEK technique, including peripheral stromal scraping. On the first postoperative day, the graft was adherent and thin. The uncorrected visual acuity (UCVA) was 20/100. At the 1-week examination, the UCVA was 20/80 and the IOP was 15 mm Hg. The histopathology report of the removed failed graft described multilayered surface conjunctival epithelial cells with occasional goblet cells extending over the surgical margin of the specimen and onto the posterior surface. These findings were consistent with epithelial downgrowth (Figure 2) originating from the conjunctiva. Despite the findings of epithelial downgrowth, the patient continued to improve postoperatively, with no signs of recurrence. Postoperatively, what was thought to be a small
Figure 2. Histopathology of the removed DSAEK graft demonstrating multilayered surface conjunctival epithelial cells with occasional goblet cells (arrows) extending over the surgical margin of the specimen and onto the posterior surface, consistent with epithelial downgrowth.
J CATARACT REFRACT SURG - VOL 35, JANUARY 2009
CASE REPORT: EPITHELIAL DOWNGROWTH AFTER DSAEK
epithelial inclusion cyst was noted peripheral to the donor graft on the endothelial surface of the host. However, with a follow-up of more than 18 months, the cyst has not enlarged and the patient’s graft has remained clear. The UCVA is 20/20-2 and the endothelial cell count, 1997 cells/mm2 (Figure 1, B).
DISCUSSION Although epithelial downgrowth into the anterior chamber after DSAEK might be considered rare, we have presented a case that was discovered in a patient after 2 failed DSAEK grafts. Epithelial ingrowth into the interface between the donor and recipient stroma has been described.12–15 In one of the reports, the epithelium was noted to extend outside the graft–host interface,15 leading to its designation as epithelial downgrowth. However, epithelial downgrowth with the epithelium invading the anterior chamber and growing over the host endothelium has not been reported following DSAEK. The presence of graft failure in the setting of epithelial downgrowth and the presence of goblet cells, indicating the conjunctival origin of the invasive cells, are unique to this case. In 2 previous case reports,14,15 epithelial ingrowth did not lead to graft failure, as corneal edema was not present in either case. In our case, the donor graft had failed before DSAEK was repeated. What is unclear, however, is whether the epithelial downgrowth led to or was the result of the first or second graft failure in this patient. The possible causes of epithelial downgrowth in this case include those inherent in intraocular surgery, including possible implantation of epithelium at the time of surgery; inadequate tissue closure, leading to subclinical wound leakage; corneoscleral suture tracks; damaged or unhealthy endothelium; multiple surgical procedures; and inflammation. It is important to note that a repeat DSAEK, including a thorough vitrectomy with careful wound closure, appears to have been a successful treatment in this case, without having to resort to a full-thickness PKP. This patient had several risk factors, including multiple surgeries and, possibly more important, the presence of vitreous within the surgical wound. The formed vitreous probably acted as a scaffold for the migration of conjunctival epithelium from the conjunctival tissue adjacent to a compromised wound. Given the nature of DSAEK surgery, poor endothelial function may have also played a role. Most risk factors should theoretically be minimized by DSAEK compared with standard PKP, and it is therefore tempting to dismiss this incident of epithelial downgrowth as a ‘‘chance’’ occurrence related to the history of multiple intraocular surgeries, the presence of vitreous in the wound, or the incidental
195
