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Corneal endothelial decompensation after iris-claw phakic intraocular lens implantation
CASE REPORT
Corneal endothelial decompensation after iris-claw phakic intraocular lens implantation Min Kim, MD, Jin Kook Kim, MD, Hyung Keun Lee, MD
A 25-year-old man received iris-claw phakic intraocular lenses (pIOLs) (Artisan, Ophtec) of 11.5 diopters (D) in the right eye and 13.0 D in the left eye; both pIOLs had a 6.0 mm optic and 8.5 mm haptics. Twenty months postoperatively, the best corrected visual acuity was 20/400 in the right eye and 20/25 in the left eye. Slitlamp examination revealed microcystic bullae, keratic precipitates, stromal edema, and ciliary injection in both eyes. Central corneal thickness was 704 mm in the right eye and 639 mm in the left eye; specular biomicroscopy showed reduced endothelial cell density of 548 cells/mm2 and 564 cells/mm2, respectively. The pIOL in the right eye was eventually explanted. J Cataract Refract Surg 2008; 34:517–519 Q 2008 ASCRS and ESCRS
Previous studies suggest that the iris-claw phakic intraocular lens (pIOL) (Artisan, Ophtec) may be safe and effective for the correction of myopia.1 However, recent long-term studies report significant reductions in endothelial cell density after 3 years,2,3 and recent case reports show severe endothelial cell loss after uneventful pIOL implantation for high myopia.4,5 We describe a patient who developed corneal endothelial decompensation after Artisan pIOL implantation in both eyes. CASE REPORT A 25-year-old Korean man who had Artisan pIOL implantation in both eyes at a local clinic 20 months earlier was referred to us due to progressive loss of vision in the right eye. The patient had no medical or ocular surgery history except pIOL implantation. Preoperatively, the manifest refraction was 8.50 1.50 5 in the right eye and 10.00 1.50 5 in the left eye, with a Snellen best corrected visual acuity (BCVA) of 20/25 in both eyes. At the time of surgery, the central corneal thickness was 531 mm in the right eye and 533 mm
Accepted for publication October 31, 2007. From the Institute of Vision Research (M. Kim, Lee), Department of Ophthalmology, Yonsei University College of Medicine, and the BS Balgensesang Ophthalmologic Clinic (J.K. Kim), Seoul, Korea. No author has a financial or proprietary interest in any material or method mentioned. Corresponding author: Hyung Keun Lee, Department of Ophthalmology, College of Medicine Yonsei University, 146-92 Dogokdong, Kangnam-gu, Seoul, Korea, 135-720. E-mail: shadik@ yumc.yonsei.ac.kr. Q 2008 ASCRS and ESCRS Published by Elsevier Inc.
in the left eye. The corneal diameters were 11.2 mm and 11.3 mm, respectively. Anterior and posterior segment evaluations were otherwise unremarkable. An ultrasonic A-scan showed the axial length was 27.13 mm in the right eye and 27.35 mm in the left eye and the anterior chamber depth was 4.03 mm and 4.09 mm, respectively. The initial preoperative specular microscopy results showed endothelial cell density of 2631 cells/mm2 in the right eye and 2544 cells/mm2 in the left eye, with no pleomorphism or polymegathism. The pIOL in the right eye was 11.5 diopters (D) and in the left eye, 13.0 D; both IOLs had a 6.0 mm optic and 8.5 mm haptics. The implantation surgery was uneventful. One week postoperatively, the uncorrected visual acuity was 20/20. At 1 month, endothelial cell count was 2272 cells/mm2 in the right eye and 2245 cells/mm2 in the left eye. The patient then moved to China and was lost to further follow-up. Twenty months postoperatively, the patient was referred to our department because of decreased visual acuity. Ocular examination indicated that the BCVA had decreased to 20/400 in the right eye and 20/25 in the left eye; the intraocular pressure was 17 mm Hg and 13 mm Hg, respectively. Slitlamp examination revealed microcystic bullae, keratic precipitates, stromal edema, and ciliary injection in both eyes (Figure 1). Although the anterior chamber was deep, many inflammatory cells and flares were observed and peripheral anterior synechias (PAS) were present in both eyes. The pIOL did not appear to be stable; mild trembling was observed in association with eyeball movement. Pupil ovalization in the left eye and vaulting of the pIOLs in both eyes was also noted. Central corneal thickness was 704 mm in the right eye and 639 mm in the left eye, and specular biomicroscopy showed a reduced endothelial cell density of 548 cells/mm2 and 564 cells/mm2, respectively. The pIOL in the right eye was explanted, and systemic and topical steroid therapy was started immediately to control the chamber reaction. Five months after the pIOL was explanted, the chamber reaction had resolved in both eyes. The patient is currently awaiting penetrating keratoplasty. 0886-3350/08/$dsee front matter doi:10.1016/j.jcrs.2007.10.030
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CASE REPORT: ENDOTHELIAL DECOMPENSATION AFTER IRIS-CLAW IOL IMPLANTATION
Figure 1. Examination of the patient’s cornea. Limbal injection and iris-claw pIOL with peripheral anterior synechia in the right eye (upper right) and left eye (upper left) were noted. Higher magnification shows keratic precipitates in the right eye (lower left). Decreased endothelial cell density is shown by specular microscopy (lower right).
