A CASE OF VASOPROLIFERATIVE RETINAL TUMOR COMPLICATED BY NEOVASCULAR GLAUCOMA Yosuke Nakamura, MD, PhD,* Norio Takeda, MD, PhD,* Makoto Mochizuki, MD, PhD†
Purpose: To report a case of vasoproliferative retinal tumor complicated by neovascular glaucoma that showed remission after vitrectomy surgery to remove the tumor. Methods: A 78-year-old man was referred to the hospital with a complaint of visual loss in his right eye. Corrected visual acuity was 0.5 in the right eye and 1.2 in the left eye. The right eye showed mild vitreous hemorrhage and an elevated lesion in the lower fundus. Fluorescein angiography demonstrated leakage from the tumor, and a 4-mm lesion of high density was seen on computed tomography, and we diagnosed it as retinal capillary hemangioma. In this case, von Hippel–Lindau disease was negative. During the course of the disease, peripheral anterior synechia and neovascularization was seen in the iris and angle, and vitreous surgery was enforced to remove the tumor because of increased intraocular pressure. The tumor was removed as almost one mass. Histologically, the tumor was composed of glial cells and small vessels proliferation. We diagnosed vasoproliferative retinal tumor. Results: Seven months after surgery, the intraocular pressure stabilized, and neovascularization of the iris and angle disappeared. Visual acuity was 0.03 due to epiretinal membrane and optic atrophy. There were no signs of recurrence. Conclusion: The vitreous surgery is one of the effective treatment methods against vasoproliferative retinal tumor complicated by neovascular glaucoma. RETINAL CASES & BRIEF REPORTS 7:338–342, 2013
From the Departments of *Ophthalmology and †Pathology, Hospital, National Center for Global Health and Medicine, Tokyo, Japan.
Case Report We report the case of a 78-year-old man whose chief complaint was reduced visual acuity on the right eye. In February 2009, the patient became aware of reduced visual acuity on the right eye and consulted the Department of Ophthalmology, Hospital, National Center for Global Health and Medicine. The patient’s history of ocular disease was not noteworthy. Approximately 1 year previously, he began to receive corticosteroid therapy for polymyalgia rheumatica. He was additionally taking a hypotensive drug for the treatment of hypertension. He had untreated thoracic aortic aneurysm. His family history was not informative. The findings during the first visit was that his visual acuity was 0.5 on the right eye and 1.2 on the left eye, and intraocular pressure (IOP) was 15 mmHg on the right eye and 16 mmHg on the left eye. His right eye was found to have posterior subcapsular cataract, vitreous hemorrhage of severity not masking the fundus, and yellow-white elevation lesion in the lower retinal periphery (Figure 1). The left eye was free of abnormalities. When fluorescein angiography was performed, the shadow of tumor vessels, probably representing vessels entering the tumor, was not clear, but leakage of fluorescein was noted to be consistent with the yellow-white elevated lesion of the lower retinal periphery (Figure 2). In addition, a high-density nodule, being 4 mm in diameter and showing intense contrast enhancement, was revealed
V
asoproliferative retinal tumor1 is a proliferative disease involving vessels of a nontumorous nature. According to our literature search, no case of vasoproliferative retinal tumor complicated by neovascular glaucoma (NVG) has been reported. We recently encountered a case of acquired vasoproliferative retinal tumor complicated by NVG where the tumor was removed by vitreous surgery, resulting in NVG to settle down. This case report is presented in this study.
The authors have no financial or conflicts of interest to disclose. Reprint requests: Yosuke Nakamura, MD, Department of Ophthalmology, Hospital, National Center for Global Health and Medicine. 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan; e-mail: [email protected]
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Fig. 1. Fundus photographs during the first visit; A, postpolar; B, lower retinal periphery. His right eye was found to have mild vitreous hemorrhage and yellow-white elevation lesion in the lower retinal periphery.