implantation of epithelial cells at the time of surgery rather than to the DSAEK procedure specifically. However, previous studies have implicated pathological or damaged endothelium in epithelial migration through loss of contact inhibition.16 If unhealthy endothelium does play a role in allowing intraocular epithelium to thrive and migrate, the endothelial damage that occurs during DSAEK procedures must be considered. Although the epithelial downgrowth may have been a result of multiple previous surgeries in our patient, it is probably most important to address the more modifiable risk factors. In this case, the presence of vitreous in the posterior wound could have easily been avoided and a prophylactic anterior vitrectomy should always be performed in any case where the posterior capsule integrity is in question and vitreous in the anterior chamber is suspected. Wound construction and approximation with sutures should be a priority, and excessive postoperative inflammation should be avoided. Finally, an attempt to avoid excessive endothelial cell damage, which might provide an easy path to the overgrowth of epithelial cells, should always be made. REFERENCES 1. Maumenee AE, Shannon CR. Epithelial invasion of the anterior chamber. Am J Ophthalmol 1956; 41:929–942 2. Chen SH. Pineda R II. Epithelial and fibrous downgrowth: mechanisms of disease. Ophthalmol Clin North Am 2002; 15(1):41–48 3. Maumenee AE. Treatment of epithelial downgrowth and intraocular fistula following cataract extraction. Trans Am Ophthalmol Soc 1964; 62:153–163; discussion 163–166. Available at: http:// www.pubmedcentral.nih.gov/picrender.fcgi?artidZ1310154& blobtypeZpdf. Accessed August 8, 2008 4. Stark WJ, Michels RG, Maumenee AE, Cupples H. Surgical management of epithelial ingrowth. Am J Ophthalmol 1978; 85:772–780 5. Weiner MJ, Trentacoste J, Pon DM, Albert DM. Epithelial downgrowth: a 30-year clinicopathological review. Br J Ophthalmol 1989; 73:6–11 6. Blodi FC. Failures of the cataract extractions and their pathologic explanation. J Iowa State Med Soc 1954; 44:514–516 7. Tillett CW. Posterior lamellar keratoplasty. Am J Ophthalmol 1956; 41:530–533 8. Melles GRJ, Eggink FAGJ, Lander F, Pels E, Rietveld FJR, Beekhuis WH, Binder PS. A surgical technique for posterior lamellar keratoplasty. Cornea 1998; 17:618–626 9. Terry MA, Ousley PJ. Deep lamellar endothelial keratoplasty in the first United States patients; early clinical results. Cornea 2001; 20:239–243; errata, 353 10. Price FW Jr, Price MO. Descemet’s stripping with endothelial keratoplasty in 50 eyes: a refractive neutral corneal transplant. J Refract Surg 2005; 21:339–345 11. Barry JS, Spiteri A, Habib NE. Traumatic wound dehiscence of old extracapsular cataract extraction incision after endothelial keratoplasty [letter]. Cornea 2008; 27:127;127; reply by PK Nagra, KH Hammersmith, EJ Cohen, CJ Rapuano and MA Terry, 127–128
J CATARACT REFRACT SURG - VOL 35, JANUARY 2009
196
CASE REPORT: EPITHELIAL DOWNGROWTH AFTER DSAEK
12. Culbertson WW. Descemet stripping endothelial keratoplasty. Int Ophthalmol Clin 2006; 46(3):155–168 13. Suh LH, Yoo SH, Deobhakta A, Donaldson KE, Alfonso AC, Culbertson WW, O’Brien TP. Complications of Descemet’s stripping with automated endothelial keratoplasty; survey of 118 eyes at one Institute. In press, Ophthalmology 2008 14. Koenig SB, Covert DJ. Epithelial ingrowth after Descemetstripping automated endothelial keratoplasty. Cornea 2008; 27:727–729 15. Walker BM, Hindman HB, Ebrahimi KB, Green WR, Eberhart CG, Garcia I, Jun AS. Epithelial downgrowth following Descemet’s-stripping automated endothelial keratoplasty [letter]. Arch Ophthalmol 2008; 126:278–280
16. Cameron JD, Flaxman BA, Yanoff M. In vitro studies of corneal wound healing: epithelial-endothelial interactions. Invest Ophthalmol 1974; 13:575–579. Available at: http://www.iovs. org/cgi/reprint/13/8/575. Accessed August 8, 2008
J CATARACT REFRACT SURG - VOL 35, JANUARY 2009
First author: Paul M. Phillips, MD Devers Eye Institute, Portland, Oregon