DISCUSSION Twenty months after Artisan pIOL implantation, the corneal endothelial cell density had decreased by 79% in the right eye (from 2631 cells/mm2 to 548 cells/mm2) and 78% in the left eye (from 2544 cells/mm2 to 564 cells/mm2). This corneal endothelial decompensation eventually resulted in bullous keratopathy and loss of vision. Considering the patient’s ocular surgery history, slitlamp examination finding, and the reduced anterior chamber reaction after pIOL removal, it seems reasonable to conclude that Artisan pIOL implantation was the sole, or at least a contributing cause, of the endothelial decompensation, although other factors might have been associated with the corneal endothelial damage. The initial examination in our clinic revealed instability of the pIOL in both eyes; ie, slight tilting of the pIOL toward the corneal endothelium indicated that it was not properly fixated at the midperipheral iris. The pIOL moved when the iris was constricted by light even though it was enclavated and attached to the iris. A detailed examination of the clipped site showed that the pIOL was fixated to the superficial iris surface and that insufficient iris stromal tissue was clipped. Moreover, the iris enclavation point was not located in a horizontal plane (3 o’clock and 9 o’clock positions),
resulting in pIOL movement toward the corneal endothelium on slight movement of the iris or globe. Also, when the patient looked downward, the uppermost part of the optic was extremely close to the cornea, although the pIOL was not observed to touch the endothelium. The distance between the pIOL and the posterior corneal surface measured by Pentacam (Oculus, Inc.) was 722 mm in the right eye and 716 mm in the left eye, which was well below the 1.5 mm minimum clearance distance between IOL and endothelium proposed by Ba¨ikoff.6 Considering the preoperative and immediate postoperative data, the corneal endothelial failure was probably caused by postoperative events. Although the exact cause of endothelial failure could not be determined, there are several possible explanations. Loose fixation of the Artisan pIOL to the iris surface may have resulted in pIOL movement. Intraocular lens trembling may have caused loss of the safety margin or even intermittent contact between the pIOL and endothelium when the patient rubbed his eye, eventually causing endothelial cell loss and corneal edema. Also, diffuse PAS may have moved the iris plane forward, contributing to the decreased distance between the pIOL and endothelium and causing damage to the endothelial cell layer because of its close proximity to
J CATARACT REFRACT SURG - VOL 34, MARCH 2008
CASE REPORT: ENDOTHELIAL DECOMPENSATION AFTER IRIS-CLAW IOL IMPLANTATION
the cornea. An oversized IOL can lead to IOL vaulting. Asian eyes are known to have distinct characteristics that may make IOL fixation difficult during surgery; eg, a smaller corneal diameter and darker pigmentation of the iris can lead to pigment dispersion during surgery.7 Furthermore, the enclavation points are situated more peripherally than in Caucasian eyes, which can lead to IOL movement and accompanying pupil movement and, eventually, to corneal endothelial damage.1 However, the sufficient preoperative corneal size and deep anterior chamber depth suggest the anatomical characteristics of Asian eyes may not be a direct contributing factor in our case. Our case may provide important insights for refractive surgeons using this type of pIOL to correct myopia. Patients must be carefully observed after surgery for possible endothelial cell loss and damage, and long-term endothelial checkups using a specular microscope are critical. Furthermore, firm and stable iris enclavation of the IOL at the exact location, with sufficient iris tissue, is essential for long-term protection of endothelial cells. If a patient has a loosely fixated pIOL, intraoperative reenclavation to prevent further damage to the corneal endothelium may be
