Saudi Journal of Ophthalmology (2014) xxx, xxx—xxx
Case Report
Retino-choroidal ischemia in central retinal vein occlusion Nazimul Hussain, MS, DNB, FACS a,⇑; Anjli Hussain, MS b
Abstract A 41-year-old gentleman with insulin dependent diabetes had decreased vision in the right eye due to non-ischemic central retinal vein occlusion with macular edema. One month following intravitreal ranibizumab, he developed retino-choroidal ischemia with further loss of vision. Authors show the fluorescein angiographic transition from non-ischemic central retinal vein occlusion to retino-choroidal ischemia. Keywords: Central retinal vein occlusion, Macular edema, Retinochoroidal ischemia 2014 Saudi Ophthalmological Society, King Saud University. Production and hosting by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.sjopt.2014.02.004
Introduction The common causes for visual decrease in central retinal vein occlusion are macular edema, macular ischemia and vitreous hemorrhage. Early treatment may be required to improve vision in macular edema before irreversible photoreceptor damage occurs. Retinal vein occlusion is associated with varying amounts of retinal ischemia or macular edema that results in the expression of vascular endothelial growth factor (VEGF). Various reports and short-term studies in the literature have shown that intravitreal bevacizumab and ranibizumab are effective and safe in the treatment of macular edema secondary to retinal vein occlusion.1,2 We report a case of central retinal vein occlusion with macular edema that developed retino-choroidal ischemia following intravitreal ranibizumab.
Case report A 41-year-old gentleman came with complaints of decreased vision in the right eye since 2 weeks. He gave history of undergoing Laser-Assisted in situ Keratomileusis
(LASIK) in both eyes 6 years ago. He is a known diabetic since 5 years on conventional insulin therapy. On examination, his visual acuity was 0.2+2 in the right eye and 1.0 3 in the left eye. Anterior segment examination was unremarkable and there was no afferent pupillary defect in both eyes. Intraocular pressure was 16 mmHg in both eyes. Dilated fundus examination showed clear ocular media in both eyes and the left eye was unremarkable. Right eye showed scattered blot retinal hemorrhages, tortuous and congested venules with cystoid macular edema. Disk showed cup disk ration (CDR) 0.3 with healthy neuroretinal rim in both eyes. A diagnosis of central retinal vein occlusion with cystoid macular edema in the right eye was made. His lab test showed erythrocyte sedimentation rate (ESR) 08 mm/hr, HbA1c 10.6%, serum homocysteine 10.28 micromol/L, slight increase in total cholesterol (5.57 micromol/L) and low density lipoproteins (LDL) cholesterol (3.63 micromol/L). He was referred to the endocrinologist for management. Fundus fluorescein angiography (FFA) and optical coherence tomography (OCT) were done. The right eye FFA showed delayed venous filling with dilated and tortuous venules. Late phase showed pooling of dye in petalloid
Received 26 January 2014; received in revised form 10 February 2014; accepted 17 February 2014; available online xxxx. a b
Department of Ophthalmology, Al Zahra Hospital, Sharjah, United Arab Emirates Buhairah Corniche, Al Majaz Street 3, Sharjah, United Arab Emirates
⇑ Corresponding author. Address: Department of Ophthalmology, Al Zahra Hospital, Al Zahra Square, P.O. Box: 3499, Sharjah, United Arab Emirates. Tel./fax: +971 06 5619999. e-mail address: [email protected] (N. Hussain). Peer review under responsibility of Saudi Ophthalmological Society, King Saud University
Production and hosting by Elsevier
Access this article online: www.saudiophthaljournal.com www.sciencedirect.com
Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
2 pattern around the fovea with late perivenous staining (Fig. 1). The left eye showed normal study. OCT of the right eye showed elevated foveal contour with extensive intraretinal cystic changes and serous foveal detachment. The central macular thickness was 592 microns and foveal thickness was 619 microns in the right eye. Based on this evaluation, he was diagnosed to have non-ischemic central retinal vein occlusion with cystoid macular edema in the right eye. Three weeks after the control of diabetes, he underwent intravitreal ranibizumab (0.5 mg) in the right eye. Post-injection period was uneventful. One month later, he came with complaints of decreased vision in the right eye since 10 days. His visual acuity was 0.1 in the right eye and 1.0 in the left eye. Anterior segment examination was unremarkable in both eyes. Intraocular pressure was 16 mmHg in the right eye and 15 mmHg in the left eye. Dilated fundus examination showed attached retina, scattered retinal hemorrhage and an area of outer retinal opacification was seen in the macula involving the fovea (Fig. 2). No gross macular thickening was observed. An impression of resolved CRVO and acute branch retinal artery occlusion or possible choroidal ischemia was made in the right eye. He was advised FFA, OCT and advised cardiological opinion. He underwent FFA, which showed macular infarct with whole of temporal retina showing lack of arteriolar and venular perfusion as well as choroidal non-filling of dye suggestive of both outer retina-choroid and inner retinal ischemia in the right eye. The retinal arterioles appeared straightened and attenuated. The venular filling was differential between the nasal and temporal side of the retina across the optic disk (Fig. 3). Left eye angiographic phases were all within normal limits. OCT showed
N. Hussain, A. Hussain
Figure 2. Color fundus photograph of the right eye showing scattered retinal hemorrhage and an area of outer retinal opacification in the macula involving the temporal horizontal raphe and inferior fovea.