by computed tomography, suggesting retinal hemangioma (Figure 3). Because the abnormality was unilateral and because the patient had no systemic symptom or no positive family history, von Hippel–Lindau disease was considered unlikely, and the patient seemed to have solitary acquired retinal capillary hemangioma. Because vitreous hemorrhage showed no tendency for exacerbation and the patient had no desire to undergo surgery, we followed the patient without active treatment. In December 2009, formation of new vessels along the full circumference of the iris and formation of vessels in part of the angle and peripheral anterior synechia were noted (Figure 4). Carotid artery ultrasonography revealed no abnormality, allowing us to rule out ocular ischemic syndrome. Because IOP remained within the normal range and the patient did not desire surgery, the patient was followed without active treatment. Later, observation of the fundus became difficult because of iris posterior synechia and progression of the severity of posterior subcapsular cataract. The patient thus underwent cataract surgery in February 2010. After cataract surgery, his visual acuity improved to 0.5, and vitreous hemorrhage tended to be absorbed. Fluorescein angiography, conducted at that time, revealed nonperfusion area or no sign of vasculitis, although leakage of fluorescein from the hemangioma was noted. Intraocular pressure subsequently rose gradually, reaching 38 mmHg in April 2010. At that time, formation of new vessels along the full iris and peripheral anterior synechia along the full angle appeared. For this reason, surgical freeing of angular adhesion and vitreous surgery for removal of the tumor were carried out in May 2010. The operation, using a 23-gauge system, removed the tumor almost en bloc. Immediately before and after removal, the tumor and its surrounding retinal tissue were photocoagulated, and endodiathermy was then performed on the tortuous vessels feeding the tumor. The
Fig. 2. Fluorescein angiography during the first visit; A, early stage; B, late stage. Leakage of fluorescein was noted to be consistent with the yellow-white elevated lesion of the lower retinal periphery.
Fig. 3. Findings of computed tomography. A high-density nodule, being 4 mm in diameter and showing intense contrast enhancement was revealed by computed tomography.
operation was completed after replacement with air. Histologically, the removed tissue showed mild vascular proliferation with mild inflammatory infiltrates, fibrin deposits, and glial cell proliferation. No marked vascular proliferation resembling hemangioma and no clear cells of hemangioblastoma were identified (Figure 5). One month after the surgery, the new vessels formed in the iris had subsided and IOP had stabilized in the normal range (Figure 6). As of December 2010, the visual acuity remained low (0.03) because of epiretinal membrane and optic atrophy, but fluorescein angiography revealed no leakage of fluorescein from the tumor stump (Figure 7). Intraocular pressure remained in the first half of the 10 to 19 mmHg range and the new vessels formed along the iris and angle also subsided. There were no signs of recurrence.
Fig. 4. Anterior segment photographs in December 2009. Formation of new vessels along the full circumference of the iris were noted.
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Fig. 5. Histological features of vasoproliferative retinal tumor. A. hematoxylin and eosin staining; B. glial fibrillary acidic protein. C. HE staining; D. glial fibrillary acidic protein. The removed tissue contained fibrin deposits interposed with inflammatory cells infiltrate glial fibrillary acidic protein negative as well as vascular gathering glial cells proliferation (glial fibrillary acidic protein positive) and vessels. C and D are high magnification of A and B. No marked vascular proliferation as hemangioma and no clear cells of hemangioblastoma were identified.
Discussion Vasoproliferative retinal tumor1 is a proliferative disease involving vessels of a nontumorous nature. Approximately 75% of cases are idiopathic, and 25% are secondary to other ocular diseases such as retinitis pigmentosa, uveitis, and congenital toxoplasmosis. Idiopathic vasoproliferative retinal tumor is unilateral and solitary, and the differential diagnosis includes retinal capillary hemangioma, the latter being divided into congenital and acquired types. Congenital retinal capillary hemangioma, accompanied by systemic symptoms such as cerebellar hemangioma, is a mani-
Fig. 6. Anterior segment photographs after surgery. The new vessels formed in the iris had subsided.