519
appropriate; in cases of bullous keratopathy, prompt surgical pIOL explantation should be considered. REFERENCES 1. Asano-Kato N, Toda I, Hori-Komai Y, et al. Experience with the Artisan phakic intraocular lens in Asian eyes. J Cataract Refract Surg 2005; 31:910–915 2. Saxena R, Boekhoorn SS, Mulder PGH, et al. Long-term follow-up of endothelial cell change after Artisan phakic intraocular lens implantation. In press, Ophthalmology 2008 3. Tehrani M, Dick HB. Endothelial cell loss after toric iris-fixated phakic intraocular lens implantation: three-year follow-up. J Refract Surg 2007; 23:172–177 4. Coullet J, Mahieu L, Malecaze F, et al. Severe endothelial cell loss following uneventful angle-supported phakic intraocular lens implantation for high myopia. J Cataract Refract Surg 2007; 33:1477–1481 5. Patel SR, Chu DS, Ayres BD, Hersh PS. Corneal edema and penetrating keratoplasty after anterior chamber phakic intraocular lens implantation. J Cataract Refract Surg 2005; 31: 2212–2215 6. Baı¨koff G. Anterior segment OCT and phakic intraocular lenses: a perspective. J Cataract Refract Surg 2006; 32:1827–1835 7. Matsuda LM, Woldorff CL, Kame RT, Hayashida JK. Clinical comparison of corneal diameter and curvature in Asian eyes with those of Caucasian eyes. Optom Vis Sci 1992; 69: 51–54
J CATARACT REFRACT SURG - VOL 34, MARCH 2008
Corneal endothelial decompensation after iris-claw phakic intraocular lens implantation Min Kim, MD, Jin Kook Kim, MD, Hyung Keun Lee, MD
A 25-year-old man received iris-claw phakic intraocular lenses (pIOLs) (Artisan, Ophtec) of 11.5 diopters (D) in the right eye and 13.0 D in the left eye; both pIOLs had a 6.0 mm optic and 8.5 mm haptics. Twenty months postoperatively, the best corrected visual acuity was 20/400 in the right eye and 20/25 in the left eye. Slitlamp examination revealed microcystic bullae, keratic precipitates, stromal edema, and ciliary injection in both eyes. Central corneal thickness was 704 mm in the right eye and 639 mm in the left eye; specular biomicroscopy showed reduced endothelial cell density of 548 cells/mm2 and 564 cells/mm2, respectively. The pIOL in the right eye was eventually explanted. J Cataract Refract Surg 2008; 34:517–519 Q 2008 ASCRS and ESCRS
Previous studies suggest that the iris-claw phakic intraocular lens (pIOL) (Artisan, Ophtec) may be safe and effective for the correction of myopia.1 However, recent long-term studies report significant reductions in endothelial cell density after 3 years,2,3 and recent case reports show severe endothelial cell loss after uneventful pIOL implantation for high myopia.4,5 We describe a patient who developed corneal endothelial decompensation after Artisan pIOL implantation in both eyes. CASE REPORT A 25-year-old Korean man who had Artisan pIOL implantation in both eyes at a local clinic 20 months earlier was referred to us due to progressive loss of vision in the right eye. The patient had no medical or ocular surgery history except pIOL implantation. Preoperatively, the manifest refraction was 8.50 1.50 5 in the right eye and 10.00 1.50 5 in the left eye, with a Snellen best corrected visual acuity (BCVA) of 20/25 in both eyes. At the time of surgery, the central corneal thickness was 531 mm in the right eye and 533 mm
Accepted for publication October 31, 2007. From the Institute of Vision Research (M. Kim, Lee), Department of Ophthalmology, Yonsei University College of Medicine, and the BS Balgensesang Ophthalmologic Clinic (J.K. Kim), Seoul, Korea. No author has a financial or proprietary interest in any material or method mentioned. Corresponding author: Hyung Keun Lee, Department of Ophthalmology, College of Medicine Yonsei University, 146-92 Dogokdong, Kangnam-gu, Seoul, Korea, 135-720. E-mail: shadik@ yumc.yonsei.ac.kr. Q 2008 ASCRS and ESCRS Published by Elsevier Inc.
