- Email: [email protected]
Pseudophakic pigmentary glaucoma
1350
LETTERS
apex location will shift from its preoperative position with photoablation. We have analyzed the central total power measurements provided with apex, pupil, and fixation point centration in our data set. While a detailed description of this analysis is beyond the scope of this letter and is planned for a future submission, there was no statistically significant difference between 2.0 mm TMP (PR.15 for all 3 centration methods compared with BCKH2), 4.0 mm TOP (PR.40), and 5.0 mm total axial power (TAP) (PR.27) values obtained via apex, pupil, or fixation centration to BCKH2, with all Pearson’s correlations being R0.96. There was no statistically significant difference between the 2.0 mm TMP (PR.09), 4.0 mm TOP (PR.08), and 5.0 mm TAP (PR.35) obtained with apex, pupil, and fixation centration for each Orbscan metric. The nomenclature of the Orbscan and other videokeratography units can be a source of some confusion. So´nego-Krone et al.1 used ‘‘spherical equivalent’’ in their definition of mean power, suggesting that this metric represents the refractive contribution of the cornea, which is better described by optical power, the latter using ray-tracing techniques while the former is a measurement of regional curvature. We described mean ‘‘power’’ as the average of 2 principal curvatures at a given point, which is equivalent to averaging many equally spaced meridians.4,5 Total mean power is calculated as the average of all the values within the region of interest combining the contributions of the anterior and posterior cornea and a nominal dioptric contribution for thickness. Curvature is a 2-dimensional quantity, whether applied to a 2-dimensional or 3-dimensional object of interest. In the 3-dimensional case, a plane of intersection must be defined to calculate the 2-dimensional curvature value. Thus, the fundamental rationale for calculating mean curvature (which Orbscan calls power) is to better describe the shape at a specified point, taking into account 2 principal meridians. This is not equivalent to power unless Snell’s law of refraction is applied (as with the TOP map), which is not done in the TMP map. However, within 2.0 to 3.0 mm of the corneal center, the paraxial approximation is valid and reasonable estimates of power are possible using the TMP map. Outside this central region, the approximation is not valid and the values are not equivalent to power.6–8 A typographical error in the methods section of our manuscript4 refers to ‘‘total anterior power,’’ which should instead read ‘‘total axial power’’; no statistical data were presented for total ‘‘anterior’’ power as this is not found on the Orbscan and is not a standard topographic metric. In summary, Arce et al. raise important considerations about the central reference point of
videokeratographic maps and alternative nomenclature approaches. Their general comment that total Orbscan power maps with small central regions of analysis should be used for estimation of corneal power following myopic keratorefractive surgery is supported by our findings, which show (in a small data set) that central Orbscan total power maps, in conjunction with the Holladay 2 formula, can be directly used to calculate corneal power independent of the availability of refractive data prior to LASIK. We look forward to future investigations that validate these finding in larger cohorts.dMujtaba A. Qazi, MD, Cynthia J. Roberts, PhD, Irwin Y. Cua, MD, Jay S. Pepose, MD, PhD REFERENCES 1. So´nego-Krone S, Lo´pez-Moreno G, Beaujon-Balbi OV, et al. A direct method to measure the power of the central cornea after myopic in situ keratomileusis. Arch Ophthalmol 2004; 122:159–166 2. Arce CG, Schor P, Campos M. Corneal power measurement after laser in situ keratomileusis [letter]. Arch Ophthalmol 2005; 123:410–411 3. Srivannaboon S, Reinstein DZ, Sutton HFS, Holland SP. Accuracy of Orbscan total optical power maps in detecting refractive change after myopic laser in situ keratomileusis. J Cataract Refract Surg 1999; 25:1596–1599 4. Qazi MA, Cua IY, Roberts CJ, Pepose JS. Determining corneal power using Orbscan II videokeratography for intraocular lens calculation after excimer laser surgery for myopia. J Cataract Refractive Surg 2007; 33:21–30 5. Roberts C. Corneal topography: a review of terms and concepts. J Cataract Refract Surg 1996; 22:624–629 6. Roberts C. The accuracy of ‘‘power’’ maps to display curvature data in corneal topography systems. Invest Ophthalmol Vis Sci 1994; 35:3525–3532 7. Roberts C. Principles of corneal topography. In: Elander R, Rich L, Robin JB, eds, Principles and Practice of Refractive Surgery. Philadelphia, PA, Saunders, 1997; 475–497 8. Roberts C. Corneal topography. In: Azar DT, eds, Refractive Surgery, 2nd ed. St Louis, Mosby, 2007; 103–116
