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Volume 19 Number 3 / June 2015 2. Peterson EC, Elhammady MS, Quintero-Wolfe S, Murray TG, Aziz-Sultan MA. Selective ophthalmic artery infusion of chemotherapy for advanced intraocular retinoblastoma: initial experience with 17 tumors. J Neurosurg 2011;114:1603-8. 3. Gobin YP, Dunkel IJ, Marr BP, Brodie SE, Abramson DH. Intraarterial chemotherapy for the management of retinoblastoma: fouryear experience. Arch Ophthalmol 2011;129:732-7. 4. Muen WJ, Kingston JE, Robertson F, Brew S, Sagoo MS, Reddy MA. Efficacy and complications of super-selective intra-ophthalmic artery melphalan for the treatment of refractory retinoblastoma. Ophthalmology 2012;119:611-16. 5. Abramson DH, Marr BP, Brodie SE, et al. Intraocular hemorrhage after intra-arterial chemotherapy for retinoblastoma in sickle cell trait. Open Ophthalmol J 2012;6:1-3. 6. Shields CL, Bianciotto CG, Jabbour P, et al. Intra-arterial chemotherapy for retinoblastoma: report no. 2, treatment complications. Arch Ophthalmol 2011;129:1407-15. 7. Tse BC, Steinle JJ, Johnson D, Haik BG, Wilson MW. Superselective intraophthalmic artery chemotherapy in a nonhuman primate model: histopathologic findings. JAMA Ophthalmol 2013;131:903-11. 8. Abramson DH. Chemosurgery for retinoblastoma: what we know after 5 years. Arch Ophthalmol 2011;129:1492-4. 9. Inomata M, Kaneko A. Chemosensitivity profiles of primary and cultured human retinoblastoma cells in a human tumor clonogenic assay. Jpn J Cancer Res 1987;78:858-68. 10. Jabbour P, Chalouhi N, Tjoumakaris S, et al. Pearls and pitfalls of intraarterial chemotherapy for retinoblastoma. J Neurosurg Pediatr 2012;10:175-81.
Retinal vein-to-vein anastomoses in Sturge-Weber syndrome documented by ultra-widefield fluorescein angiography Ann V. Quan, BS,a Grant H. Moore, MD,b and Irena Tsui, MDc FIG 2. A, Staining of retinal tissue section (hematoxylin and eosin, original magnification 40). Subretinal tumor with areas of calcification and necrosis and an overlying retinal detachment. The tumor extends to the prelaminar optic nerve with vitreous seeding noted. B, Staining of retinal tissue section (hematoxylin and eosin, original magnification 100). Prelaminar extension of the tumor is shown in high power magnification with a retained preretinal hemorrhage and notable areas (approximately 20%) of persistently viable tumor.
with laminar flow. Pulsatile infusion of the drug then leads to vacillating perfusion pressures within the vessels, which yields more homogeneous drug concentrations but probable damage to already fragile blood vessels.2 The net result of these hemorrhages is impaired monitoring for viable tumor and impeded laser photocoagulation. As such, post-IAC hemorrhage appears to be an early risk factor for IAC treatment failure. References 1. Yamane T, Kaneko A, Mohri M. The technique of ophthalmic arterial infusion therapy for patients with intraocular retinoblastoma. Int J Clin Oncol 2004;9:69-73.
We report the case of a 6-year-old boy with Sturge-Weber syndrome and unilateral glaucoma in his left eye. He was born with a port wine mark involving his upper left eyelid. On ultra-widefield fluorescein angiography, he was found to have several vein-to-vein anastomoses in his left retina. To our knowledge, this is the first documentation of retinal vein-to-vein anastomoses in Sturge-Weber syndrome.
Author affiliations: aCharles R. Drew University of Medicine & Science, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, CA; bJules Stein Eye Institute, University of California–Los Angeles; cPediatric and Adult Retina, Stein Doheny Eye Institute, University of California–Los Angeles Presented at the Annual Meeting of the Association of Pediatric Retina Specialists, Cabo San Lucas, Mexico, February 13-15, 2014. Submitted September 4, 2014. Revision accepted January 17, 2015. Published online May 2, 2015. Correspondence: Irena Tsui, MD, 100 Stein Plaza, Los Angeles, CA 90095 (email: [email protected]). J AAPOS 2015;19:270-272. Copyright Ó 2015 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.01.014
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FIG 1. Ultra-widefield retinal imaging of the left eye. A, Fundus photograph. B, Fluorescein angiogram. C, Early phase fluorescein angiogram. Arrows are pointing to the venous-to-venous anastomoses.