widening of foveal contour and intraretinal edema was evident. An impression of retino-choridal ischemia was made. His cardiological evaluation was normal and he was put on aspirin, lipitor and continued on antidiabetic treatment. Three months later, his visual acuity was counting fingers 1.5 meters in the right eye. The fundus examination was same as before.
Figure 1. Color photograph of the right eye showing scattered retinal hemorrhages, tortuous vessels and cystoid macular edema (Top left) and the left eye showed normal finding (Top right). FFA of the left eye showed normal angiographic features (Bottom left) and late phase FFA of the right eye showed disk staining, perivenous staining, tortuous vessels and typical petalloid appearance of the macula suggestive of cystoid macular edema (Bottom right). Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
3
Retino-choroidal ischemia in central retinal vein occlusion
Figure 3. Early phase FA showing non-filling venules, straightening of arterioles and conspicuous absence of choroidal filling (Top left). Mid-phase FA shows complete absence of inner retinal and choroidal filling in the temporal and superior quadrant and evident lamellar venous flow in the nasal quadrant (Top left). FA images in the bottom (left/right) highlight the narrowing of arterioles, blunted end of vessels at the ischemic and non-ischemic zone and complete absence of retino-choroidal angiographic characteristics in the ischemic area.
Discussion Central retinal vein occlusion is one of the most common retinal vascular diseases and often associated with moderate to severe visual loss.3 It has been reported that monthly intravitreal ranibizumab for macular edema from retinal vein occlusion contributes to greater improvement in vision related function compared to sham treated patients through 6 months.1,4 It has also found to be safe and effective with significant impact on visual finction.5 No new safety events were identified with long-term use of ranibizumab and rates of serious adverse events potentially related to treatment were consistent with prior ranibizumab trials.2 All available data, suggest that intravitreal ranibizumab provided an effective treatment for macular edema secondary to central retinal vein occlusion.1–5 Retino-choroidal infarction is an uncommon ophthalmic complication in central retinal vein occlusion. The persistent visual loss in our patient is caused by ischemic damage to the retina and choroid. Reported cases of retinal choroidal ischemia have been caused following intralesional steroid injection,6,7 during the treatment of acute lymphoblastic leukemia8 and in pregnancy induced hypertension and dessiminated intravascular coagulation.9 The risk factors for central retinal vein occlusion are systemic hypertension, diabetes mellitus and open angle glaucoma.9 In women, the risk of occlusion decreased with the use of postmenopausal estrogens and increased with higher erythrocyte sedimentation rates. Cardiovascular disease, electrocardiographic abnormalities, history of treatment of diabetes mellitus, higher blood glucose levels, lower albumin-globulin ratios, and higher alpha-globulin levels were associated with increased risk only for ischemic CRVO.9 Higher total plasma level of homocysteine was also found to be an independent risk factor for central retinal vein occlusion (odds
ratio 13)10 and thrombophilia.11 We do know that progressive retinal vein occlusion can cause extensive ischemia of the retina, however, choroidal ischemia occurs as a result of defective retro-ocular circulation. This can only happen when blood flow to the choroidal perfusion is affected. Choroidal vascular compromise can acutely occur in malignant hypertension and pre-eclampsia.12 Perfusion abnormality depends primarily on the focal effect on choriocapillaries or effect on larger arterioles. Inflammatory conditions like giant cell arteritis and Wegener’s granulomatosis can also cause inflammatory occlusion of choriocapillaries or occlusion of intra-orbital part of ophthalmic artery13 so does vaso-occlusive diseases in a variety of diseases.14–16 This condition results in varieties of choroidal infarction or choroidal ischemia. In the present case, the cause for retino-choroidal ischemia could not be determined. However, it is possible that such an undesirable vascular event could have happened due to occlusion of short posterior ciliary arteries with reasons not known to us. The only risk factor was uncontrolled blood sugar (HbA1c 10.6%) at the time of presentation. This case demonstrates the fluorescein angiographic characteristics of retino-choroidal ischemia occurring after the treatment for central retinal vein occlusion and highlights that such an event can occur in patients with central retinal vein occlusion.
Conflict of interest The authors declared that there is no conflict of interest.
