- Email: [email protected]
May consultation # 4
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CONSULTATION SECTION
astigmatism. These findings may be contributing to the monocular diplopia the patient is experiencing. In this case, a trial with a rigid gas-permeable (RGP) contact lens may elucidate the source of the problem and become a potential short- or long-term clinical solution. My second thought is ectasia. After 2 LASIK procedures (one for 10.00 D) and a cataract extraction procedure, cornea ectasia becomes a concern. This may be supported by the myopic shift and the irregular high astigmatism on the current topography (1.70 D). In addition, there is a significant change in the posterior elevation that looks to be in the 0.040 mm range. An RGP contact lens trial may be able to shed more light in this case. If ectasia is established, collagen crosslinking could be considered as a stabilizing measure.1 A third thought is that PCO may be contributing to or be the main reason for the diplopia. My impression from the retroillumination photograph is that the PCO is probably not severe yet. If PCO were a contributing factor, a neodymium:YAG (Nd:YAG) capsulotomy could be considered. Fourth, the patient may have a macula problem. As this patient is monocular, is in his 50s, and has very high myopia, I would perform an Amsler grid evaluation and perhaps a macula optical coherence tomography (OCT) to rule out a Fuchs-like subretinal pathology ‘‘cooking.’’ Finally, as a cornea surgeon, I would perform a more complete evaluation of the fellow blind eye. I would be interested in whether the cornea is intact and has good endothelial cell counts. An extreme thought, but one I believe is important, is that if the cornea pathology in the seeing eye necessitates lamellar or penetrating keratoplasty, the blind eye may become a unique homograft cornea donor. I would make sure that any of these diagnoses (or ones I missed) are well documented as the last thing this patient needs is a new procedure that may further complicate his visual function. A. John Kanellopoulos, MD Athens, Greece New York, New York, USA REFERENCE 1. Kanellopoulos AJ. Post-LASIK ectasia [letter]. Ophthalmology 2007; 114:1230
- A 50-year-old man is blind in 1 eye and reportedly had amblyopia is the fellow eye. We do not know his best corrected visual acuity (BCVA) before the eye surgeries. He had LASIK for 16.00 D of myopia 5 years
ago. Postoperatively, the refraction is 6.00 D, but we still do not know the BCVA. He had cataract surgery 2 years previously and ended up with C1.00 D; however, we still do not know the BCVA. One year ago, the patient has repeat LASIK and now reports decreased vision and monocular diplopia. With a 2.50 D refraction, the BCVA is 1/17. Early PCO is noted. Assuming the posterior segment has been examined and determined to be normal, there are 3 likely potential reasons for poor vision: (1) amblyopia, (2) irregular astigmatism, and (3) PCO. Monocular diplopia, perhaps better described as ‘‘shadow vision,’’ can be caused by irregular astigmatism or PCO, but typically not by amblyopia. The Orbscan overview (Figure 1) does not show significant irregular astigmatism or evidence of ectasia. The thinnest area of cornea is central and measures 358 mm, which is consistent with excimer laser treatment of very high myopia. Note that the accuracy of the Orbscan’s posterior corneal measurements may not be perfect after excimer laser surgery. The slitlamp photograph (Figure 2) shows some PCO. A rigid contact lens over-refraction should be performed to neutralize any irregular astigmatism. If the shadow vision improves, the patient could be fit with a rigid contact lens. If the patient is contact lens intolerant, custom LASIK enhancement or surface ablation might help the symptoms. Given the moderately thin cornea, surface ablation with mitomycin-C is probably a safer option than repeat LASIK. If a rigid contact lens does not improve vision, an Nd:YAG laser posterior capsulotomy should be performed. Clearing the PCO should improve the shadow vision, if not the actual visual acuity, which may be limited by amblyopia. If neither improves the visual symptoms, the posterior segment, including the optic nerve, should be examined more carefully, including testing such as OCT and automated visual field assessments. Christopher J. Rapuano, MD Philadelphia, Pennsylvania, USA
- The case history shows a monocular patient with high myopia and a history of myopic LASIK. This was followed by cataract surgery with PC IOL implantation, which was followed by hyperopic LASIK in the only-seeing eye, the amblyopic right eye. We are not given the important information of the pre-cataract and/or pre-LASIK BSCVA. At present, the patient reports diplopia in his only eye. The question is whether the diplopia is due to corneal irregularity or from the IOL and/or PCO. Review of the Orbscan topography reveals irregular astigmatism and central corneal thinning. There is
J CATARACT REFRACT SURG - VOL 34, MAY 2008
CONSULTATION SECTION