Case Report
A
6-year-old boy diagnosed with Sturge-Weber syndrome was born with a large port wine mark that involved his upper left eyelid in an area concurrent with the V1 nerve distribution. He had received multiple pulsed dye laser treatments with cosmetic improvement. He had been followed by a neurologist since birth and had undergone serial magnetic resonance imaging, none of which had shown evidence of leptomeningeal involvement. The patient also had unilateral glaucoma in his left eye, for which he was treated with dorzolamide 1drop 3 times daily. On examination at Stein Eye Institute, his visual acuity was 20/30 in the right eye and 20/40 in the left eye. Intraocular pressure (IOP) was measured at18 mm Hg in the right eye and 20 mm Hg in the left eye. Gonioscopy revealed open angles in both eyes. Dilated fundus examination was remarkable for increased cupping of the optic disk in the left eye. On ultra-widefield fluorescein angiography (Optos, Dunfermline, Scotland), the patient was noted to have several vein-to-vein anastomoses and retinal venous dilatation and tortuosity in his left fundus (Figure 1). Color photographs and intravenous fluorescein angiography photographs of the normal right fundus are provided for comparison (Figure 2).
Discussion Nevus flammeus, or port wine mark, is a congenital capillary malformation that occurs in approximately 0.3% of newborns.1 The skin lesions are characterized by macular, nonpalpable marks with a dark red color.1 The pathogenesis of port wine marks is unclear; however, the incidence of Sturge-Weber syndrome is approximately 3% to 6% in patients with a facial port wine mark, with an increased risk with involvement of the V1 nerve distribution.2,3 Sturge-Weber syndrome is defined by the concurrent presentation of facial port wine mark, ipsilateral leptomeningeal vascular malformation with associated mental and neurological deficits, and increased IOP.2-4
Journal of AAPOS
FIG 2. Ultra-widefield retinal imaging of the normal right eye. A, Fundus photograph. B, Fluorescein angiogram.
We present a 6-year-old boy with the Sturge-Weber syndrome who had left-side facial port wine mark, ipsilateral glaucoma, and retinal vein-to-vein malformations. Hennedige and colleagues2 demonstrated that in patients with involvement of only the V1 dermatome, the risk of glaucoma is 6.7% and the risk of the Sturge-Weber syndrome is 26.7 percent. The literature shows that port wine marks can be associated with retinal arteriovenous malformations and
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also retinal venous malformations.4-7 Ward and Katz reported a 17-year-old female with nevus flammeus, seizures, and calcification associated with an arteriovenous malformation in her parieto-occipital lobe, classic for Sturge-Weber syndrome.5 She also had ipsilateral retinal arteriovenous anastomoses consistent with WyburnMason syndrome. Shin and Demer reported a 7-year-old girl with ipsilateral nevus flammeus, glaucoma, retinal arteriovenous anastomoses, facial hypertrophy, and cafe-au-lait spots.6 Mehney documented tortuous retinal vein-to-vein communications in a patient with nevus flammeus associated with chronic glaucoma.7 To the best of our knowledge, this report is the first to document retinal vein-to-vein anastomoses in Sturge-Weber syndrome on UWFFA. UWFFA is a noncontact high-resolution, widefield imaging tool that allows 80% of the retinal vasculature to be captured; it may prove an important modality for detecting retinal vascular malformations in patients with the Sturge-Weber syndrome. Port wine marks are thought to result from postcapillary venule ectasias,8 and several mechanisms for their development have been hypothesized, including lack of neuronal control of blood flow and overexpression of vascular endothelial growth factor.8,9 Shirley and colleagues10 identified a specific somatic mosaic activating mutation in the GNAQ gene in samples of affected tissue from 88% of participants (23 of 26) with Sturge-Weber syndrome and 92% of participants (12 of 13) with nonsyndromic port wine marks. The data indicates that there is an underlying mechanism for the SturgeWeber syndrome and nonsyndromic port wine marks and adds a molecular basis for a decades-old hypothesis regarding somatic mutations as the cause of the malformations.10 Recently Parsa4 proposed that port wine marks and the other vascular malformations of Sturge-Weber syndrome occur as part of the primary venous dysplasia and prenatal venous thrombo-occlusion rather than neural dysfunction. According to this hypothesis, occlusion leads to impaired drainage and congestion in the area drained by the vein in question. In our patient, we hypothesize occlusion of the superior ophthalmic vein distal to its drainage into the cavernous sinus contributed to congestion of cutaneous venules forming a port wine mark, episcleral veins contributing to increased IOP, and branch retinal veins leading to vein-to-vein anastomoses. The presence of venous anastomoses in the retina suggests uneven venous pressure draining differentials, with the superior ophthalmic venous pressure being higher than that of the inferior ophthalmic vein.
