Letters
Figure 2. Quantitative Fundus Autofluorescence (qAF) Values by Age for Study Patient With RPGR Mutation vs Patients With Stargardt Disease 1 and Healthy Individuals
800
Author Affiliations: Department of Ophthalmology, Columbia University, New York, New York (Marsiglia, Lee, Zernant, Tsang, Sparrow); Department of Ophthalmology and Visual Sciences, University of Iowa, Iowa City (Mahajan); Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts (Delori); Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts (Delori).
600
Corresponding Author: Janet R. Sparrow, PhD, Department of Ophthalmology, Columbia University, 630 W 168th St, New York, NY 10032 (jrs88@columbia .edu).
Autofluorescence, qAF Units
1000
Patients with Stargardt disease 1 Patient with RPGR mutation
Published Online: November 6, 2014. doi:10.1001/jamaophthalmol.2014.4507. 400
200
0 0
10
20
30
40
50
60
Age, y
The qAF values (arbitrary grayscale units) acquired from each eye of our patient with an RPGR mutation and qAF values from patients with Stargardt disease 1 are plotted by age.4 Solid line indicates mean qAF values from 277 healthy individuals; dashed lines, 95% confidence interval.4
of RPGR (c.3070G>T, pGlu1024X, OMIM #312610). The mean qAF values of the patient were found to be within the range observed in healthy eyes. The patient’s mean values were also lower than in many patients of the same age with STGD14 (Figure 1 and Figure 2). Discussion | X-linked retinitis pigmentosa accounts for up to 20% of families with retinitis pigmentosa, and RPGR is the most frequently mutated gene in X-linked retinitis pigmentosa.6 In our proband, the inheritance pattern was typical of X-linked disease and the report of a tapetal reflex in the mother was consistent with X-linked retinitis pigmentosa. It was ultimately apparent that the BEM phenotype had also been conferred by the mutation in RPGR. Nevertheless, given that disease caused by mutations in ABCA4 can manifest as BEM, that diseasecausing variants in ABCA4 are copious (approximately 800 sequence variants), and that a second mutation is frequently not detected in the presence of clinical disease, it was initially reasonable to consider ABCA4 pathogenicity on the basis of a single allele and the clinical presentation. Here was a case in which an additional clinical tool, qAF, could guide genetic screening so as to potentially avoid the pitfalls of phenotypic and genetic heterogeneity. Subsequent to the identification of the ABCA4 variant p.E471K by array screening, data available from the Exome Variant Server7 indicated that this allele is unlikely to be disease causing.
Author Contributions: Dr Sparrow had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Marsiglia, Tsang, Sparrow. Acquisition, analysis, or interpretation of data: All authors. Drafting of the manuscript: Marsiglia, Mahajan, Zernant, Sparrow. Critical revision of the manuscript for important intellectual content: Marsiglia, Lee, Delori, Tsang, Sparrow. Statistical analysis: Delori, Sparrow. Obtained funding: Sparrow. Administrative, technical, or material support: Marsiglia, Lee, Mahajan, Zernant, Sparrow. Study supervision: Tsang, Sparrow. Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported. Funding/Support: This work was supported by grants EY024091, EY019861, and P30EY019007 from the National Eye Institute and a grant from Research to Prevent Blindness to the Department of Ophthalmology, Columbia University. Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. 1. Thiadens AA, Phan TM, Zekveld-Vroon RC, et al; Writing Committee for the Cone Disorders Study Group Consortium. Clinical course, genetic etiology, and visual outcome in cone and cone-rod dystrophy. Ophthalmology. 2012;119(4): 819-826. 2. Bassuk AG, Sujirakul T, Tsang SH, Mahajan VB. A novel RPGR mutation masquerading as Stargardt disease. Br J Ophthalmol. 2014;98(5):709-711. 3. Zernant J, Schubert C, Im KM, et al. Analysis of the ABCA4 gene by next-generation sequencing. Invest Ophthalmol Vis Sci. 2011;52(11):8479-8487. 4. Burke TR, Duncker T, Woods RL, et al. Quantitative fundus autofluorescence in recessive Stargardt disease. Invest Ophthalmol Vis Sci. 2014;55(5):2841-2852. 5. Acton JH, Greenberg JP, Greenstein VC, et al. Evaluation of multimodal imaging in carriers of X-linked retinitis pigmentosa. Exp Eye Res. 2013;113:41-48. 6. Thompson DA, Khan NW, Othman MI, et al. Rd9 is a naturally occurring mouse model of a common form of retinitis pigmentosa caused by mutations in RPGR-ORF15. PLoS One. 2012;7(5):e35865. 7. National Heart, Lung, and Blood Institute Grand Opportunity Exome Sequencing Project. Exome Variant Server. http://evs.gs.washington.edu/EVS/. Accessed June 5, 2014.