festation of von Hippel–Lindau syndrome; it is often bilateral, and its onset is familial in nature in 20% of cases. On the contrary, acquired retinal capillary hemangioma was first reported in 1983 by Shields et al2 as a unilateral, nonfamilial, and solitary disease. Unlike congenital retinal capillary hemangioma, vasoproliferative retinal tumor shows a comparatively gradual onset, and from the viewpoints of therapy, counseling, and prognosis, it is important to differentiate the two diseases. In 1995, Shields et al3 described a series of 129 vasoproliferative retinal tumors in 113 eyes of 103 patients, together with the associated ophthalmic diseases, clinical features, and treatment modalities. Although both discriminate from a fundus or clinical course in many cases, diagnostic resection was often performed and a final diagnosis was obtained by histopathology. The tumor consists mostly of glial cells interlaced with a fine capillary network and dilated hyalinized blood vessels, some of which are occluded.1,4 Exudates, macrophages, and foreign body giant cells are also present, and as the histology is not indicative of a “vasoproliferative” tumor, the term “reactionary retinal glioangiosis” has been proposed.4 In this case, the removed tissue contained fibrin deposits interposed by inflammatory cell infiltrates as well as vascular tangles and glial cell proliferation. These findings allowed a diagnosis of vasoproliferative retinal tumor discrete from retinal capillary hemangioma. Ocular complications reported in patients with vasoproliferative retinal tumor include vitreous hemorrhage, epiretinal membrane, and so on.1 According to our literature search, no cases of this disease complicated by NVG have been reported. Diseases possibly inducing NVG include diabetic retinopathy, retinal vein occlusion, ocular ischemic syndrome, aortitis syndrome,5 and so on. The patient in the present study was free of diabetes mellitus and fundus hemorrhage. Carotid artery ultrasonography revealed no abnormality, allowing us to rule out ocular ischemic syndrome. Although the patient had been taking corticosteroid for the treatment of polymyalgia rheumatica, he was free of other collagen disease and aortitis syndrome. It has been reported that patients with NVG secondary to diabetic retinopathy or retinal vein occlusion show elevation in ocular vascular endothelial growth factor (VEGF) level and appearance of new vessels in the iris and angle. Involvement of VEGF in retinal hemangioma has been reported,6 and hypoxiainducible factors are often expressed in retinal hemangioma associated with von Hippel–Lindau disease, resulting in induction of VEGF formation by hypoxiainducible factors. Also, in the patient in the present report, new vessels formed in the iris were subsiding
A CASE OF VRT COMPLICATED BY NVG
341
Fig. 7. Fundus photographs (top) and fluorescein angiography (bottom) after surgery. A. postpolar; B. lower retinal periphery; C. early stage; D. late stage. Epiretinal membrane and optic atrophy are presented. Fluorescein angiography reveals no leakage of fluorescein from the tumor stump. There are no sign of recurrence.
1 month after surgery, suggesting that NVG had been induced by VEGF formed in retinal hemangioma preoperatively. Methods used for the treatment of vasoproliferative retinal tumor include photocoagulation, cryopexy, photodynamic therapy,7 intravitreal of anti-VEGF antibody, and pars plana vitrectomy.8–10 According to some investigators,3 application of vitreous surgery for the treatment of this disease has been reported in cases complicated by vitreous hemorrhage or epiretinal membrane.In the present case, vitreous surgery was selected for the purpose of alleviating the accompanying vitreous hemorrhage and enabling definite diagnosis and subsequent treatment of retinal hemangioma by resection. Before the tumor was resected, the tumor itself and the surrounding tissue were adequately photocoagulated. Subsequently, the tumor was resected during careful diathermic coagulation. In this way, the operation could be carried out safely, with minimum intraoperative bleeding. Yeh et al.9 have reported a vasoproliferative retinal tumor in a 31-year-old woman who underwent pars plana vitrectomy and endoresection of the tumor. They performed confluent indirect laser irradiation for
360° around the tumor, followed by endodiathermy of the tortuous vessels feeding the tumor. Air–fluid exchange was then performed, followed by instillation of 16% C3F8 gas. At 9 months after surgery, there were no signs of recurrence and the course was favorable. Gaudric et al10 reported vitreoretinal surgery for severe retinal capillary hemangiomas associated with von Hippel–Lindau syndrome in 23 eyes of 21 patients. In 9 eyes, retinectomy was performed to remove the tumor; at 6 months after surgery, 5 of these eyes were blind, and 4 had NVG. In the present case study, visual acuity after treatment was low because of optic atrophy and the postoperative complication by epiretinal membrane. Patients developing epiretinal membrane after vitreous surgery for retinal hemangioma, like the patient in the study, have been reported previously.10 Because the patient we encountered in this study had no desire for epiretinal membrane surgery, we have been following the patient without active treatment of epiretinal membrane. As far as NVG in this case is concerned, the new vessels formed in the iris and angle are showing a tendency to subside, and IOP stabilized in the first half of the 10 to 19 mmHg range. Retinal hemangioma has not recurred
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in this case. In view of a report on a case where NVG developed several years after vitreous surgery for retinal hemangioma leading to blindness,10 we see the necessity of following this patient from now on, paying close attention to relapse of NVG. Key words: neovascular glaucoma, vasoproliferative retinal tumor, vascular endothelial growth factor, vitrectomy. References 1. Bertil D. Vasoproliferative retinal tumor. Br J Ophthalmol 2006;90:399–400. 2. Shields JA, Decker WL, Sanborn GE, et al. Presumed acquired retinal hemangiomas. Ophthalmology 1983;90:1292–1300. 3. Shields CL, Shields JA, Barrett J, De Potter P. Vasoproliferative tumors of the ocular fundus: classification and clinical manifestations in 103 patients. Arch Ophthalmol 1995;113:615–623.
