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RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES 2015 VOLUME 35 NUMBER 7
Thus, there are two possible causes of serous neurosensory macular detachment related to a thick choroid: choroidal effusion and choroidal neovascularization. The authors thank Pang and Freund for their contribution. Scott E. Pautler, MD* David J. Browning, MD, PhD† *Retina Vitreous Associates, Tampa, Florida † Charlotte Eye and Ear Associates, Charlotte, North Carolina None of the authors have any financial/conflicting interests to disclose. References 1. Pang CE, Freund KB. Pachychoroid neovasculopathy. Retina 2015;35:1–9. 2. Pautler SE, Browning DJ. Isolated posterior uveal effusion: expanding the spectrum of the uveal effusion syndrome. Clin Ophthalmol 2014;9:43–49. 3. Elagouz M, Stanescu-Segall D, Jackson TL. Uveal effusion syndrome. Surv Ophthalmol 2010;55:134–145. 4. Harada T, Machida S, Fujiwara T, et al. Choroidal findings in idiopathic uveal effusion syndrome. Clin Ophthalmol 2011;5: 1599–1601.
Reply To the Editor: We appreciate the interest of Pautler and Browning in our article, entitled “Pachychoroid neovasculopathy”1 and wish to thank them for their comments. They have brought attention to an interesting phenomenon of serous macular detachment occurring in hyperopic eyes with a localized posterior pachychoroid (thickened choroid), which they term “isolated posterior uveal effusion.”2 However, the latter does not involve choroidal neovascularization and should not be confused with pachychoroid neovasculopathy. Pachychoroid neovasculopathy is type 1 (subretinal pigment epithelium) choroidal neovascularization associated with choroid thickening and/or dilated choroidal vessels.1 The purpose of our original article was to establish pachychoroid as a potential cause of choroidal neovascularization in the absence of other causes of choroidal neovascularization, such as agerelated macular degeneration, myopic degeneration, inflammatory diseases, or a history of acute or chronic central serous chorioretinopathy. We agree with Pautler and Browning2 that a pachychoroid may be associated with serous macular detachment due to an increased transudation of plasma from the
thickened choroid. This hyperpermeability of the thickened choroid is demonstrable by indocyanine green angiography in the midphase and late-phase study. However, in addition to pachychoroid macular effusion and pachychoroid neovasculopathy, the manifestation of serous neuorosensory macular detachment related to pachychoroid can also occur in various other entities, including central serous chorioretinopathy, inflammatory diseases such as Vogt–Koyanagi–Harada syndrome, and infiltrative disorders such as lymphoma. Although there have been no large cohort studies, the authors have also observed the atypical occurrence of serous macular detachment in entities such as acute, posterior multifocal placoid pigment epitheliopathy and the multiple evanescent white dot syndrome when these entities occur in patients having a preexisting baseline pachychoroid. Future studies based on choroidal thickness in relation to the occurrence of serous macular detachment in various diseases are highly anticipated. Claudine E. Pang, MD*† K. Bailey Freund, MD*†‡ *Vitreous, Retina, Macula Consultants of New York, New York †LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear and Throat Hospital, New York, New York ‡Department of Ophthalmology, New York University School of Medicine, New York, New York Supported by the Macula Foundation, Inc, New York, NY. K. B. Freund is a consultant to Genentech, Regeneron, ThromboGenics, Ohr Pharmaceutical, Bayer HealthCare, and Heidelberg Engineering. C. E. Pang has no financial/ conflicting interests to disclose. References 1. Pang CE, Freund KB. Pachychoroid neovasculopathy. Retina 2015;35:1–9. 2. Pautler SE, Browning DJ. Isolated posterior uveal effusion: expanding the spectrum of uveal effusion syndrome. Clin Ophthalmol 2014;30:43–49.