OBSERVATIONS
Endothelial Circles After Nd:YAG Posterior Capsulotomy The Nd:YAG laser uses infrared light focused at 1064 nm.1 Using a short pulse and high power, it causes plasma formation, resulting in shock or acoustic waves that disrupt target tissue.2,3 It is commonly used for laser periphery iridotomies and posterior capsulotomies. Common complications after Nd:YAG capsulotomy include intraocular pressure elevation, intraocu-
Marcela Marsiglia, MD, PhD Winston Lee, BS Vinit B. Mahajan, MD, PhD Jana Zernant, MS François C. Delori, PhD 220
Stephen H. Tsang, MD, PhD Janet R. Sparrow, PhD
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Letters
lar lens damage, and anterior uveitis.4,5 Herein, we describe 3 eyes in 2 patients with endothelial damage after Nd:YAG capsulotomy. Report of Cases | Case 1. A man in his late 80s with a history of Fuchs endothelial dystrophy had undergone uncomplicated phacoemulsification in both eyes and subsequent Nd:YAG capsulotomy. The settings for the right eye were a pulse energy of 5 to 6 mJ with a total of 23 pulses distributed in a circular pattern. One month later, the patient underwent Nd:YAG capsulotomy in the left eye with a pulse energy of 6.6 mJ with a total of 33 applications distributed in a circular pattern. On presentation, visual acuity was 20/125 OD and 20/80 OS. Slitlamp examination showed central corneal edema associated with subepithelial fibrosis and guttata, consistent with a diagnosis of Fuchs endothelial dystrophy. There were deep circular endothelial lesions oriented in a circle in the central cornea. There was a posterior chamber intraocular lens with a posterior capsule open in a circular pattern (Figure, A and B). Findings on dilated examination were unremarkable. Case 2. A man in his late 70s with a history of advanced glaucoma underwent uncomplicated phacoemulsification in the left eye. One month later, he underwent Nd:YAG posterior capsulotomy in the left eye with a pulse energy of 2.6 mJ with a total of 61 applications distributed in a cruciate pattern. On examination, visual acuity was 20/100 OS, limited by advanced glaucoma. Slitlamp examination of the left eye revealed deep circular endothelial lesions oriented in a cruciate pattern with an otherwise clear cornea (Figure, C). There was a posterior chamber intraocular lens with a posterior capsule open in a cruciate pattern. Findings on dilated fundus examination were unremarkable other than evidence of advanced optic nerve cupping. Discussion | The Nd:YAG laser induces tissue breakdown by resulting in plasma formation and induc ing shock waves.2,3,5 Studies suggest that corneal injury occurs at the level of the endothelium and Descemet membrane.2,3 The endothelial damage induced depends on the pulse power of the laser, the total energy used, the distance of the corneal endothelium from the site of optical breakdown, and the point of laser focus.2,6 We report deep, central corneal circles representing damage to the corneal endothelium as a result of Nd:YAG posterior capsulotomy. The pattern of the corneal lesions follows precisely the areas of laser application when creating a circular or cruciate opening in the posterior capsule. Each circular lesion appears to be the result of an Nd:YAG laser–induced shock wave. The distinct pattern of damage is suspicious of Nd:YAG laser when used at a high-pulse setting and when the laser energy is too anteriorly focused. Although our patients reported no visual symptoms, it is unclear whether these areas of endothelial damage are of visual consequence; our patients had decreased visual acuity from other ocular pathology. However, in our patient with Fuchs endothelial dystrophy with a low functional endothelial cell reserve, it is possible that the damage could have resulted in additional cell loss, jamaophthalmology.com
Figure. Endothelial Circles After Nd:YAG Posterior Capsulotomy A
B
C
A, Circular endothelial lesions corresponding to the treatment area of posterior capsulotomy. B, The open, circular posterior capsule. C, Endothelial circles with a cruciate orientation, corresponding to a cruciate posterior capsulotomy.