Literature Search The PubMed Central and MEDLINE database were searched (1974 to present) using the following terms: Sturge-Weber syndrome and retina. References 1. Jacobs AH, Walton RG. The incidence of birthmarks in the neonate. Pediatrics 1976;58:218-22.
Volume 19 Number 3 / June 2015 2. Hennedige AA, Quaba AA, Al-Nakib K. Sturge-Weber syndrome and dermatomal facial port-wine stains: incidence, association with glaucoma, and pulsed tunable dye laser treatment effectiveness. Plast and Recons Surg 2008;121:1173-80. 3. Piram M, Lorette G, Sirinelli D, Herbreteau D, Giraudeau B, Maruani A. Sturge-Weber syndrome in patients with facial portwine stain. Pediatr Dermatol 2012;29:32-7. 4. Parsa CF. Focal venous hypertension as a pathophysiologic mechanism for tissue hypertrophy, port-wine stains, the Sturge-Weber Syndrome, and related disorders: proof of concept with novel hypothesis for underlying etiological cause. Trans Am Ophthalmol Soc 2013;111:180-202. 5. Ward JB, Katz NN. Combined phakomatoses: a case report of Sturge-Weber and Wyburn-Mason syndrome occurring in the same individual. Ann Ophthalmol 1983;15:1112-16. 6. Shin GS, Demer JL. Retinal arteriovenous communications associated with features of the Sturge-Weber syndrome. Am J Ophthalmol 1994;117:115-17. 7. Mehney GH. Naevus flammeus associated with glaucoma: report of a case. Arch Ophthalmol 1937;17:1018-23. 8. Chang CJ, Yu JS, Nelson JS. Confocal microscopy study of neurovascular distribution in facial port wine stains (capillary malformation). J Formos Med Assoc 2008;107:559. 9. Vural E, Ramakrishnan J, Cetin N, et al. The expression of vascular endothelial growth factor and its receptors in port-wine stains. Otolaryngol Head Neck Surg 2008;139:560-64. 10. Shirley MD, Tang H, Gallione CJ, et al. Sturge-Weber syndrome and port-wine stains caused by somatic mutation in GNAQ. N Engl J Med 2013;368:1971-9.
Pediatric adenoid cystic carcinoma of the lacrimal gland treated with intra-arterial cytoreductive chemotherapy Amaka Eneh, MD,a Kami Parsa, MD,b Kenneth W. Wright, MD,c and Yi Ning J. Strube, MD, FRCSCa Adenoid cystic carcinoma (ACC) of the lacrimal gland is the most common primary malignant tumor of the lacrimal gland. It typically affects patients in the fifth decade of life and presents with rapid progression of pain, ptosis, motility disturbances, and sensory deficits of less than 1 year’s duration. ACC is rare in children. Due to early,
Author affiliations: aDepartment of Ophthalmology, Hotel Dieu Hospital, Queen’s University, Kingston, Ontario, Canada; bCedars-Sinai Medical Center, Los Angeles, California; cWright Foundation for Pediatric Ophthalmology, Los Angeles, California, United States of America Presented at the International Pediatric Ophthalmology and Strabismus (IPOS IV) meeting, Chicago, Illinois, October 15, 2010. Submitted July 29, 2014. Revision accepted January 18, 2015. Published online April 15, 2015. Correspondence: Yi Ning J. Strube, MD, MS, FRCSC, DABO, 166 Brock Street, Department of Ophthalmology, Hotel Dieu Hospital, Kingston, Ontario, Canada (email: [email protected]). J AAPOS 2015;19:272-274. Copyright Ó 2015 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.01.016
Journal of AAPOS
Quan, Moore, and Tsui