Correspondence To the Editor: I read with great interest the article by Jusufbegovic et al1 titled, “Changing Trends in the Management of Diabetic Macular Edema at a Single Institution Over
Correspondence
the Past Decade.” Although the study has several interesting results, the finding that stood out most was the 2013 cohort’s 0.3 logMAR (equivalent of 2 Snellen lines) improvement in visual acuity particularly when compared with the near zero (0.01 logMAR) improvement in the 2003 cohort. Having a visual acuity outcome in a “real-world” population that compares as closely as the 2013 cohort’s does to diabetic macular edema (DME) clinical trial results represents a tremendous accomplishment for the ophthalmologists who treated these patients. This study uses a large sample size that alone suggests a certain degree of validity to the results; however, confirming this through replication in other populations will be difficult because of the omission of several important details from the original manuscript. Certainly, one question is whether the apparent magnitude of improvement between the 2003 and 2013 cohorts is due to differences in the composition of the 2 cohorts. With the multitude of clinical trials demonstrating the superior visual results from antivascular endothelial growth factor agents relative to focal laser for DME, few would disagree that injections are the new standard of care for the majority of patients with DME. The majority, however, does not mean all, and currently, little guidance exists on the benefit of treating patients with DME not involving the fovea or DME involving the fovea with very good vision (better than 20/40) with anti-vascular endothelial growth factor agents. This becomes an important point when reviewing this study and may explain part of the visual acuity differences seen between the 2003 cohort and the 2013 cohort. Given the study requires a patient to have received at least 1 treatment for inclusion, the 2003 cohort likely had more patients with a better starting visual acuity. This would be due to the classic guidelines for treating clinical significant macular edema including edema adjacent to the fovea, but not necessarily involving the fovea, with focal laser therapy. It is unclear what percent of these patients were included in the 2003 cohort or how these patients were dealt with in the 2013 cohort. If nonfovea-involving DME was treated by this practice with bevacizumab, then attaining a 0.3 logMAR visual improvement is even more impressive because most of these patients are not able to improve by 2 Snellen lines of acuity. Although determining percentages of patients with fovea-involving DME would be difficult, this issue could be partially clarified by reporting results based on two to three categories of starting vision, or at the very least, the initial and end visual acuities of each cohort. Other important population characteristics that affect change in vision after treatment are also not
e41
specified. For example, could patients with DME be carried over from 1 year’s cohort to another, or were only new patients included? If the patients were new, did they have to be treatment naive or just new to the practice? Given the 2013 cohort’s visual acuity results, it is most likely that these were treatmentnaive patients (bevacizumab-treated patients would not be expected to average a 2 Snellen line improvement in the middle of a therapeutic course), but these characteristics are never explicitly stated. Nor were the follow-up requirements for inclusion in the study provided. Presumably, each patient had to have at least two visits in the cohort period for beginning and end comparisons. Alternatively, it is unclear if a patient with DME first seen in September 2013 would be followed for a full-calendar year for precomparisons and postcomparisons or only until the last visit before the stated end of the study, November 2013. This has direct implications for interpreting the average number of office visits (if all data is cut off in November 2013, then the visit number is likely an underestimation) and may also inform why the visual change seen in the 2003 cohort (0.01 logMAR improvement) was so little. In the protocol I DRCRnet trial, the focal laser-only arm had gradual visual improvement throughout the last 6 months of the first year of treatment, which if the author’s 2003 cohort had an arbitrary cutoff of December 31, then many treated patients would not have the potential for full improvement.2 Finally, new studies are most beneficial when they are placed within the context of other previous reports. This represents the first “real-world” experience that mirrors the results seen in clinical trials for DME. Before this, one “real-world” DME study using administrative claims data showed an average of 3.6 injections over 5.3 office visits3 and another practice-based study demonstrated 2.6 injections in the first year of treatment with a mean 3.7 letter increase in vision.4 These results led Kiss et al4 to speculate that the difference between clinical trial and real-world visual acuity results is likely due to a lower rate of injections received. This study demonstrates that an average of 9 visits (compared with 13 per year in most clinical trials) can obtain clinical trial level visual acuity results, but without injection frequency data, the reader is unable to fully determine how the ophthalmologists in the practice accomplished this. The study by Jusufbegovic et al has set a high mark for visual outcomes in a typical clinic setting that the rest of the DME-treating community will have to try and match. However, comparisons between this population and others have been greatly limited by the report’s omission of important features of the study cohorts
e42
RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES 2015 VOLUME 35 NUMBER 7
and methods for calculating change in visual acuity. Inclusion of these study characteristics would greatly aid the replication of this study in other populations. Brian L. VanderBeek, MD, MPH*†‡ *Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania †Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania ‡Leonard Davis Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania The author has no financial/conflicting interests to disclose. References 1. Jusufbegovic D, Mugavin MO, Schaal S. Evolution of controlling diabetic retinopathy: changing trends in the management of diabetic macular edema at a single institution over the past decade. Retina 2015;35:929–934. 2. Elman MJ, et al. Randomized trial evaluating ranibizumab plus prompt or deferred laser or triamcinolone plus prompt laser for diabetic macular edema. Ophthalmology 2010;117: 1064–1077. 3. Kiss S, et al. Clinical utilization of anti-vascular endothelial growth-factor agents and patient monitoring in retinal vein occlusion and diabetic macular edema. Clin Ophthalmol 2014; 8:1611–1621. 4. Kiss S, Almony A, Ingram H, et al. Real world vision outcomes in DME treated with anti-VEGF injections-an analysis of EMR data from a large integrated U.S. health system. Paper presented at: The Retina Society Annual Meeting; Sep 14, 2014; Philadelphia, PA.
Reply To the Editor: We would like to thank Brian VanderBeek for his interest in our recent article titled “Changing Trends in the Management of Diabetic Macular Edema at a Single Institution Over the Past Decade”: Retina PAP.1 We studied the treatment choices for diabetic macular edema (DME) at our institution from 2003 to 2013 and their effect on visual acuity and anatomical outcomes in our patient population. We reported the abandonment of laser photocoagulation at our institution and the exclusive use of anti-vascular endothelial growth factor (anti-VEGF) injections for the management of DME. As a result of the change in treatment modality,
we have observed a significant improvement in visual acuity in patients treated with anti-VEGF injections (0.3 logMAR; equivalent of 2 Snellen lines in 2013) compared with laser photocoagulation (0.01 logMAR; equivalent of ,1 Snellen line in 2003). Dr. VanderBeek raised several important questions that are imperative for further discussion and deeper understanding of the results of our study. First, Dr. VanderBeek wonders whether the magnitude of visual improvement between 2003 and 2013 was related to differences in the composition of the study groups such as smaller rate of fovea-involving DME in the laser group. Although laser photocoagulation is recommended for the treatment of “clinically significant macular edema” as defined by the Early Treatment Diabetic Retinopathy Study and might not necessarily involve the fovea,2 all patients included in our study had fovea-involving DME documented by fluorescein angiography and/or optical coherence tomography and reduction in visual acuity. Specifically, there was no statistically significant difference in the pretreatment visual acuity between the laser photocoagulation and anti-VEGF groups. Thus, the smaller magnitude of visual acuity improvement observed in the laser photocoagulation group cannot be explained by the ceiling effect or by selection bias. Second, several comments were raised regarding the inclusion criteria and follow-up of patients in our study. In the study, we included treatment-naive patients who had at least 3 months of follow-up. However, the average follow-up in both cohorts was .12 months. Although there was a slight trend of longer follow-up in the laser photocoagulation group given that most of the laser treatments occurred in 2003 and 2004, there was no statistically significant difference in the overall length of follow-up period between the 2 groups. Accordingly, the length of follow-up period was shorter for patients who presented in November 2013 (which was still at least 3 months). Nevertheless, the study results were comparable between 2012 and 2013 cohorts (see Figures 3–5 in the original article1). Regarding the grouping of patients to specific years, patients who presented to our practice in 2003 were kept in 2003 cohort. For example, a patient who presented in September 2003 and had the last documented follow-up in January 2005 was only included in 2003 cohort. In the same example, the difference between initial and final visual acuities was calculated using the data points from September 2003 to January 2005. The patient follow-up was not cut off at the end of calendar year 2003. Lastly, Dr. VanderBeek commented on the frequency of follow-up in our patient population and the frequency of injections required to maintain the visual improvements. We have confirmed superior visual
RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES 2015 VOLUME 35 NUMBER 7
Thus, there are two possible causes of serous neurosensory macular detachment related to a thick choroid: choroidal effusion and choroidal neovascularization. The authors thank Pang and Freund for their contribution. Scott E. Pautler, MD* David J. Browning, MD, PhD† *Retina Vitreous Associates, Tampa, Florida † Charlotte Eye and Ear Associates, Charlotte, North Carolina None of the authors have any financial/conflicting interests to disclose. References 1. Pang CE, Freund KB. Pachychoroid neovasculopathy. Retina 2015;35:1–9. 2. Pautler SE, Browning DJ. Isolated posterior uveal effusion: expanding the spectrum of the uveal effusion syndrome. Clin Ophthalmol 2014;9:43–49. 3. Elagouz M, Stanescu-Segall D, Jackson TL. Uveal effusion syndrome. Surv Ophthalmol 2010;55:134–145. 4. Harada T, Machida S, Fujiwara T, et al. Choroidal findings in idiopathic uveal effusion syndrome. Clin Ophthalmol 2011;5: 1599–1601.