worsening or hastening the onset of corneal edema. Nonetheless, this is an additional reminder to use only the minimal energy required and only precisely focused laser energy with the Nd:YAG laser. Shivali A. Menda, MD David Palay, MD Stephen McLeod, MD Author Affiliations: Department of Ophthalmology, University of California, San Francisco (Menda, McLeod); Atlanta Ophthalmology Associates, Atlanta, Georgia (Palay); Francis I. Proctor Foundation, University of California, San Francisco (McLeod). Corresponding Author: Stephen McLeod, MD, Department of Ophthalmology and Francis I. Proctor Foundation, University of California, San Francisco, 10 Koret Way, San Francisco, CA 94143 ([email protected]). Published Online: October 30, 2014. doi:10.1001/jamaophthalmol.2014.4289. Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported. (Reprinted) JAMA Ophthalmology February 2015 Volume 133, Number 2
Copyright 2015 American Medical Association. All rights reserved.
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221
Letters
Additional Contributions: Ashley Brito, BA, Department of Ophthalmology, University of California, San Francisco, photographed the endothelial lesions and Sarah DeParis, MD, Department of Ophthalmology, University of California, San Francisco, helped in creating the figure; they received no compensation for these contributions. 1. Slomovic AR, Parrish RK II, Forster RK, Cubillas A. Neodymium-YAG laser posterior capsulotomy: central corneal endothelial cell density. Arch Ophthalmol. 1986;104(4):536-538. 2. Vaikoussis E, Bisogiannis Z, Margaritis L. Corneal endothelial damage after Nd:YAG laser anterior capsulotomy: an experimental study on rabbits. Doc Ophthalmol. 1993;83(4):279-286. 3. Kerr Muir MG, Sherrard ES. Damage to the corneal endothelium during Nd/YAG photodisruption. Br J Ophthalmol. 1985;69(2):77-85. 4. Channell MM, Beckman H. Intraocular pressure changes after neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol. 1984;102(7): 1024-1026. 5. Aslam TM, Devlin H, Dhillon B. Use of Nd:YAG laser capsulotomy. Surv Ophthalmol. 2003;48(6):594-612. 6. Bath PE, Hoffer KJ, Aron-Rosa D, Dang Y. Glare disability secondary to YAG laser intraocular lens damage. J Cataract Refract Surg. 1987;13(3):309-313.
Presumed Bee Stinger Retained Intraocularly in the Absence of Inflammation There are multiple reports in the literature describing ocular trauma due to bee and wasp stings, and most of the complications are caused by either venom or the local inflammatory reaction, 1 potentially leading to corneal edema, uveitis, cataract,1,2 and, less frequently, optic neuritis.3 Although there are controversies in the management of retained bee stingers, surgical removal is usually indicated.4 We report an unusual case of a presumed intraocular bee stinger embedded in the lens for 5 years with surrounding cataract but no signs of intraocular inflammation. Report of a Case | A man in his late 50s presented to the local eye clinic after being invited to an ophthalmological examination for a population-based survey on prevalence of blindness. He was satisfied with his visual acuity and reported a slight decrease in the upper visual field of his left eye. His bestcorrected distance visual acuity was 20/20 OD and 20/32 OS; intraocular pressure was 10 mm Hg OD and 12 mm Hg OS. On slitlamp examination, the right eye showed only a small pin-
guecula. His left eye also showed a pinguecula, no signs of conjunctival hyperemia, a mild paracentral corneal opacification, and an intraocular foreign body embedded in the lens and touching the upper temporal pupil border (Figure 1A). There were no signs of anterior chamber inflammatory reaction. After instillation of tropicamide, 1%, and phenylephrine hydrochloride, 10%, we observed that the surrounding lens was opaque (Figure 1B). Once we noticed the intraocular foreign body, we asked him whether he had a history of ocular trauma. He reported that 5 years earlier, he had gotten multiple bee stings while riding a horse in the local rural area. At that time, he had severe pain and traveled to the next nearest eye clinic. The local ophthalmologist removed multiple stingers from both eyes and prescribed topical drugs; the patient felt better a few days later and never returned for an ocular evaluation. Optical