Pseudophakic pigmentary glaucoma I commend Detry-Morel et al.1 on their interesting case on the clinical problem of pigmentary glaucoma in the presence of an intraocular lens (IOL). In this scenario, the surgeon is required to decide between IOL exchange (implying that the IOL is at fault) or continuing medical therapy alone. Their case is a good example of the complexity of this decision. Although Detry-Morel et al. thought their patient’s transient pigmentary glaucoma was due to the IOL, I would like to suggest why this is unlikely. The case involves the left eye of a 43-year-old myopic man who had uneventful bilateral endocapsular phacoemulsification with implantation of a C4.00
J CATARACT REFRACT SURG - VOL 33, AUGUST 2007
LETTERS
diopter AcrySof MA60 IOL (Alcon Laboratories) in the capsular bag 2 years previously. The man complained of intermittent, painless, blurred vision with intraocular pressure reaching 40 mm Hg and anterior chamber cells, which began a few weeks after bilateral neodymium:YAG (Nd:YAG) laser capsulotomies. He responded well to atropine and dorzolamide–timolol eyedrops and was adequately controlled on medical therapy alone. Both haptics were in the bag, with the optic anterior to the capsulorhexis. Optical coherence tomography (OCT) and ultrasound biomicroscopy (UBM) showed iris–optic contact. Detry-Morel et al. speculate that secondary cataract displaced the posterior chamber IOL out of the capsular bag, causing iris chafing, and that the small Nd:YAG capsulotomy may have played a role in the accumulation of Elschnig pearls just behind the optic edge. I believe an inflammatory mechanism due to the release of sequestered lens proteins into the vitreous by the laser capsulotomy is more likely than an IOL–iris chafing mechanism. Another possibility is recurrent idiopathic anterior uveitic glaucoma. My reasons are as follows: 1. The problem began late, 2 years after surgery, and was related to the laser capsulotomy. 2. It is difficult to understand how an in-the-bag IOL with angulated haptics, even with the optic anterior to the capsulorhexis, can exert enough pressure on the iris pigment epithelium to cause chafing and mechanical pigment dispersion. Upside down IOL implantation may make this possible, but the authors exclude this. Likewise, the possibility of pseudophacodonesis was excluded. 3. No hyperopic shift (expected if the IOL was pushed forward) was noted. 4. The glaucoma and anterior chamber cells were transient. The problem resolved without any anatomical change. 5. There were no Krukenberg spindles, usually a sensitive sign of pigment dispersion. 6. The iris epithelial defects were noted within a month of symptoms; they usually require 6 to 12 months of iris chafing to develop.2,3 7. Regarding the OCT and UBM findings: Demonstrating iris–optic contact is not good evidence of iris chafing; in normal eyes, the iris is often in contact with the IOL. More convincing evidence of IOL chafing, which UBM easily demonstrates, is IOL tilt4,5 or haptic subluxation out of the bag and into the ciliary sulcus.6 The authors speculate that Elschnig pearl proliferation at the edge of the small posterior capsulotomy pushed the IOL anteriorly against the posterior iris surface. If so, why not attempt widening the
1351
capsulotomy to alleviate the forward pressure on the IOL optic? Understanding the mechanism of the glaucoma is important. If IOL chafing is the cause, surgery or immobilizing the iris with miotics would be the solution. If the mechanism is inflammatory, surgery may worsen the glaucoma; treatment would be antiinflammatory medication. Russell Pokroy, MD Rehovot, Israel