References 1. Varma R, Beassler NM, Suner I, Dolan CM, Ward J, Colman S, et al. Improved vision-related function after ranibizumab for macular
Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
4
2.
3. 4. 5.
6.
7.
N. Hussain, A. Hussain edema after retinal vein occlusion: results from the BRAVO and CRUISE trials: BRAVO and CRUISE study groups. Ophthalmology 2012 Oct;119(10):2108–18. Heier JS, Campochiaro PA, Yau L, Li Z, Saroj N, Rubio RG, et al. Ranibizumab for macular edema due to retinal vein occlusions: longterm follow-up in the HORIZON trial. Ophthalmology 2012;119(4):802–9. Hayreh SS. Classification of central retinal vein occlusion. Ophthalmology 1983;90:458–74. Campochiaro PA, Brown DM, Awh CC, Lee SY, Gray S, Saroj N, et al. Ophthalmology 2011 Oct;118(10):2041–9. Pece A, Isola V, Piermarocchi S, Calori G. Efficacy and safety of antivascular endothelial growth factor (VEGF) therapy with Intravitreal ranibizumab (Lucentis) for naïve retinal vein occlusion: 1 year follow up. Br J Ophthalmol 2011;95:56–68. Amjadi S, Brown TM, Masselos K, Wang LW, Figuiera EC, Francis IC. Anterior segment ischemia and retinochoroidal vascular occlusion after intralesional steroid injection. Reply to Editor. Ophthal Plast Reconstr Surg 2009;25(3):253–4. Yagci A, Palamar M, Egrilmez S, Sahbazov C, Ozbek SS. Anterior segment ischemia and retinochoroidal vascular occlusion after intralesional steroid injection. Ophthal Plast Reconstr Surg 2008;24(1):55–7.
8. Kato Y, Takano Y, Kobayashi M, Ito F, Hara T, Yanagisawa T, et al. Retinochoroidal infarction during treatment of acute lymphoblastic leukemia. Pediatrics Int 2006;48:495–7. 9. Risk factor for central retinal vein occlusion. The eye disease casecontrol study group. Arch Ophthalmol 1996;115(5):545–54. 10. Lahiri KD, Dutta J, Datta H, Das HN. Hyperhomocysteinemia, as an independent risk factor for retinal venous occlusion in an Indian population. Indian J Clin Biochem 2013 Jan;28(1):61–4. 11. Chapin J, Carlson K, Christos PJ, Desancho MT. Risk factors and treatment strategies in patients with retinal vascular occlusions. Clin Appl Thromb Hemost 2013 [Epub ahead of print]. 12. Gaudric A, Coscas G, Bird AC. Choroidal ischemia. Am J Ophthalmol 1982;94:489–98. 13. Iida T, Spaide RF, Kantor J. Retinal and choroidal arterial occlusion in Wegener’s granulomatosis. Am J Ophthalmol 2002;133:151–2. 14. Kinyoun JL, Kalina RE. Visual loss from choroidal ischemia. Am J Ophthalmol 1986;101:650–6. 15. Melton RC, Spaide RF. Visual problems as a presenting sign for thrombotic thrombocytopenic purpura. Retina 1996;16:78–80. 16. Spaide RF, Goldbaum M, Wong DW, Tang KC, Iida T. Serous detachment of the retina. Retina 2003;23:820–46.
Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
Case Report
Retino-choroidal ischemia in central retinal vein occlusion Nazimul Hussain, MS, DNB, FACS a,⇑; Anjli Hussain, MS b
Abstract A 41-year-old gentleman with insulin dependent diabetes had decreased vision in the right eye due to non-ischemic central retinal vein occlusion with macular edema. One month following intravitreal ranibizumab, he developed retino-choroidal ischemia with further loss of vision. Authors show the fluorescein angiographic transition from non-ischemic central retinal vein occlusion to retino-choroidal ischemia. Keywords: Central retinal vein occlusion, Macular edema, Retinochoroidal ischemia 2014 Saudi Ophthalmological Society, King Saud University. Production and hosting by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.sjopt.2014.02.004
Introduction The common causes for visual decrease in central retinal vein occlusion are macular edema, macular ischemia and vitreous hemorrhage. Early treatment may be required to improve vision in macular edema before irreversible photoreceptor damage occurs. Retinal vein occlusion is associated with varying amounts of retinal ischemia or macular edema that results in the expression of vascular endothelial growth factor (VEGF). Various reports and short-term studies in the literature have shown that intravitreal bevacizumab and ranibizumab are effective and safe in the treatment of macular edema secondary to retinal vein occlusion.1,2 We report a case of central retinal vein occlusion with macular edema that developed retino-choroidal ischemia following intravitreal ranibizumab.