Volume 19 Number 3 / June 2015 2. Peterson EC, Elhammady MS, Quintero-Wolfe S, Murray TG, Aziz-Sultan MA. Selective ophthalmic artery infusion of chemotherapy for advanced intraocular retinoblastoma: initial experience with 17 tumors. J Neurosurg 2011;114:1603-8. 3. Gobin YP, Dunkel IJ, Marr BP, Brodie SE, Abramson DH. Intraarterial chemotherapy for the management of retinoblastoma: fouryear experience. Arch Ophthalmol 2011;129:732-7. 4. Muen WJ, Kingston JE, Robertson F, Brew S, Sagoo MS, Reddy MA. Efficacy and complications of super-selective intra-ophthalmic artery melphalan for the treatment of refractory retinoblastoma. Ophthalmology 2012;119:611-16. 5. Abramson DH, Marr BP, Brodie SE, et al. Intraocular hemorrhage after intra-arterial chemotherapy for retinoblastoma in sickle cell trait. Open Ophthalmol J 2012;6:1-3. 6. Shields CL, Bianciotto CG, Jabbour P, et al. Intra-arterial chemotherapy for retinoblastoma: report no. 2, treatment complications. Arch Ophthalmol 2011;129:1407-15. 7. Tse BC, Steinle JJ, Johnson D, Haik BG, Wilson MW. Superselective intraophthalmic artery chemotherapy in a nonhuman primate model: histopathologic findings. JAMA Ophthalmol 2013;131:903-11. 8. Abramson DH. Chemosurgery for retinoblastoma: what we know after 5 years. Arch Ophthalmol 2011;129:1492-4. 9. Inomata M, Kaneko A. Chemosensitivity profiles of primary and cultured human retinoblastoma cells in a human tumor clonogenic assay. Jpn J Cancer Res 1987;78:858-68. 10. Jabbour P, Chalouhi N, Tjoumakaris S, et al. Pearls and pitfalls of intraarterial chemotherapy for retinoblastoma. J Neurosurg Pediatr 2012;10:175-81.
Retinal vein-to-vein anastomoses in Sturge-Weber syndrome documented by ultra-widefield fluorescein angiography Ann V. Quan, BS,a Grant H. Moore, MD,b and Irena Tsui, MDc FIG 2. A, Staining of retinal tissue section (hematoxylin and eosin, original magnification 40). Subretinal tumor with areas of calcification and necrosis and an overlying retinal detachment. The tumor extends to the prelaminar optic nerve with vitreous seeding noted. B, Staining of retinal tissue section (hematoxylin and eosin, original magnification 100). Prelaminar extension of the tumor is shown in high power magnification with a retained preretinal hemorrhage and notable areas (approximately 20%) of persistently viable tumor.
with laminar flow. Pulsatile infusion of the drug then leads to vacillating perfusion pressures within the vessels, which yields more homogeneous drug concentrations but probable damage to already fragile blood vessels.2 The net result of these hemorrhages is impaired monitoring for viable tumor and impeded laser photocoagulation. As such, post-IAC hemorrhage appears to be an early risk factor for IAC treatment failure. References 1. Yamane T, Kaneko A, Mohri M. The technique of ophthalmic arterial infusion therapy for patients with intraocular retinoblastoma. Int J Clin Oncol 2004;9:69-73.
We report the case of a 6-year-old boy with Sturge-Weber syndrome and unilateral glaucoma in his left eye. He was born with a port wine mark involving his upper left eyelid. On ultra-widefield fluorescein angiography, he was found to have several vein-to-vein anastomoses in his left retina. To our knowledge, this is the first documentation of retinal vein-to-vein anastomoses in Sturge-Weber syndrome.
Author affiliations: aCharles R. Drew University of Medicine & Science, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, CA; bJules Stein Eye Institute, University of California–Los Angeles; cPediatric and Adult Retina, Stein Doheny Eye Institute, University of California–Los Angeles Presented at the Annual Meeting of the Association of Pediatric Retina Specialists, Cabo San Lucas, Mexico, February 13-15, 2014. Submitted September 4, 2014. Revision accepted January 17, 2015. Published online May 2, 2015. Correspondence: Irena Tsui, MD, 100 Stein Plaza, Los Angeles, CA 90095 (email: [email protected]). J AAPOS 2015;19:270-272. Copyright Ó 2015 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.01.014
Journal of AAPOS
Volume 19 Number 3 / June 2015
Quan, Moore, and Tsui
271
FIG 1. Ultra-widefield retinal imaging of the left eye. A, Fundus photograph. B, Fluorescein angiogram. C, Early phase fluorescein angiogram. Arrows are pointing to the venous-to-venous anastomoses.