4. Irvine F, O’Donnell N, Kemp E, Lee WR. Retinal vasoproliferative tumors: surgical management and histological findings. Arch Ophthalmol 2000;118:563–569. 5. Milea D, Cassoux N, Lehoang P, et al. Neovascular glaucoma after bypass surgery in Takayasu’s disease. Eye 1999;13: 786–789. 6. Chan CC, Vortmeyer AO, Chew EY, et al. VHL gene deletion and enhanced VEGF gene expression detected in the stromal cells of retinal angioma. Arch Ophthalmol 1999;117:625–630. 7. Chan RP, Lai TY. Photodynamic therapy with verteporfin for vasoproliferative tumor of the retina. Acta Ophthalmol 2010;88:711–712. 8. Gibran SK. Trans-vitreal endoresection for vasoproliferative retinal tumors. Clin Experiment Ophthalmol 2008;36:712–716. 9. Yeh S, Wilson DJ. Pars plana vitrectomy and endoresection of a retinal vasoproliferative tumor. Arch Ophthalmol 2010;128:1196–1199. 10. Gaudric A, Krivosic V, Duguid G, et al. Vitreoretinal surgery for severe retinal capillary hemangiomas in von Hippel-Lindau disease. Ophthalmology 2011;118:142–149.
Purpose: To report a case of vasoproliferative retinal tumor complicated by neovascular glaucoma that showed remission after vitrectomy surgery to remove the tumor. Methods: A 78-year-old man was referred to the hospital with a complaint of visual loss in his right eye. Corrected visual acuity was 0.5 in the right eye and 1.2 in the left eye. The right eye showed mild vitreous hemorrhage and an elevated lesion in the lower fundus. Fluorescein angiography demonstrated leakage from the tumor, and a 4-mm lesion of high density was seen on computed tomography, and we diagnosed it as retinal capillary hemangioma. In this case, von Hippel–Lindau disease was negative. During the course of the disease, peripheral anterior synechia and neovascularization was seen in the iris and angle, and vitreous surgery was enforced to remove the tumor because of increased intraocular pressure. The tumor was removed as almost one mass. Histologically, the tumor was composed of glial cells and small vessels proliferation. We diagnosed vasoproliferative retinal tumor. Results: Seven months after surgery, the intraocular pressure stabilized, and neovascularization of the iris and angle disappeared. Visual acuity was 0.03 due to epiretinal membrane and optic atrophy. There were no signs of recurrence. Conclusion: The vitreous surgery is one of the effective treatment methods against vasoproliferative retinal tumor complicated by neovascular glaucoma. RETINAL CASES & BRIEF REPORTS 7:338–342, 2013
From the Departments of *Ophthalmology and †Pathology, Hospital, National Center for Global Health and Medicine, Tokyo, Japan.