Reply To the Editor: We appreciate the interest of Pautler and Browning in our article, entitled “Pachychoroid neovasculopathy”1 and wish to thank them for their comments. They have brought attention to an interesting phenomenon of serous macular detachment occurring in hyperopic eyes with a localized posterior pachychoroid (thickened choroid), which they term “isolated posterior uveal effusion.”2 However, the latter does not involve choroidal neovascularization and should not be confused with pachychoroid neovasculopathy. Pachychoroid neovasculopathy is type 1 (subretinal pigment epithelium) choroidal neovascularization associated with choroid thickening and/or dilated choroidal vessels.1 The purpose of our original article was to establish pachychoroid as a potential cause of choroidal neovascularization in the absence of other causes of choroidal neovascularization, such as agerelated macular degeneration, myopic degeneration, inflammatory diseases, or a history of acute or chronic central serous chorioretinopathy. We agree with Pautler and Browning2 that a pachychoroid may be associated with serous macular detachment due to an increased transudation of plasma from the
thickened choroid. This hyperpermeability of the thickened choroid is demonstrable by indocyanine green angiography in the midphase and late-phase study. However, in addition to pachychoroid macular effusion and pachychoroid neovasculopathy, the manifestation of serous neuorosensory macular detachment related to pachychoroid can also occur in various other entities, including central serous chorioretinopathy, inflammatory diseases such as Vogt–Koyanagi–Harada syndrome, and infiltrative disorders such as lymphoma. Although there have been no large cohort studies, the authors have also observed the atypical occurrence of serous macular detachment in entities such as acute, posterior multifocal placoid pigment epitheliopathy and the multiple evanescent white dot syndrome when these entities occur in patients having a preexisting baseline pachychoroid. Future studies based on choroidal thickness in relation to the occurrence of serous macular detachment in various diseases are highly anticipated. Claudine E. Pang, MD*† K. Bailey Freund, MD*†‡ *Vitreous, Retina, Macula Consultants of New York, New York †LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear and Throat Hospital, New York, New York ‡Department of Ophthalmology, New York University School of Medicine, New York, New York Supported by the Macula Foundation, Inc, New York, NY. K. B. Freund is a consultant to Genentech, Regeneron, ThromboGenics, Ohr Pharmaceutical, Bayer HealthCare, and Heidelberg Engineering. C. E. Pang has no financial/ conflicting interests to disclose. References 1. Pang CE, Freund KB. Pachychoroid neovasculopathy. Retina 2015;35:1–9. 2. Pautler SE, Browning DJ. Isolated posterior uveal effusion: expanding the spectrum of uveal effusion syndrome. Clin Ophthalmol 2014;30:43–49.