in the left eye. The corneal diameters were 11.2 mm and 11.3 mm, respectively. Anterior and posterior segment evaluations were otherwise unremarkable. An ultrasonic A-scan showed the axial length was 27.13 mm in the right eye and 27.35 mm in the left eye and the anterior chamber depth was 4.03 mm and 4.09 mm, respectively. The initial preoperative specular microscopy results showed endothelial cell density of 2631 cells/mm2 in the right eye and 2544 cells/mm2 in the left eye, with no pleomorphism or polymegathism. The pIOL in the right eye was 11.5 diopters (D) and in the left eye, 13.0 D; both IOLs had a 6.0 mm optic and 8.5 mm haptics. The implantation surgery was uneventful. One week postoperatively, the uncorrected visual acuity was 20/20. At 1 month, endothelial cell count was 2272 cells/mm2 in the right eye and 2245 cells/mm2 in the left eye. The patient then moved to China and was lost to further follow-up. Twenty months postoperatively, the patient was referred to our department because of decreased visual acuity. Ocular examination indicated that the BCVA had decreased to 20/400 in the right eye and 20/25 in the left eye; the intraocular pressure was 17 mm Hg and 13 mm Hg, respectively. Slitlamp examination revealed microcystic bullae, keratic precipitates, stromal edema, and ciliary injection in both eyes (Figure 1). Although the anterior chamber was deep, many inflammatory cells and flares were observed and peripheral anterior synechias (PAS) were present in both eyes. The pIOL did not appear to be stable; mild trembling was observed in association with eyeball movement. Pupil ovalization in the left eye and vaulting of the pIOLs in both eyes was also noted. Central corneal thickness was 704 mm in the right eye and 639 mm in the left eye, and specular biomicroscopy showed a reduced endothelial cell density of 548 cells/mm2 and 564 cells/mm2, respectively. The pIOL in the right eye was explanted, and systemic and topical steroid therapy was started immediately to control the chamber reaction. Five months after the pIOL was explanted, the chamber reaction had resolved in both eyes. The patient is currently awaiting penetrating keratoplasty. 0886-3350/08/$dsee front matter doi:10.1016/j.jcrs.2007.10.030
517
518
CASE REPORT: ENDOTHELIAL DECOMPENSATION AFTER IRIS-CLAW IOL IMPLANTATION
Figure 1. Examination of the patient’s cornea. Limbal injection and iris-claw pIOL with peripheral anterior synechia in the right eye (upper right) and left eye (upper left) were noted. Higher magnification shows keratic precipitates in the right eye (lower left). Decreased endothelial cell density is shown by specular microscopy (lower right).