also a suggestion of inferotemporal thinning to a milder degree. Wavefront aberrometry may be helpful to determine whether significant coma or another higherorder aberration is contributing to the complaints of diplopia. The first step is a contact lens fitting to see whether it alleviates the diplopia and improves the patient’s vision. If it is successful, I would recommend stopping at this intervention and fitting the patient with a gas permeable or hybrid type lens. There is no mention of the patient being contact lens intolerant, and I would be conservative and try to minimize further surgical interventions in this amblyopic 1-eyed patient. If the diplopia is only partially relieved with the contact lens fitting, I would obtain an OCT to see whether there is evidence of untreated cystoid macular edema (CME) that could be contributing to this situation. I would avoid further LASIK or surface ablation in this patient as he already has a thin, weakened cornea after 2 LASIK procedures. The slitlamp photograph reveals mild PCO. An Nd:YAG capsulotomy could be considered if the contact lens trial were only partially successful and there was no evidence of CME (or after appropriate treatment of the CME). The IOL appears well centered, so it seems unlikely that the diplopia is secondary to IOL tilt or decentration. The most important aspect to this case is to be sure that the patient has realistic expectations and to be conservative in trying to maximize as well as to maintain the vision in this amblyopic 1-eyed patient. In addition, it will be important to monitor him for signs of corneal ectasia that may require further interventions. Audrey Talley-Rostov, MD Seattle, Washington, USA
- This monocular patient has symptomatic monocular diplopia and blurred vision in an amblyopic eye after previous LASIK, phacoemulsification with IOL implantation, and LASIK enhancement. As the diplopia did not occur at the time of IOL implantation, it is safe to assume that there is nothing intrinsically wrong with the IOL or the IOL position (such as lens tilt) to explain the patient’s symptoms. The last LASIK enhancement left him overcorrected with a 2.50 D spherical subjective refraction, and the diplopia presented after this enhancement, which also was approximately 9 months after phacoemulsification. In general, the options for correction of the diplopia and blurred vision include LASIK enhancement, photorefractive keratectomy (PRK) treatment, Intacs segment implantation, Nd:YAG capsulotomy, and RGP
723
contact lens fitting; however, few of these options appear appropriate for this individual. As this patient is monocular and has had numerous surgical procedures, I would be hesitant to offer aggressive surgical alternatives at this juncture. The Orbscan II topography shows a relatively flat central cornea (approximately 35.0 to 37.0 D) and irregular astigmatism in the visual axis. With a central corneal thickness measurement of 365 mm, it is safe to assume the residual stromal bed is less than 250 mm. Therefore, I would not offer LASIK enhancement because I do not believe it would alleviate the patient’s symptoms and may in fact make them worse. Also, further tissue removal could stimulate the development of corneal ectasia. A second option would be PRK treatment on top of the LASIK flap. Although this should preserve the current biomechanical integrity of the cornea, it will further flatten the central cornea and would be no more effective in treating the patient’s irregular astigmatism. Furthermore, there is a likely higher risk for corneal haze formation when treating on top of LASIK. Therefore, I would not offer PRK treatment. A third option would be Intacs segment implantation. The patient’s subjective refraction of 2.50 D sphere is within treatment range, and this option would be less likely to affect the biomechanical integrity of the cornea. However, even successful Intacs placement would further flatten the central cornea and would not address the central corneal irregularity. Also, the thin peripheral cornea could predispose the patient to segment erosion. Therefore, I would not offer the patient Intacs implantation. A fourth option would be Nd:YAG capsulotomy. The timing of the onset of diplopia suggests that LASIK enhancement caused this symptom; however, the monocular diplopia could have easily been caused by increasing PCO 9 months after phacoemulsification. This procedure has limited downsides and a huge potential upside if it eliminates the diplopia. Therefore, an Nd:YAG capsulotomy would be my first choice for intervention. Assuming that Nd:YAG capsulotomy was ineffective or only partially effective in alleviating the patient’s symptoms, the most appropriate option would be RGP contact lens fitting. An RGP lens should mask the corneal irregularities and maximize the patient’s visual acuity. Furthermore, as a nonsurgical option, RGP lens fitting is more amenable to changes in the patient’s visual status as he ages and therefore would provide greater flexibility for this monocular patient in the future. J. Bradley Randleman, MD Atlanta, Georgia, USA