coherence tomographic images (iVue 100; Optovue) of the anterior chamber demonstrated stromal opacification of the cornea presumably at the stinger inoculation site (Figure 2A). The presumed stinger reached 1.04 mm into the anterior chamber (Figure 2B), while its intralenticular part could not be adequately measured. Discussion | This presumed stinger is most likely from Apis mellifera (Vera Lucia Imperatriz-Fonseca, PhD, written communication, November 20, 2013); surgical removal of the stinger and further analysis could confirm this hypothesis. Apis bees, Pogonomyrmex ants, and multiple wasps have a barbed sting lancet and are able to perform sting autotomy, the selfamputation of the stinger and poison sac (which remain in their target) as a form of self-defense from vertebrate predators.5 Considering the stinger’s dimensions and the patient’s corneal thickness (594 μm centrally) and anterior chamber depth, it is unclear how the stinger became embedded in the lens. One possible explanation is an indentation of the globe at the moment of trauma, temporarily reducing its axial dimension. To our knowledge, this is only the second report in the literature of a presumed innocuous intraocular bee stinger attached to the lens1 and the first time that optical coherence tomographic images were used to analyze the presumed stinger.
Figure 1. Clinical Photographs Showing Presumed Bee Stinger A
B
A, Presumed bee stinger (arrowhead). B, Bee stinger with associated lens opacification (arrowhead), after instillation of mydriatic agents. Images were captured with an iPhone 5 (Apple Inc) in front of the slitlamp optics. 222
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Figure 2. Quantitative Fundus Autofluorescence (qAF) Values by Age for Study Patient With RPGR Mutation vs Patients With Stargardt Disease 1 and Healthy Individuals
800
Author Affiliations: Department of Ophthalmology, Columbia University, New York, New York (Marsiglia, Lee, Zernant, Tsang, Sparrow); Department of Ophthalmology and Visual Sciences, University of Iowa, Iowa City (Mahajan); Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts (Delori); Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts (Delori).
600
Corresponding Author: Janet R. Sparrow, PhD, Department of Ophthalmology, Columbia University, 630 W 168th St, New York, NY 10032 (jrs88@columbia .edu).
Autofluorescence, qAF Units
1000
Patients with Stargardt disease 1 Patient with RPGR mutation
Published Online: November 6, 2014. doi:10.1001/jamaophthalmol.2014.4507. 400
200
0 0
10
20
30
40
50
60
Age, y
The qAF values (arbitrary grayscale units) acquired from each eye of our patient with an RPGR mutation and qAF values from patients with Stargardt disease 1 are plotted by age.4 Solid line indicates mean qAF values from 277 healthy individuals; dashed lines, 95% confidence interval.4
of RPGR (c.3070G>T, pGlu1024X, OMIM #312610). The mean qAF values of the patient were found to be within the range observed in healthy eyes. The patient’s mean values were also lower than in many patients of the same age with STGD14 (Figure 1 and Figure 2). Discussion | X-linked retinitis pigmentosa accounts for up to 20% of families with retinitis pigmentosa, and RPGR is the most frequently mutated gene in X-linked retinitis pigmentosa.6 In our proband, the inheritance pattern was typical of X-linked disease and the report of a tapetal reflex in the mother was consistent with X-linked retinitis pigmentosa. It was ultimately apparent that the BEM phenotype had also been conferred by the mutation in RPGR. Nevertheless, given that disease caused by mutations in ABCA4 can manifest as BEM, that diseasecausing variants in ABCA4 are copious (approximately 800 sequence variants), and that a second mutation is frequently not detected in the presence of clinical disease, it was initially reasonable to consider ABCA4 pathogenicity on the basis of a single allele and the clinical presentation. Here was a case in which an additional clinical tool, qAF, could guide genetic screening so as to potentially avoid the pitfalls of phenotypic and genetic heterogeneity. Subsequent to the identification of the ABCA4 variant p.E471K by array screening, data available from the Exome Variant Server7 indicated that this allele is unlikely to be disease causing.