Case Report We report the case of a 78-year-old man whose chief complaint was reduced visual acuity on the right eye. In February 2009, the patient became aware of reduced visual acuity on the right eye and consulted the Department of Ophthalmology, Hospital, National Center for Global Health and Medicine. The patient’s history of ocular disease was not noteworthy. Approximately 1 year previously, he began to receive corticosteroid therapy for polymyalgia rheumatica. He was additionally taking a hypotensive drug for the treatment of hypertension. He had untreated thoracic aortic aneurysm. His family history was not informative. The findings during the first visit was that his visual acuity was 0.5 on the right eye and 1.2 on the left eye, and intraocular pressure (IOP) was 15 mmHg on the right eye and 16 mmHg on the left eye. His right eye was found to have posterior subcapsular cataract, vitreous hemorrhage of severity not masking the fundus, and yellow-white elevation lesion in the lower retinal periphery (Figure 1). The left eye was free of abnormalities. When fluorescein angiography was performed, the shadow of tumor vessels, probably representing vessels entering the tumor, was not clear, but leakage of fluorescein was noted to be consistent with the yellow-white elevated lesion of the lower retinal periphery (Figure 2). In addition, a high-density nodule, being 4 mm in diameter and showing intense contrast enhancement, was revealed
V
asoproliferative retinal tumor1 is a proliferative disease involving vessels of a nontumorous nature. According to our literature search, no case of vasoproliferative retinal tumor complicated by neovascular glaucoma (NVG) has been reported. We recently encountered a case of acquired vasoproliferative retinal tumor complicated by NVG where the tumor was removed by vitreous surgery, resulting in NVG to settle down. This case report is presented in this study.
The authors have no financial or conflicts of interest to disclose. Reprint requests: Yosuke Nakamura, MD, Department of Ophthalmology, Hospital, National Center for Global Health and Medicine. 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan; e-mail: [email protected]
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Fig. 1. Fundus photographs during the first visit; A, postpolar; B, lower retinal periphery. His right eye was found to have mild vitreous hemorrhage and yellow-white elevation lesion in the lower retinal periphery.
by computed tomography, suggesting retinal hemangioma (Figure 3). Because the abnormality was unilateral and because the patient had no systemic symptom or no positive family history, von Hippel–Lindau disease was considered unlikely, and the patient seemed to have solitary acquired retinal capillary hemangioma. Because vitreous hemorrhage showed no tendency for exacerbation and the patient had no desire to undergo surgery, we followed the patient without active treatment. In December 2009, formation of new vessels along the full circumference of the iris and formation of vessels in part of the angle and peripheral anterior synechia were noted (Figure 4). Carotid artery ultrasonography revealed no abnormality, allowing us to rule out ocular ischemic syndrome. Because IOP remained within the normal range and the patient did not desire surgery, the patient was followed without active treatment. Later, observation of the fundus became difficult because of iris posterior synechia and progression of the severity of posterior subcapsular cataract. The patient thus underwent cataract surgery in February 2010. After cataract surgery, his visual acuity improved to 0.5, and vitreous hemorrhage tended to be absorbed. Fluorescein angiography, conducted at that time, revealed nonperfusion area or no sign of vasculitis, although leakage of fluorescein from the hemangioma was noted. Intraocular pressure subsequently rose gradually, reaching 38 mmHg in April 2010. At that time, formation of new vessels along the full iris and peripheral anterior synechia along the full angle appeared. For this reason, surgical freeing of angular adhesion and vitreous surgery for removal of the tumor were carried out in May 2010. The operation, using a 23-gauge system, removed the tumor almost en bloc. Immediately before and after removal, the tumor and its surrounding retinal tissue were photocoagulated, and endodiathermy was then performed on the tortuous vessels feeding the tumor. The
Fig. 2. Fluorescein angiography during the first visit; A, early stage; B, late stage. Leakage of fluorescein was noted to be consistent with the yellow-white elevated lesion of the lower retinal periphery.
Fig. 3. Findings of computed tomography. A high-density nodule, being 4 mm in diameter and showing intense contrast enhancement was revealed by computed tomography.
operation was completed after replacement with air. Histologically, the removed tissue showed mild vascular proliferation with mild inflammatory infiltrates, fibrin deposits, and glial cell proliferation. No marked vascular proliferation resembling hemangioma and no clear cells of hemangioblastoma were identified (Figure 5). One month after the surgery, the new vessels formed in the iris had subsided and IOP had stabilized in the normal range (Figure 6). As of December 2010, the visual acuity remained low (0.03) because of epiretinal membrane and optic atrophy, but fluorescein angiography revealed no leakage of fluorescein from the tumor stump (Figure 7). Intraocular pressure remained in the first half of the 10 to 19 mmHg range and the new vessels formed along the iris and angle also subsided. There were no signs of recurrence.