DISCUSSION Twenty months after Artisan pIOL implantation, the corneal endothelial cell density had decreased by 79% in the right eye (from 2631 cells/mm2 to 548 cells/mm2) and 78% in the left eye (from 2544 cells/mm2 to 564 cells/mm2). This corneal endothelial decompensation eventually resulted in bullous keratopathy and loss of vision. Considering the patient’s ocular surgery history, slitlamp examination finding, and the reduced anterior chamber reaction after pIOL removal, it seems reasonable to conclude that Artisan pIOL implantation was the sole, or at least a contributing cause, of the endothelial decompensation, although other factors might have been associated with the corneal endothelial damage. The initial examination in our clinic revealed instability of the pIOL in both eyes; ie, slight tilting of the pIOL toward the corneal endothelium indicated that it was not properly fixated at the midperipheral iris. The pIOL moved when the iris was constricted by light even though it was enclavated and attached to the iris. A detailed examination of the clipped site showed that the pIOL was fixated to the superficial iris surface and that insufficient iris stromal tissue was clipped. Moreover, the iris enclavation point was not located in a horizontal plane (3 o’clock and 9 o’clock positions),
resulting in pIOL movement toward the corneal endothelium on slight movement of the iris or globe. Also, when the patient looked downward, the uppermost part of the optic was extremely close to the cornea, although the pIOL was not observed to touch the endothelium. The distance between the pIOL and the posterior corneal surface measured by Pentacam (Oculus, Inc.) was 722 mm in the right eye and 716 mm in the left eye, which was well below the 1.5 mm minimum clearance distance between IOL and endothelium proposed by Ba¨ikoff.6 Considering the preoperative and immediate postoperative data, the corneal endothelial failure was probably caused by postoperative events. Although the exact cause of endothelial failure could not be determined, there are several possible explanations. Loose fixation of the Artisan pIOL to the iris surface may have resulted in pIOL movement. Intraocular lens trembling may have caused loss of the safety margin or even intermittent contact between the pIOL and endothelium when the patient rubbed his eye, eventually causing endothelial cell loss and corneal edema. Also, diffuse PAS may have moved the iris plane forward, contributing to the decreased distance between the pIOL and endothelium and causing damage to the endothelial cell layer because of its close proximity to
J CATARACT REFRACT SURG - VOL 34, MARCH 2008
CASE REPORT: ENDOTHELIAL DECOMPENSATION AFTER IRIS-CLAW IOL IMPLANTATION
the cornea. An oversized IOL can lead to IOL vaulting. Asian eyes are known to have distinct characteristics that may make IOL fixation difficult during surgery; eg, a smaller corneal diameter and darker pigmentation of the iris can lead to pigment dispersion during surgery.7 Furthermore, the enclavation points are situated more peripherally than in Caucasian eyes, which can lead to IOL movement and accompanying pupil movement and, eventually, to corneal endothelial damage.1 However, the sufficient preoperative corneal size and deep anterior chamber depth suggest the anatomical characteristics of Asian eyes may not be a direct contributing factor in our case. Our case may provide important insights for refractive surgeons using this type of pIOL to correct myopia. Patients must be carefully observed after surgery for possible endothelial cell loss and damage, and long-term endothelial checkups using a specular microscope are critical. Furthermore, firm and stable iris enclavation of the IOL at the exact location, with sufficient iris tissue, is essential for long-term protection of endothelial cells. If a patient has a loosely fixated pIOL, intraoperative reenclavation to prevent further damage to the corneal endothelium may be
519
appropriate; in cases of bullous keratopathy, prompt surgical pIOL explantation should be considered. REFERENCES 1. Asano-Kato N, Toda I, Hori-Komai Y, et al. Experience with the Artisan phakic intraocular lens in Asian eyes. J Cataract Refract Surg 2005; 31:910–915 2. Saxena R, Boekhoorn SS, Mulder PGH, et al. Long-term follow-up of endothelial cell change after Artisan phakic intraocular lens implantation. In press, Ophthalmology 2008 3. Tehrani M, Dick HB. Endothelial cell loss after toric iris-fixated phakic intraocular lens implantation: three-year follow-up. J Refract Surg 2007; 23:172–177 4. Coullet J, Mahieu L, Malecaze F, et al. Severe endothelial cell loss following uneventful angle-supported phakic intraocular lens implantation for high myopia. J Cataract Refract Surg 2007; 33:1477–1481 5. Patel SR, Chu DS, Ayres BD, Hersh PS. Corneal edema and penetrating keratoplasty after anterior chamber phakic intraocular lens implantation. J Cataract Refract Surg 2005; 31: 2212–2215 6. Baı¨koff G. Anterior segment OCT and phakic intraocular lenses: a perspective. J Cataract Refract Surg 2006; 32:1827–1835 7. Matsuda LM, Woldorff CL, Kame RT, Hayashida JK. Clinical comparison of corneal diameter and curvature in Asian eyes with those of Caucasian eyes. Optom Vis Sci 1992; 69: 51–54
J CATARACT REFRACT SURG - VOL 34, MARCH 2008