Author Contributions: Dr Sparrow had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Marsiglia, Tsang, Sparrow. Acquisition, analysis, or interpretation of data: All authors. Drafting of the manuscript: Marsiglia, Mahajan, Zernant, Sparrow. Critical revision of the manuscript for important intellectual content: Marsiglia, Lee, Delori, Tsang, Sparrow. Statistical analysis: Delori, Sparrow. Obtained funding: Sparrow. Administrative, technical, or material support: Marsiglia, Lee, Mahajan, Zernant, Sparrow. Study supervision: Tsang, Sparrow. Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported. Funding/Support: This work was supported by grants EY024091, EY019861, and P30EY019007 from the National Eye Institute and a grant from Research to Prevent Blindness to the Department of Ophthalmology, Columbia University. Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. 1. Thiadens AA, Phan TM, Zekveld-Vroon RC, et al; Writing Committee for the Cone Disorders Study Group Consortium. Clinical course, genetic etiology, and visual outcome in cone and cone-rod dystrophy. Ophthalmology. 2012;119(4): 819-826. 2. Bassuk AG, Sujirakul T, Tsang SH, Mahajan VB. A novel RPGR mutation masquerading as Stargardt disease. Br J Ophthalmol. 2014;98(5):709-711. 3. Zernant J, Schubert C, Im KM, et al. Analysis of the ABCA4 gene by next-generation sequencing. Invest Ophthalmol Vis Sci. 2011;52(11):8479-8487. 4. Burke TR, Duncker T, Woods RL, et al. Quantitative fundus autofluorescence in recessive Stargardt disease. Invest Ophthalmol Vis Sci. 2014;55(5):2841-2852. 5. Acton JH, Greenberg JP, Greenstein VC, et al. Evaluation of multimodal imaging in carriers of X-linked retinitis pigmentosa. Exp Eye Res. 2013;113:41-48. 6. Thompson DA, Khan NW, Othman MI, et al. Rd9 is a naturally occurring mouse model of a common form of retinitis pigmentosa caused by mutations in RPGR-ORF15. PLoS One. 2012;7(5):e35865. 7. National Heart, Lung, and Blood Institute Grand Opportunity Exome Sequencing Project. Exome Variant Server. http://evs.gs.washington.edu/EVS/. Accessed June 5, 2014.
OBSERVATIONS
Endothelial Circles After Nd:YAG Posterior Capsulotomy The Nd:YAG laser uses infrared light focused at 1064 nm.1 Using a short pulse and high power, it causes plasma formation, resulting in shock or acoustic waves that disrupt target tissue.2,3 It is commonly used for laser periphery iridotomies and posterior capsulotomies. Common complications after Nd:YAG capsulotomy include intraocular pressure elevation, intraocu-
Marcela Marsiglia, MD, PhD Winston Lee, BS Vinit B. Mahajan, MD, PhD Jana Zernant, MS François C. Delori, PhD 220
Stephen H. Tsang, MD, PhD Janet R. Sparrow, PhD
JAMA Ophthalmology February 2015 Volume 133, Number 2 (Reprinted)
Copyright 2015 American Medical Association. All rights reserved.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/27/2015
jamaophthalmology.com
Letters
lar lens damage, and anterior uveitis.4,5 Herein, we describe 3 eyes in 2 patients with endothelial damage after Nd:YAG capsulotomy. Report of Cases | Case 1. A man in his late 80s with a history of Fuchs endothelial dystrophy had undergone uncomplicated phacoemulsification in both eyes and subsequent Nd:YAG capsulotomy. The settings for the right eye were a pulse energy of 5 to 6 mJ with a total of 23 pulses distributed in a circular pattern. One month later, the patient underwent Nd:YAG capsulotomy in the left eye with a pulse energy of 6.6 mJ with a total of 33 applications distributed in a circular pattern. On presentation, visual acuity was 20/125 OD and 20/80 OS. Slitlamp examination showed central corneal edema associated with subepithelial fibrosis and