REFERENCES 1. Detry-Morel ML, Van Acker E, Pourjavan S, et al. Anterior segment imaging using optical coherence tomography and ultrasound biomicroscopy in secondary pigmentary glaucoma associated with in-the-bag intraocular lens. J Cataract Refract Surg 2006; 32:1866–1869 2. Mastropasqua L, Lobefalo L, Gallenga PE. Iris chafing in pseudophakia. Doc Ophthalmol 1994; 87:139–144 3. Mackool RJ. Pigmentary dispersion syndrome [letter]. J Cataract Refract Surg 2001; 27:1341; reply by R Wintle, M Austin, 1341– 1342 4. Loya N, Lichter H, Barash D, et al. Posterior chamber intraocular lens implantation after capsular tear: ultrasound biomicroscopy evaluation. J Cataract Refract Surg 2001; 27:1423–1427 5. Apple DJ, Reidy JJ, Googe JM, et al. A comparison of ciliary sulcus and capsular bag fixation of posterior chamber intraocular lenses. Am Intra-Ocular Implant Soc J 1985; 11:44–63 6. LeBoyer RM, Werner L, Snyder ME, et al. Acute haptic-induced ciliary sulcus irritation associated with single-piece AcrySof intraocular lenses. J Cataract Refract Surg 2005; 31:1421–1427
REPLY: We appreciate Pokroy’s interest in our article and thank him for his pertinent comments and constructive suggestions. Pokroy has some doubt about the pathogenic mechanism we described based on the clinical examination and the anterior segment OCT (AS-OCT) and UBM images. He suggested that an inflammatory mechanism due to the release of sequestered lens proteins into the anterior chamber and the vitreous by the laser capsulotomy was more likely that an IOL–iris chafing mechanism. This hypothesis of hypertensive uveitis was quite plausible. We had considered it at the beginning of our management of the patient. However, the absence of cells in the vitreous and the chronic pigmented cells in the anterior chamber as well as the morphology of the iris atrophy and the trabecular hyperpigmentation are arguments against hypertensive uveitis. Moreover, 3 weeks of corticosteroid therapy was administered without a significant clinical effect and was therefore discontinued. The lack of a Krukenberg spindle, which has been less frequently described in secondary than in primary pigmentary dispersion syndrome (PDS), does not argue against our diagnosis.
J CATARACT REFRACT SURG - VOL 33, AUGUST 2007
LETTERS
apex location will shift from its preoperative position with photoablation. We have analyzed the central total power measurements provided with apex, pupil, and fixation point centration in our data set. While a detailed description of this analysis is beyond the scope of this letter and is planned for a future submission, there was no statistically significant difference between 2.0 mm TMP (PR.15 for all 3 centration methods compared with BCKH2), 4.0 mm TOP (PR.40), and 5.0 mm total axial power (TAP) (PR.27) values obtained via apex, pupil, or fixation centration to BCKH2, with all Pearson’s correlations being R0.96. There was no statistically significant difference between the 2.0 mm TMP (PR.09), 4.0 mm TOP (PR.08), and 5.0 mm TAP (PR.35) obtained with apex, pupil, and fixation centration for each Orbscan metric. The nomenclature of the Orbscan and other videokeratography units can be a source of some confusion. So´nego-Krone et al.1 used ‘‘spherical equivalent’’ in their definition of mean power, suggesting that this metric represents the refractive contribution of the cornea, which is better described by optical power, the latter using ray-tracing techniques while the former is a measurement of regional curvature. We described mean ‘‘power’’ as the average of 2 principal curvatures at a given point, which is equivalent to averaging many equally spaced meridians.4,5 Total mean power is calculated as the average of all the values within the region of interest combining the contributions of the anterior and posterior cornea and a nominal dioptric contribution for thickness. Curvature is a 2-dimensional quantity, whether applied to a 2-dimensional or 3-dimensional object of interest. In the 3-dimensional case, a plane of intersection must be defined to calculate the 2-dimensional curvature value. Thus, the fundamental rationale for calculating mean curvature (which Orbscan calls power) is to better describe the shape at a specified point, taking into account 2 principal meridians. This is not equivalent to power unless Snell’s law of refraction is applied (as with the TOP