Fig. 4. Anterior segment photographs in December 2009. Formation of new vessels along the full circumference of the iris were noted.
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Fig. 5. Histological features of vasoproliferative retinal tumor. A. hematoxylin and eosin staining; B. glial fibrillary acidic protein. C. HE staining; D. glial fibrillary acidic protein. The removed tissue contained fibrin deposits interposed with inflammatory cells infiltrate glial fibrillary acidic protein negative as well as vascular gathering glial cells proliferation (glial fibrillary acidic protein positive) and vessels. C and D are high magnification of A and B. No marked vascular proliferation as hemangioma and no clear cells of hemangioblastoma were identified.
Discussion Vasoproliferative retinal tumor1 is a proliferative disease involving vessels of a nontumorous nature. Approximately 75% of cases are idiopathic, and 25% are secondary to other ocular diseases such as retinitis pigmentosa, uveitis, and congenital toxoplasmosis. Idiopathic vasoproliferative retinal tumor is unilateral and solitary, and the differential diagnosis includes retinal capillary hemangioma, the latter being divided into congenital and acquired types. Congenital retinal capillary hemangioma, accompanied by systemic symptoms such as cerebellar hemangioma, is a mani-
Fig. 6. Anterior segment photographs after surgery. The new vessels formed in the iris had subsided.
festation of von Hippel–Lindau syndrome; it is often bilateral, and its onset is familial in nature in 20% of cases. On the contrary, acquired retinal capillary hemangioma was first reported in 1983 by Shields et al2 as a unilateral, nonfamilial, and solitary disease. Unlike congenital retinal capillary hemangioma, vasoproliferative retinal tumor shows a comparatively gradual onset, and from the viewpoints of therapy, counseling, and prognosis, it is important to differentiate the two diseases. In 1995, Shields et al3 described a series of 129 vasoproliferative retinal tumors in 113 eyes of 103 patients, together with the associated ophthalmic diseases, clinical features, and treatment modalities. Although both discriminate from a fundus or clinical course in many cases, diagnostic resection was often performed and a final diagnosis was obtained by histopathology. The tumor consists mostly of glial cells interlaced with a fine capillary network and dilated hyalinized blood vessels, some of which are occluded.1,4 Exudates, macrophages, and foreign body giant cells are also present, and as the histology is not indicative of a “vasoproliferative” tumor, the term “reactionary retinal glioangiosis” has been proposed.4 In this case, the removed tissue contained fibrin deposits interposed by inflammatory cell infiltrates as well as vascular tangles and glial cell proliferation. These findings allowed a diagnosis of vasoproliferative retinal tumor discrete from retinal capillary hemangioma. Ocular complications reported in patients with vasoproliferative retinal tumor include vitreous hemorrhage, epiretinal membrane, and so on.1 According to our literature search, no cases of this disease complicated by NVG have been reported. Diseases possibly inducing NVG include diabetic retinopathy, retinal vein occlusion, ocular ischemic syndrome, aortitis syndrome,5 and so on. The patient in the present study was free of diabetes mellitus and fundus hemorrhage. Carotid artery ultrasonography revealed no abnormality, allowing us to rule out ocular ischemic syndrome. Although the patient had been taking corticosteroid for the treatment of polymyalgia rheumatica, he was free of other collagen disease and aortitis syndrome. It has been reported that patients with NVG secondary to diabetic retinopathy or retinal vein occlusion show elevation in ocular vascular endothelial growth factor (VEGF) level and appearance of new vessels in the iris and angle. Involvement of VEGF in retinal hemangioma has been reported,6 and hypoxiainducible factors are often expressed in retinal hemangioma associated with von Hippel–Lindau disease, resulting in induction of VEGF formation by hypoxiainducible factors. Also, in the patient in the present report, new vessels formed in the iris were subsiding
A CASE OF VRT COMPLICATED BY NVG
341
Fig. 7. Fundus photographs (top) and fluorescein angiography (bottom) after surgery. A. postpolar; B. lower retinal periphery; C. early stage; D. late stage. Epiretinal membrane and optic atrophy are presented. Fluorescein angiography reveals no leakage of fluorescein from the tumor stump. There are no sign of recurrence.