guttata, consistent with a diagnosis of Fuchs endothelial dystrophy. There were deep circular endothelial lesions oriented in a circle in the central cornea. There was a posterior chamber intraocular lens with a posterior capsule open in a circular pattern (Figure, A and B). Findings on dilated examination were unremarkable. Case 2. A man in his late 70s with a history of advanced glaucoma underwent uncomplicated phacoemulsification in the left eye. One month later, he underwent Nd:YAG posterior capsulotomy in the left eye with a pulse energy of 2.6 mJ with a total of 61 applications distributed in a cruciate pattern. On examination, visual acuity was 20/100 OS, limited by advanced glaucoma. Slitlamp examination of the left eye revealed deep circular endothelial lesions oriented in a cruciate pattern with an otherwise clear cornea (Figure, C). There was a posterior chamber intraocular lens with a posterior capsule open in a cruciate pattern. Findings on dilated fundus examination were unremarkable other than evidence of advanced optic nerve cupping. Discussion | The Nd:YAG laser induces tissue breakdown by resulting in plasma formation and induc ing shock waves.2,3,5 Studies suggest that corneal injury occurs at the level of the endothelium and Descemet membrane.2,3 The endothelial damage induced depends on the pulse power of the laser, the total energy used, the distance of the corneal endothelium from the site of optical breakdown, and the point of laser focus.2,6 We report deep, central corneal circles representing damage to the corneal endothelium as a result of Nd:YAG posterior capsulotomy. The pattern of the corneal lesions follows precisely the areas of laser application when creating a circular or cruciate opening in the posterior capsule. Each circular lesion appears to be the result of an Nd:YAG laser–induced shock wave. The distinct pattern of damage is suspicious of Nd:YAG laser when used at a high-pulse setting and when the laser energy is too anteriorly focused. Although our patients reported no visual symptoms, it is unclear whether these areas of endothelial damage are of visual consequence; our patients had decreased visual acuity from other ocular pathology. However, in our patient with Fuchs endothelial dystrophy with a low functional endothelial cell reserve, it is possible that the damage could have resulted in additional cell loss, jamaophthalmology.com
Figure. Endothelial Circles After Nd:YAG Posterior Capsulotomy A
B
C
A, Circular endothelial lesions corresponding to the treatment area of posterior capsulotomy. B, The open, circular posterior capsule. C, Endothelial circles with a cruciate orientation, corresponding to a cruciate posterior capsulotomy.
worsening or hastening the onset of corneal edema. Nonetheless, this is an additional reminder to use only the minimal energy required and only precisely focused laser energy with the Nd:YAG laser. Shivali A. Menda, MD David Palay, MD Stephen McLeod, MD Author Affiliations: Department of Ophthalmology, University of California, San Francisco (Menda, McLeod); Atlanta Ophthalmology Associates, Atlanta, Georgia (Palay); Francis I. Proctor Foundation, University of California, San Francisco (McLeod). Corresponding Author: Stephen McLeod, MD, Department of Ophthalmology and Francis I. Proctor Foundation, University of California, San Francisco, 10 Koret Way, San Francisco, CA 94143 ([email protected]). Published Online: October 30, 2014. doi:10.1001/jamaophthalmol.2014.4289. Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported. (Reprinted) JAMA Ophthalmology February 2015 Volume 133, Number 2
Copyright 2015 American Medical Association. All rights reserved.