map), which is not done in the TMP map. However, within 2.0 to 3.0 mm of the corneal center, the paraxial approximation is valid and reasonable estimates of power are possible using the TMP map. Outside this central region, the approximation is not valid and the values are not equivalent to power.6–8 A typographical error in the methods section of our manuscript4 refers to ‘‘total anterior power,’’ which should instead read ‘‘total axial power’’; no statistical data were presented for total ‘‘anterior’’ power as this is not found on the Orbscan and is not a standard topographic metric. In summary, Arce et al. raise important considerations about the central reference point of
videokeratographic maps and alternative nomenclature approaches. Their general comment that total Orbscan power maps with small central regions of analysis should be used for estimation of corneal power following myopic keratorefractive surgery is supported by our findings, which show (in a small data set) that central Orbscan total power maps, in conjunction with the Holladay 2 formula, can be directly used to calculate corneal power independent of the availability of refractive data prior to LASIK. We look forward to future investigations that validate these finding in larger cohorts.dMujtaba A. Qazi, MD, Cynthia J. Roberts, PhD, Irwin Y. Cua, MD, Jay S. Pepose, MD, PhD REFERENCES 1. So´nego-Krone S, Lo´pez-Moreno G, Beaujon-Balbi OV, et al. A direct method to measure the power of the central cornea after myopic in situ keratomileusis. Arch Ophthalmol 2004; 122:159–166 2. Arce CG, Schor P, Campos M. Corneal power measurement after laser in situ keratomileusis [letter]. Arch Ophthalmol 2005; 123:410–411 3. Srivannaboon S, Reinstein DZ, Sutton HFS, Holland SP. Accuracy of Orbscan total optical power maps in detecting refractive change after myopic laser in situ keratomileusis. J Cataract Refract Surg 1999; 25:1596–1599 4. Qazi MA, Cua IY, Roberts CJ, Pepose JS. Determining corneal power using Orbscan II videokeratography for intraocular lens calculation after excimer laser surgery for myopia. J Cataract Refractive Surg 2007; 33:21–30 5. Roberts C. Corneal topography: a review of terms and concepts. J Cataract Refract Surg 1996; 22:624–629 6. Roberts C. The accuracy of ‘‘power’’ maps to display curvature data in corneal topography systems. Invest Ophthalmol Vis Sci 1994; 35:3525–3532 7. Roberts C. Principles of corneal topography. In: Elander R, Rich L, Robin JB, eds, Principles and Practice of Refractive Surgery. Philadelphia, PA, Saunders, 1997; 475–497 8. Roberts C. Corneal topography. In: Azar DT, eds, Refractive Surgery, 2nd ed. St Louis, Mosby, 2007; 103–116
Pseudophakic pigmentary glaucoma I commend Detry-Morel et al.1 on their interesting case on the clinical problem of pigmentary glaucoma in the presence of an intraocular lens (IOL). In this scenario, the surgeon is required to decide between IOL exchange (implying that the IOL is at fault) or continuing medical therapy alone. Their case is a good example of the complexity of this decision. Although Detry-Morel et al. thought their patient’s transient pigmentary glaucoma was due to the IOL, I would like to suggest why this is unlikely. The case involves the left eye of a 43-year-old myopic man who had uneventful bilateral endocapsular phacoemulsification with implantation of a C4.00
J CATARACT REFRACT SURG - VOL 33, AUGUST 2007
LETTERS
diopter AcrySof MA60 IOL (Alcon Laboratories) in the capsular bag 2 years previously. The man complained of intermittent, painless, blurred vision with intraocular pressure reaching 40 mm Hg and anterior chamber cells, which began a few weeks after bilateral neodymium:YAG (Nd:YAG) laser capsulotomies. He responded well to atropine and dorzolamide–timolol eyedrops and was adequately controlled on medical therapy alone. Both haptics were in the bag, with the optic anterior to the capsulorhexis. Optical coherence tomography (OCT) and ultrasound biomicroscopy (UBM) showed iris–optic contact. Detry-Morel et al. speculate that secondary cataract displaced the posterior chamber IOL out of the capsular bag, causing iris chafing, and that the small Nd:YAG capsulotomy may have played a role in the accumulation of Elschnig pearls just behind the optic edge. I believe an inflammatory mechanism due to the release of sequestered lens proteins into the vitreous by the laser capsulotomy is more likely than an IOL–iris chafing mechanism. Another possibility is recurrent idiopathic anterior uveitic glaucoma. My reasons are as follows: 1. The problem began late, 2 years after surgery, and was related to the laser capsulotomy. 