Correspondence To the Editor: I read with great interest the article by Jusufbegovic et al1 titled, “Changing Trends in the Management of Diabetic Macular Edema at a Single Institution Over
Correspondence
the Past Decade.” Although the study has several interesting results, the finding that stood out most was the 2013 cohort’s 0.3 logMAR (equivalent of 2 Snellen lines) improvement in visual acuity particularly when compared with the near zero (0.01 logMAR) improvement in the 2003 cohort. Having a visual acuity outcome in a “real-world” population that compares as closely as the 2013 cohort’s does to diabetic macular edema (DME) clinical trial results represents a tremendous accomplishment for the ophthalmologists who treated these patients. This study uses a large sample size that alone suggests a certain degree of validity to the results; however, confirming this through replication in other populations will be difficult because of the omission of several important details from the original manuscript. Certainly, one question is whether the apparent magnitude of improvement between the 2003 and 2013 cohorts is due to differences in the composition of the 2 cohorts. With the multitude of clinical trials demonstrating the superior visual results from antivascular endothelial growth factor agents relative to focal laser for DME, few would disagree that injections are the new standard of care for the majority of patients with DME. The majority, however, does not mean all, and currently, little guidance exists on the benefit of treating patients with DME not involving the fovea or DME involving the fovea with very good vision (better than 20/40) with anti-vascular endothelial growth factor agents. This becomes an important point when reviewing this study and may explain part of the visual acuity differences seen between the 2003 cohort and the 2013 cohort. Given the study requires a patient to have received at least 1 treatment for inclusion, the 2003 cohort likely had more patients with a better starting visual acuity. This would be due to the classic guidelines for treating clinical significant macular edema including edema adjacent to the fovea, but not necessarily involving the fovea, with focal laser therapy. It is unclear what percent of these patients were included in the 2003 cohort or how these patients were dealt with in the 2013 cohort. If nonfovea-involving DME was treated by this practice with bevacizumab, then attaining a 0.3 logMAR visual improvement is even more impressive because most of these patients are not able to improve by 2 Snellen lines of acuity. Although determining percentages of patients with fovea-involving DME would be difficult, this issue could be partially clarified by reporting results based on two to three categories of starting vision, or at the very least, the initial and end visual acuities of each cohort. Other important population characteristics that affect change in vision after treatment are also not
e41
specified. For example, could patients with DME be carried over from 1 year’s cohort to another, or were only new patients included? If the patients were new, did they have to be treatment naive or just new to the practice? Given the 2013 cohort’s visual acuity results, it is most likely that these were treatmentnaive patients (bevacizumab-treated patients would not be expected to average a 2 Snellen line improvement in the middle of a therapeutic course), but these characteristics are never explicitly stated. Nor were the follow-up requirements for inclusion in the study provided. Presumably, each patient had to have at least two visits in the cohort period for beginning and end comparisons. Alternatively, it is unclear if a patient with DME first seen in September 2013 would be followed for a full-calendar year for precomparisons and postcomparisons or only until the last visit before the stated end of the study, November 2013. This has direct implications for interpreting the average number of office visits (if all data is cut off in November 2013, then the visit number is likely an underestimation) and may also inform why the visual change seen in the 2003 cohort (0.01 logMAR improvement) was so little. In the protocol I DRCRnet trial, the focal laser-only arm had gradual visual improvement throughout the last 6 months of the first year of treatment, which if the author’s 2003 cohort had an arbitrary cutoff of December 31, then many treated patients would not have the potential for full improvement.2 Finally, new studies are most beneficial when they are placed within the context of other previous reports. This represents the first “real-world” experience that mirrors the results seen in clinical trials for DME. Before this, one “real-world” DME study using administrative claims data showed an average of 3.6 injections over 5.3 office visits3 and another practice-based study demonstrated 2.6 injections in the first year of treatment with a mean 3.7 letter increase in vision.4 These results led Kiss et al4 to speculate that the difference between clinical trial and real-world visual acuity results is likely due to a lower rate of injections received. This study demonstrates that an average of 9 visits (compared with 13 per year in most clinical trials) can obtain clinical trial level visual acuity results, but without injection frequency data, the reader is unable to fully determine how the ophthalmologists in the practice accomplished this. The study by Jusufbegovic et al has set a high mark for visual outcomes in a typical clinic setting that the rest of the DME-treating community will have to try and match. However, comparisons between this population and others have been greatly limited by the report’s omission of important features of the study cohorts