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221
Letters
Additional Contributions: Ashley Brito, BA, Department of Ophthalmology, University of California, San Francisco, photographed the endothelial lesions and Sarah DeParis, MD, Department of Ophthalmology, University of California, San Francisco, helped in creating the figure; they received no compensation for these contributions. 1. Slomovic AR, Parrish RK II, Forster RK, Cubillas A. Neodymium-YAG laser posterior capsulotomy: central corneal endothelial cell density. Arch Ophthalmol. 1986;104(4):536-538. 2. Vaikoussis E, Bisogiannis Z, Margaritis L. Corneal endothelial damage after Nd:YAG laser anterior capsulotomy: an experimental study on rabbits. Doc Ophthalmol. 1993;83(4):279-286. 3. Kerr Muir MG, Sherrard ES. Damage to the corneal endothelium during Nd/YAG photodisruption. Br J Ophthalmol. 1985;69(2):77-85. 4. Channell MM, Beckman H. Intraocular pressure changes after neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol. 1984;102(7): 1024-1026. 5. Aslam TM, Devlin H, Dhillon B. Use of Nd:YAG laser capsulotomy. Surv Ophthalmol. 2003;48(6):594-612. 6. Bath PE, Hoffer KJ, Aron-Rosa D, Dang Y. Glare disability secondary to YAG laser intraocular lens damage. J Cataract Refract Surg. 1987;13(3):309-313.
Presumed Bee Stinger Retained Intraocularly in the Absence of Inflammation There are multiple reports in the literature describing ocular trauma due to bee and wasp stings, and most of the complications are caused by either venom or the local inflammatory reaction, 1 potentially leading to corneal edema, uveitis, cataract,1,2 and, less frequently, optic neuritis.3 Although there are controversies in the management of retained bee stingers, surgical removal is usually indicated.4 We report an unusual case of a presumed intraocular bee stinger embedded in the lens for 5 years with surrounding cataract but no signs of intraocular inflammation. Report of a Case | A man in his late 50s presented to the local eye clinic after being invited to an ophthalmological examination for a population-based survey on prevalence of blindness. He was satisfied with his visual acuity and reported a slight decrease in the upper visual field of his left eye. His bestcorrected distance visual acuity was 20/20 OD and 20/32 OS; intraocular pressure was 10 mm Hg OD and 12 mm Hg OS. On slitlamp examination, the right eye showed only a small pin-
guecula. His left eye also showed a pinguecula, no signs of conjunctival hyperemia, a mild paracentral corneal opacification, and an intraocular foreign body embedded in the lens and touching the upper temporal pupil border (Figure 1A). There were no signs of anterior chamber inflammatory reaction. After instillation of tropicamide, 1%, and phenylephrine hydrochloride, 10%, we observed that the surrounding lens was opaque (Figure 1B). Once we noticed the intraocular foreign body, we asked him whether he had a history of ocular trauma. He reported that 5 years earlier, he had gotten multiple bee stings while riding a horse in the local rural area. At that time, he had severe pain and traveled to the next nearest eye clinic. The local ophthalmologist removed multiple stingers from both eyes and prescribed topical drugs; the patient felt better a few days later and never returned for an ocular evaluation. Optical coherence tomographic images (iVue 100; Optovue) of the anterior chamber demonstrated stromal opacification of the cornea presumably at the stinger inoculation site (Figure 2A). The presumed stinger reached 1.04 mm into the anterior chamber (Figure 2B), while its intralenticular part could not be adequately measured. Discussion | This presumed stinger is most likely from Apis mellifera (Vera Lucia Imperatriz-Fonseca, PhD, written communication, November 20, 2013); surgical removal of the stinger and further analysis could confirm this hypothesis. Apis bees, Pogonomyrmex ants, and multiple wasps have a barbed sting lancet and are able to perform sting autotomy, the selfamputation of the stinger and poison sac (which remain in their target) as a form of self-defense from vertebrate predators.5 Considering the stinger’s dimensions and the patient’s corneal thickness (594 μm centrally) and anterior chamber depth, it is unclear how the stinger became embedded in the lens. One possible explanation is an indentation of the globe at the moment of trauma, temporarily reducing its axial dimension. To our knowledge, this is only the second report in the literature of a presumed innocuous intraocular bee stinger attached to the lens1 and the first time that optical coherence tomographic images were used to analyze the presumed stinger.
Figure 1. Clinical Photographs Showing Presumed Bee Stinger A
B
A, Presumed bee stinger (arrowhead). B, Bee stinger with associated lens opacification (arrowhead), after instillation of mydriatic agents. Images were captured with an iPhone 5 (Apple Inc) in front of the slitlamp optics. 222
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