J CATARACT REFRACT SURG - VOL 34, MAY 2008
CONSULTATION SECTION
astigmatism. These findings may be contributing to the monocular diplopia the patient is experiencing. In this case, a trial with a rigid gas-permeable (RGP) contact lens may elucidate the source of the problem and become a potential short- or long-term clinical solution. My second thought is ectasia. After 2 LASIK procedures (one for 10.00 D) and a cataract extraction procedure, cornea ectasia becomes a concern. This may be supported by the myopic shift and the irregular high astigmatism on the current topography (1.70 D). In addition, there is a significant change in the posterior elevation that looks to be in the 0.040 mm range. An RGP contact lens trial may be able to shed more light in this case. If ectasia is established, collagen crosslinking could be considered as a stabilizing measure.1 A third thought is that PCO may be contributing to or be the main reason for the diplopia. My impression from the retroillumination photograph is that the PCO is probably not severe yet. If PCO were a contributing factor, a neodymium:YAG (Nd:YAG) capsulotomy could be considered. Fourth, the patient may have a macula problem. As this patient is monocular, is in his 50s, and has very high myopia, I would perform an Amsler grid evaluation and perhaps a macula optical coherence tomography (OCT) to rule out a Fuchs-like subretinal pathology ‘‘cooking.’’ Finally, as a cornea surgeon, I would perform a more complete evaluation of the fellow blind eye. I would be interested in whether the cornea is intact and has good endothelial cell counts. An extreme thought, but one I believe is important, is that if the cornea pathology in the seeing eye necessitates lamellar or penetrating keratoplasty, the blind eye may become a unique homograft cornea donor. I would make sure that any of these diagnoses (or ones I missed) are well documented as the last thing this patient needs is a new procedure that may further complicate his visual function. A. John Kanellopoulos, MD Athens, Greece New York, New York, USA REFERENCE 1. Kanellopoulos AJ. Post-LASIK ectasia [letter]. Ophthalmology 2007; 114:1230
- A 50-year-old man is blind in 1 eye and reportedly had amblyopia is the fellow eye. We do not know his best corrected visual acuity (BCVA) before the eye surgeries. He had LASIK for 16.00 D of myopia 5 years
ago. Postoperatively, the refraction is 6.00 D, but we still do not know the BCVA. He had cataract surgery 2 years previously and ended up with C1.00 D; however, we still do not know the BCVA. One year ago, the patient has repeat LASIK and now reports decreased vision and monocular diplopia. With a 2.50 D refraction, the BCVA is 1/17. Early PCO is noted. Assuming the posterior segment has been examined and determined to be normal, there are 3 likely potential reasons for poor vision: (1) amblyopia, (2) irregular astigmatism, and (3) PCO. Monocular diplopia, perhaps better described as ‘‘shadow vision,’’ can be caused by irregular astigmatism or PCO, but typically not by amblyopia. The Orbscan overview (Figure 1) does not show significant irregular astigmatism or evidence of ectasia. The thinnest area of cornea is central and measures 358 mm, which is consistent with excimer laser treatment of very high myopia. Note that the accuracy of the Orbscan’s posterior corneal measurements may not be perfect after excimer laser surgery. The slitlamp photograph (Figure 2) shows some PCO. A rigid contact lens over-refraction should be performed to neutralize any irregular astigmatism. If the shadow vision improves, the patient could be fit with a rigid contact lens. If the patient is contact lens intolerant, custom LASIK enhancement or surface ablation might help the symptoms. Given the moderately thin cornea, surface ablation with mitomycin-C is probably a safer option than repeat LASIK. If a rigid contact lens does not improve vision, an Nd:YAG laser posterior capsulotomy should be performed. Clearing the PCO should improve the shadow vision, if not the actual visual acuity, which may be limited by amblyopia. If neither improves the visual symptoms, the posterior segment, including the optic nerve, should be examined more carefully, including testing such as OCT and automated visual field assessments. Christopher J. Rapuano, MD Philadelphia, Pennsylvania, USA
- The case history shows a monocular patient with high myopia and a history of myopic LASIK. This was followed by cataract surgery with PC IOL implantation, which was followed by hyperopic LASIK in the only-seeing eye, the amblyopic right eye. We are not given the important information of the pre-cataract and/or pre-LASIK BSCVA. At present, the patient reports diplopia in his only eye. The question is whether the diplopia is due to corneal irregularity or from the IOL and/or PCO. Review of the Orbscan topography reveals irregular astigmatism and central corneal thinning. There is
J CATARACT REFRACT SURG - VOL 34, MAY 2008
CONSULTATION SECTION