e42
RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES 2015 VOLUME 35 NUMBER 7
and methods for calculating change in visual acuity. Inclusion of these study characteristics would greatly aid the replication of this study in other populations. Brian L. VanderBeek, MD, MPH*†‡ *Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania †Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania ‡Leonard Davis Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania The author has no financial/conflicting interests to disclose. References 1. Jusufbegovic D, Mugavin MO, Schaal S. Evolution of controlling diabetic retinopathy: changing trends in the management of diabetic macular edema at a single institution over the past decade. Retina 2015;35:929–934. 2. Elman MJ, et al. Randomized trial evaluating ranibizumab plus prompt or deferred laser or triamcinolone plus prompt laser for diabetic macular edema. Ophthalmology 2010;117: 1064–1077. 3. Kiss S, et al. Clinical utilization of anti-vascular endothelial growth-factor agents and patient monitoring in retinal vein occlusion and diabetic macular edema. Clin Ophthalmol 2014; 8:1611–1621. 4. Kiss S, Almony A, Ingram H, et al. Real world vision outcomes in DME treated with anti-VEGF injections-an analysis of EMR data from a large integrated U.S. health system. Paper presented at: The Retina Society Annual Meeting; Sep 14, 2014; Philadelphia, PA.
Reply To the Editor: We would like to thank Brian VanderBeek for his interest in our recent article titled “Changing Trends in the Management of Diabetic Macular Edema at a Single Institution Over the Past Decade”: Retina PAP.1 We studied the treatment choices for diabetic macular edema (DME) at our institution from 2003 to 2013 and their effect on visual acuity and anatomical outcomes in our patient population. We reported the abandonment of laser photocoagulation at our institution and the exclusive use of anti-vascular endothelial growth factor (anti-VEGF) injections for the management of DME. As a result of the change in treatment modality,
we have observed a significant improvement in visual acuity in patients treated with anti-VEGF injections (0.3 logMAR; equivalent of 2 Snellen lines in 2013) compared with laser photocoagulation (0.01 logMAR; equivalent of ,1 Snellen line in 2003). Dr. VanderBeek raised several important questions that are imperative for further discussion and deeper understanding of the results of our study. First, Dr. VanderBeek wonders whether the magnitude of visual improvement between 2003 and 2013 was related to differences in the composition of the study groups such as smaller rate of fovea-involving DME in the laser group. Although laser photocoagulation is recommended for the treatment of “clinically significant macular edema” as defined by the Early Treatment Diabetic Retinopathy Study and might not necessarily involve the fovea,2 all patients included in our study had fovea-involving DME documented by fluorescein angiography and/or optical coherence tomography and reduction in visual acuity. Specifically, there was no statistically significant difference in the pretreatment visual acuity between the laser photocoagulation and anti-VEGF groups. Thus, the smaller magnitude of visual acuity improvement observed in the laser photocoagulation group cannot be explained by the ceiling effect or by selection bias. Second, several comments were raised regarding the inclusion criteria and follow-up of patients in our study. In the study, we included treatment-naive patients who had at least 3 months of follow-up. However, the average follow-up in both cohorts was .12 months. Although there was a slight trend of longer follow-up in the laser photocoagulation group given that most of the laser treatments occurred in 2003 and 2004, there was no statistically significant difference in the overall length of follow-up period between the 2 groups. Accordingly, the length of follow-up period was shorter for patients who presented in November 2013 (which was still at least 3 months). Nevertheless, the study results were comparable between 2012 and 2013 cohorts (see Figures 3–5 in the original article1). Regarding the grouping of patients to specific years, patients who presented to our practice in 2003 were kept in 2003 cohort. For example, a patient who presented in September 2003 and had the last documented follow-up in January 2005 was only included in 2003 cohort. In the same example, the difference between initial and final visual acuities was calculated using the data points from September 2003 to January 2005. The patient follow-up was not cut off at the end of calendar year 2003. Lastly, Dr. VanderBeek commented on the frequency of follow-up in our patient population and the frequency of injections required to maintain the visual improvements. We have confirmed superior visual