1 month after surgery, suggesting that NVG had been induced by VEGF formed in retinal hemangioma preoperatively. Methods used for the treatment of vasoproliferative retinal tumor include photocoagulation, cryopexy, photodynamic therapy,7 intravitreal of anti-VEGF antibody, and pars plana vitrectomy.8–10 According to some investigators,3 application of vitreous surgery for the treatment of this disease has been reported in cases complicated by vitreous hemorrhage or epiretinal membrane.In the present case, vitreous surgery was selected for the purpose of alleviating the accompanying vitreous hemorrhage and enabling definite diagnosis and subsequent treatment of retinal hemangioma by resection. Before the tumor was resected, the tumor itself and the surrounding tissue were adequately photocoagulated. Subsequently, the tumor was resected during careful diathermic coagulation. In this way, the operation could be carried out safely, with minimum intraoperative bleeding. Yeh et al.9 have reported a vasoproliferative retinal tumor in a 31-year-old woman who underwent pars plana vitrectomy and endoresection of the tumor. They performed confluent indirect laser irradiation for
360° around the tumor, followed by endodiathermy of the tortuous vessels feeding the tumor. Air–fluid exchange was then performed, followed by instillation of 16% C3F8 gas. At 9 months after surgery, there were no signs of recurrence and the course was favorable. Gaudric et al10 reported vitreoretinal surgery for severe retinal capillary hemangiomas associated with von Hippel–Lindau syndrome in 23 eyes of 21 patients. In 9 eyes, retinectomy was performed to remove the tumor; at 6 months after surgery, 5 of these eyes were blind, and 4 had NVG. In the present case study, visual acuity after treatment was low because of optic atrophy and the postoperative complication by epiretinal membrane. Patients developing epiretinal membrane after vitreous surgery for retinal hemangioma, like the patient in the study, have been reported previously.10 Because the patient we encountered in this study had no desire for epiretinal membrane surgery, we have been following the patient without active treatment of epiretinal membrane. As far as NVG in this case is concerned, the new vessels formed in the iris and angle are showing a tendency to subside, and IOP stabilized in the first half of the 10 to 19 mmHg range. Retinal hemangioma has not recurred
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in this case. In view of a report on a case where NVG developed several years after vitreous surgery for retinal hemangioma leading to blindness,10 we see the necessity of following this patient from now on, paying close attention to relapse of NVG. Key words: neovascular glaucoma, vasoproliferative retinal tumor, vascular endothelial growth factor, vitrectomy. References 1. Bertil D. Vasoproliferative retinal tumor. Br J Ophthalmol 2006;90:399–400. 2. Shields JA, Decker WL, Sanborn GE, et al. Presumed acquired retinal hemangiomas. Ophthalmology 1983;90:1292–1300. 3. Shields CL, Shields JA, Barrett J, De Potter P. Vasoproliferative tumors of the ocular fundus: classification and clinical manifestations in 103 patients. Arch Ophthalmol 1995;113:615–623.
4. Irvine F, O’Donnell N, Kemp E, Lee WR. Retinal vasoproliferative tumors: surgical management and histological findings. Arch Ophthalmol 2000;118:563–569. 5. Milea D, Cassoux N, Lehoang P, et al. Neovascular glaucoma after bypass surgery in Takayasu’s disease. Eye 1999;13: 786–789. 6. Chan CC, Vortmeyer AO, Chew EY, et al. VHL gene deletion and enhanced VEGF gene expression detected in the stromal cells of retinal angioma. Arch Ophthalmol 1999;117:625–630. 7. Chan RP, Lai TY. Photodynamic therapy with verteporfin for vasoproliferative tumor of the retina. Acta Ophthalmol 2010;88:711–712. 8. Gibran SK. Trans-vitreal endoresection for vasoproliferative retinal tumors. Clin Experiment Ophthalmol 2008;36:712–716. 9. Yeh S, Wilson DJ. Pars plana vitrectomy and endoresection of a retinal vasoproliferative tumor. Arch Ophthalmol 2010;128:1196–1199. 10. Gaudric A, Krivosic V, Duguid G, et al. Vitreoretinal surgery for severe retinal capillary hemangiomas in von Hippel-Lindau disease. Ophthalmology 2011;118:142–149.