2. It is difficult to understand how an in-the-bag IOL with angulated haptics, even with the optic anterior to the capsulorhexis, can exert enough pressure on the iris pigment epithelium to cause chafing and mechanical pigment dispersion. Upside down IOL implantation may make this possible, but the authors exclude this. Likewise, the possibility of pseudophacodonesis was excluded. 3. No hyperopic shift (expected if the IOL was pushed forward) was noted. 4. The glaucoma and anterior chamber cells were transient. The problem resolved without any anatomical change. 5. There were no Krukenberg spindles, usually a sensitive sign of pigment dispersion. 6. The iris epithelial defects were noted within a month of symptoms; they usually require 6 to 12 months of iris chafing to develop.2,3 7. Regarding the OCT and UBM findings: Demonstrating iris–optic contact is not good evidence of iris chafing; in normal eyes, the iris is often in contact with the IOL. More convincing evidence of IOL chafing, which UBM easily demonstrates, is IOL tilt4,5 or haptic subluxation out of the bag and into the ciliary sulcus.6 The authors speculate that Elschnig pearl proliferation at the edge of the small posterior capsulotomy pushed the IOL anteriorly against the posterior iris surface. If so, why not attempt widening the
1351
capsulotomy to alleviate the forward pressure on the IOL optic? Understanding the mechanism of the glaucoma is important. If IOL chafing is the cause, surgery or immobilizing the iris with miotics would be the solution. If the mechanism is inflammatory, surgery may worsen the glaucoma; treatment would be antiinflammatory medication. Russell Pokroy, MD Rehovot, Israel
REFERENCES 1. Detry-Morel ML, Van Acker E, Pourjavan S, et al. Anterior segment imaging using optical coherence tomography and ultrasound biomicroscopy in secondary pigmentary glaucoma associated with in-the-bag intraocular lens. J Cataract Refract Surg 2006; 32:1866–1869 2. Mastropasqua L, Lobefalo L, Gallenga PE. Iris chafing in pseudophakia. Doc Ophthalmol 1994; 87:139–144 3. Mackool RJ. Pigmentary dispersion syndrome [letter]. J Cataract Refract Surg 2001; 27:1341; reply by R Wintle, M Austin, 1341– 1342 4. Loya N, Lichter H, Barash D, et al. Posterior chamber intraocular lens implantation after capsular tear: ultrasound biomicroscopy evaluation. J Cataract Refract Surg 2001; 27:1423–1427 5. Apple DJ, Reidy JJ, Googe JM, et al. A comparison of ciliary sulcus and capsular bag fixation of posterior chamber intraocular lenses. Am Intra-Ocular Implant Soc J 1985; 11:44–63 6. LeBoyer RM, Werner L, Snyder ME, et al. Acute haptic-induced ciliary sulcus irritation associated with single-piece AcrySof intraocular lenses. J Cataract Refract Surg 2005; 31:1421–1427
REPLY: We appreciate Pokroy’s interest in our article and thank him for his pertinent comments and constructive suggestions. Pokroy has some doubt about the pathogenic mechanism we described based on the clinical examination and the anterior segment OCT (AS-OCT) and UBM images. He suggested that an inflammatory mechanism due to the release of sequestered lens proteins into the anterior chamber and the vitreous by the laser capsulotomy was more likely that an IOL–iris chafing mechanism. This hypothesis of hypertensive uveitis was quite plausible. We had considered it at the beginning of our management of the patient. However, the absence of cells in the vitreous and the chronic pigmented cells in the anterior chamber as well as the morphology of the iris atrophy and the trabecular hyperpigmentation are arguments against hypertensive uveitis. Moreover, 3 weeks of corticosteroid therapy was administered without a significant clinical effect and was therefore discontinued. The lack of a Krukenberg spindle, which has been less frequently described in secondary than in primary pigmentary dispersion syndrome (PDS), does not argue against our diagnosis.
J CATARACT REFRACT SURG - VOL 33, AUGUST 2007