Case Report
A
6-year-old boy diagnosed with Sturge-Weber syndrome was born with a large port wine mark that involved his upper left eyelid in an area concurrent with the V1 nerve distribution. He had received multiple pulsed dye laser treatments with cosmetic improvement. He had been followed by a neurologist since birth and had undergone serial magnetic resonance imaging, none of which had shown evidence of leptomeningeal involvement. The patient also had unilateral glaucoma in his left eye, for which he was treated with dorzolamide 1drop 3 times daily. On examination at Stein Eye Institute, his visual acuity was 20/30 in the right eye and 20/40 in the left eye. Intraocular pressure (IOP) was measured at18 mm Hg in the right eye and 20 mm Hg in the left eye. Gonioscopy revealed open angles in both eyes. Dilated fundus examination was remarkable for increased cupping of the optic disk in the left eye. On ultra-widefield fluorescein angiography (Optos, Dunfermline, Scotland), the patient was noted to have several vein-to-vein anastomoses and retinal venous dilatation and tortuosity in his left fundus (Figure 1). Color photographs and intravenous fluorescein angiography photographs of the normal right fundus are provided for comparison (Figure 2).
Discussion Nevus flammeus, or port wine mark, is a congenital capillary malformation that occurs in approximately 0.3% of newborns.1 The skin lesions are characterized by macular, nonpalpable marks with a dark red color.1 The pathogenesis of port wine marks is unclear; however, the incidence of Sturge-Weber syndrome is approximately 3% to 6% in patients with a facial port wine mark, with an increased risk with involvement of the V1 nerve distribution.2,3 Sturge-Weber syndrome is defined by the concurrent presentation of facial port wine mark, ipsilateral leptomeningeal vascular malformation with associated mental and neurological deficits, and increased IOP.2-4
Journal of AAPOS
FIG 2. Ultra-widefield retinal imaging of the normal right eye. A, Fundus photograph. B, Fluorescein angiogram.
We present a 6-year-old boy with the Sturge-Weber syndrome who had left-side facial port wine mark, ipsilateral glaucoma, and retinal vein-to-vein malformations. Hennedige and colleagues2 demonstrated that in patients with involvement of only the V1 dermatome, the risk of glaucoma is 6.7% and the risk of the Sturge-Weber syndrome is 26.7 percent. The literature shows that port wine marks can be associated with retinal arteriovenous malformations and
272
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also retinal venous malformations.4-7 Ward and Katz reported a 17-year-old female with nevus flammeus, seizures, and calcification associated with an arteriovenous malformation in her parieto-occipital lobe, classic for Sturge-Weber syndrome.5 She also had ipsilateral retinal arteriovenous anastomoses consistent with WyburnMason syndrome. Shin and Demer reported a 7-year-old girl with ipsilateral nevus flammeus, glaucoma, retinal arteriovenous anastomoses, facial hypertrophy, and cafe-au-lait spots.6 Mehney documented tortuous retinal vein-to-vein communications in a patient with nevus flammeus associated with chronic glaucoma.7 To the best of our knowledge, this report is the first to document retinal vein-to-vein anastomoses in Sturge-Weber syndrome on UWFFA. UWFFA is a noncontact high-resolution, widefield imaging tool that allows 80% of the retinal vasculature to be captured; it may prove an important modality for detecting retinal vascular malformations in patients with the Sturge-Weber syndrome. Port wine marks are thought to result from postcapillary venule ectasias,8 and several mechanisms for their development have been hypothesized, including lack of neuronal control of blood flow and overexpression of vascular endothelial growth factor.8,9 Shirley and colleagues10 identified a specific somatic mosaic activating mutation in the GNAQ gene in samples of affected tissue from 88% of participants (23 of 26) with Sturge-Weber syndrome and 92% of participants (12 of 13) with nonsyndromic port wine marks. The data indicates that there is an underlying mechanism for the SturgeWeber syndrome and nonsyndromic port wine marks and adds a molecular basis for a decades-old hypothesis regarding somatic mutations as the cause of the malformations.10 Recently Parsa4 proposed that port wine marks and the other vascular malformations of Sturge-Weber syndrome occur as part of the primary venous dysplasia and prenatal venous thrombo-occlusion rather than neural dysfunction. According to this hypothesis, occlusion leads to impaired drainage and congestion in the area drained by the vein in question. In our patient, we hypothesize occlusion of the superior ophthalmic vein distal to its drainage into the cavernous sinus contributed to congestion of cutaneous venules forming a port wine mark, episcleral veins contributing to increased IOP, and branch retinal veins leading to vein-to-vein anastomoses. The presence of venous anastomoses in the retina suggests uneven venous pressure draining differentials, with the superior ophthalmic venous pressure being higher than that of the inferior ophthalmic vein.