also a suggestion of inferotemporal thinning to a milder degree. Wavefront aberrometry may be helpful to determine whether significant coma or another higherorder aberration is contributing to the complaints of diplopia. The first step is a contact lens fitting to see whether it alleviates the diplopia and improves the patient’s vision. If it is successful, I would recommend stopping at this intervention and fitting the patient with a gas permeable or hybrid type lens. There is no mention of the patient being contact lens intolerant, and I would be conservative and try to minimize further surgical interventions in this amblyopic 1-eyed patient. If the diplopia is only partially relieved with the contact lens fitting, I would obtain an OCT to see whether there is evidence of untreated cystoid macular edema (CME) that could be contributing to this situation. I would avoid further LASIK or surface ablation in this patient as he already has a thin, weakened cornea after 2 LASIK procedures. The slitlamp photograph reveals mild PCO. An Nd:YAG capsulotomy could be considered if the contact lens trial were only partially successful and there was no evidence of CME (or after appropriate treatment of the CME). The IOL appears well centered, so it seems unlikely that the diplopia is secondary to IOL tilt or decentration. The most important aspect to this case is to be sure that the patient has realistic expectations and to be conservative in trying to maximize as well as to maintain the vision in this amblyopic 1-eyed patient. In addition, it will be important to monitor him for signs of corneal ectasia that may require further interventions. Audrey Talley-Rostov, MD Seattle, Washington, USA
- This monocular patient has symptomatic monocular diplopia and blurred vision in an amblyopic eye after previous LASIK, phacoemulsification with IOL implantation, and LASIK enhancement. As the diplopia did not occur at the time of IOL implantation, it is safe to assume that there is nothing intrinsically wrong with the IOL or the IOL position (such as lens tilt) to explain the patient’s symptoms. The last LASIK enhancement left him overcorrected with a 2.50 D spherical subjective refraction, and the diplopia presented after this enhancement, which also was approximately 9 months after phacoemulsification. In general, the options for correction of the diplopia and blurred vision include LASIK enhancement, photorefractive keratectomy (PRK) treatment, Intacs segment implantation, Nd:YAG capsulotomy, and RGP
723
contact lens fitting; however, few of these options appear appropriate for this individual. As this patient is monocular and has had numerous surgical procedures, I would be hesitant to offer aggressive surgical alternatives at this juncture. The Orbscan II topography shows a relatively flat central cornea (approximately 35.0 to 37.0 D) and irregular astigmatism in the visual axis. With a central corneal thickness measurement of 365 mm, it is safe to assume the residual stromal bed is less than 250 mm. Therefore, I would not offer LASIK enhancement because I do not believe it would alleviate the patient’s symptoms and may in fact make them worse. Also, further tissue removal could stimulate the development of corneal ectasia. A second option would be PRK treatment on top of the LASIK flap. Although this should preserve the current biomechanical integrity of the cornea, it will further flatten the central cornea and would be no more effective in treating the patient’s irregular astigmatism. Furthermore, there is a likely higher risk for corneal haze formation when treating on top of LASIK. Therefore, I would not offer PRK treatment. A third option would be Intacs segment implantation. The patient’s subjective refraction of 2.50 D sphere is within treatment range, and this option would be less likely to affect the biomechanical integrity of the cornea. However, even successful Intacs placement would further flatten the central cornea and would not address the central corneal irregularity. Also, the thin peripheral cornea could predispose the patient to segment erosion. Therefore, I would not offer the patient Intacs implantation. A fourth option would be Nd:YAG capsulotomy. The timing of the onset of diplopia suggests that LASIK enhancement caused this symptom; however, the monocular diplopia could have easily been caused by increasing PCO 9 months after phacoemulsification. This procedure has limited downsides and a huge potential upside if it eliminates the diplopia. Therefore, an Nd:YAG capsulotomy would be my first choice for intervention. Assuming that Nd:YAG capsulotomy was ineffective or only partially effective in alleviating the patient’s symptoms, the most appropriate option would be RGP contact lens fitting. An RGP lens should mask the corneal irregularities and maximize the patient’s visual acuity. Furthermore, as a nonsurgical option, RGP lens fitting is more amenable to changes in the patient’s visual status as he ages and therefore would provide greater flexibility for this monocular patient in the future. J. Bradley Randleman, MD Atlanta, Georgia, USA
J CATARACT REFRACT SURG - VOL 34, MAY 2008