Literature Search The PubMed Central and MEDLINE database were searched (1974 to present) using the following terms: Sturge-Weber syndrome and retina. References 1. Jacobs AH, Walton RG. The incidence of birthmarks in the neonate. Pediatrics 1976;58:218-22.
Volume 19 Number 3 / June 2015 2. Hennedige AA, Quaba AA, Al-Nakib K. Sturge-Weber syndrome and dermatomal facial port-wine stains: incidence, association with glaucoma, and pulsed tunable dye laser treatment effectiveness. Plast and Recons Surg 2008;121:1173-80. 3. Piram M, Lorette G, Sirinelli D, Herbreteau D, Giraudeau B, Maruani A. Sturge-Weber syndrome in patients with facial portwine stain. Pediatr Dermatol 2012;29:32-7. 4. Parsa CF. Focal venous hypertension as a pathophysiologic mechanism for tissue hypertrophy, port-wine stains, the Sturge-Weber Syndrome, and related disorders: proof of concept with novel hypothesis for underlying etiological cause. Trans Am Ophthalmol Soc 2013;111:180-202. 5. Ward JB, Katz NN. Combined phakomatoses: a case report of Sturge-Weber and Wyburn-Mason syndrome occurring in the same individual. Ann Ophthalmol 1983;15:1112-16. 6. Shin GS, Demer JL. Retinal arteriovenous communications associated with features of the Sturge-Weber syndrome. Am J Ophthalmol 1994;117:115-17. 7. Mehney GH. Naevus flammeus associated with glaucoma: report of a case. Arch Ophthalmol 1937;17:1018-23. 8. Chang CJ, Yu JS, Nelson JS. Confocal microscopy study of neurovascular distribution in facial port wine stains (capillary malformation). J Formos Med Assoc 2008;107:559. 9. Vural E, Ramakrishnan J, Cetin N, et al. The expression of vascular endothelial growth factor and its receptors in port-wine stains. Otolaryngol Head Neck Surg 2008;139:560-64. 10. Shirley MD, Tang H, Gallione CJ, et al. Sturge-Weber syndrome and port-wine stains caused by somatic mutation in GNAQ. N Engl J Med 2013;368:1971-9.
Pediatric adenoid cystic carcinoma of the lacrimal gland treated with intra-arterial cytoreductive chemotherapy Amaka Eneh, MD,a Kami Parsa, MD,b Kenneth W. Wright, MD,c and Yi Ning J. Strube, MD, FRCSCa Adenoid cystic carcinoma (ACC) of the lacrimal gland is the most common primary malignant tumor of the lacrimal gland. It typically affects patients in the fifth decade of life and presents with rapid progression of pain, ptosis, motility disturbances, and sensory deficits of less than 1 year’s duration. ACC is rare in children. Due to early,
Author affiliations: aDepartment of Ophthalmology, Hotel Dieu Hospital, Queen’s University, Kingston, Ontario, Canada; bCedars-Sinai Medical Center, Los Angeles, California; cWright Foundation for Pediatric Ophthalmology, Los Angeles, California, United States of America Presented at the International Pediatric Ophthalmology and Strabismus (IPOS IV) meeting, Chicago, Illinois, October 15, 2010. Submitted July 29, 2014. Revision accepted January 18, 2015. Published online April 15, 2015. Correspondence: Yi Ning J. Strube, MD, MS, FRCSC, DABO, 166 Brock Street, Department of Ophthalmology, Hotel Dieu Hospital, Kingston, Ontario, Canada (email: [email protected]). J AAPOS 2015;19:272-274. Copyright Ó 2015 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.01.016
Journal of AAPOS