Case report A 41-year-old gentleman came with complaints of decreased vision in the right eye since 2 weeks. He gave history of undergoing Laser-Assisted in situ Keratomileusis
(LASIK) in both eyes 6 years ago. He is a known diabetic since 5 years on conventional insulin therapy. On examination, his visual acuity was 0.2+2 in the right eye and 1.0 3 in the left eye. Anterior segment examination was unremarkable and there was no afferent pupillary defect in both eyes. Intraocular pressure was 16 mmHg in both eyes. Dilated fundus examination showed clear ocular media in both eyes and the left eye was unremarkable. Right eye showed scattered blot retinal hemorrhages, tortuous and congested venules with cystoid macular edema. Disk showed cup disk ration (CDR) 0.3 with healthy neuroretinal rim in both eyes. A diagnosis of central retinal vein occlusion with cystoid macular edema in the right eye was made. His lab test showed erythrocyte sedimentation rate (ESR) 08 mm/hr, HbA1c 10.6%, serum homocysteine 10.28 micromol/L, slight increase in total cholesterol (5.57 micromol/L) and low density lipoproteins (LDL) cholesterol (3.63 micromol/L). He was referred to the endocrinologist for management. Fundus fluorescein angiography (FFA) and optical coherence tomography (OCT) were done. The right eye FFA showed delayed venous filling with dilated and tortuous venules. Late phase showed pooling of dye in petalloid
Received 26 January 2014; received in revised form 10 February 2014; accepted 17 February 2014; available online xxxx. a b
Department of Ophthalmology, Al Zahra Hospital, Sharjah, United Arab Emirates Buhairah Corniche, Al Majaz Street 3, Sharjah, United Arab Emirates
⇑ Corresponding author. Address: Department of Ophthalmology, Al Zahra Hospital, Al Zahra Square, P.O. Box: 3499, Sharjah, United Arab Emirates. Tel./fax: +971 06 5619999. e-mail address: [email protected] (N. Hussain). Peer review under responsibility of Saudi Ophthalmological Society, King Saud University
Production and hosting by Elsevier
Access this article online: www.saudiophthaljournal.com www.sciencedirect.com
Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
2 pattern around the fovea with late perivenous staining (Fig. 1). The left eye showed normal study. OCT of the right eye showed elevated foveal contour with extensive intraretinal cystic changes and serous foveal detachment. The central macular thickness was 592 microns and foveal thickness was 619 microns in the right eye. Based on this evaluation, he was diagnosed to have non-ischemic central retinal vein occlusion with cystoid macular edema in the right eye. Three weeks after the control of diabetes, he underwent intravitreal ranibizumab (0.5 mg) in the right eye. Post-injection period was uneventful. One month later, he came with complaints of decreased vision in the right eye since 10 days. His visual acuity was 0.1 in the right eye and 1.0 in the left eye. Anterior segment examination was unremarkable in both eyes. Intraocular pressure was 16 mmHg in the right eye and 15 mmHg in the left eye. Dilated fundus examination showed attached retina, scattered retinal hemorrhage and an area of outer retinal opacification was seen in the macula involving the fovea (Fig. 2). No gross macular thickening was observed. An impression of resolved CRVO and acute branch retinal artery occlusion or possible choroidal ischemia was made in the right eye. He was advised FFA, OCT and advised cardiological opinion. He underwent FFA, which showed macular infarct with whole of temporal retina showing lack of arteriolar and venular perfusion as well as choroidal non-filling of dye suggestive of both outer retina-choroid and inner retinal ischemia in the right eye. The retinal arterioles appeared straightened and attenuated. The venular filling was differential between the nasal and temporal side of the retina across the optic disk (Fig. 3). Left eye angiographic phases were all within normal limits. OCT showed
N. Hussain, A. Hussain
Figure 2. Color fundus photograph of the right eye showing scattered retinal hemorrhage and an area of outer retinal opacification in the macula involving the temporal horizontal raphe and inferior fovea.
widening of foveal contour and intraretinal edema was evident. An impression of retino-choridal ischemia was made. His cardiological evaluation was normal and he was put on aspirin, lipitor and continued on antidiabetic treatment. Three months later, his visual acuity was counting fingers 1.5 meters in the right eye. The fundus examination was same as before.
Figure 1. Color photograph of the right eye showing scattered retinal hemorrhages, tortuous vessels and cystoid macular edema (Top left) and the left eye showed normal finding (Top right). FFA of the left eye showed normal angiographic features (Bottom left) and late phase FFA of the right eye showed disk staining, perivenous staining, tortuous vessels and typical petalloid appearance of the macula suggestive of cystoid macular edema (Bottom right). Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
3
Retino-choroidal ischemia in central retinal vein occlusion
Figure 3. Early phase FA showing non-filling venules, straightening of arterioles and conspicuous absence of choroidal filling (Top left). Mid-phase FA shows complete absence of inner retinal and choroidal filling in the temporal and superior quadrant and evident lamellar venous flow in the nasal quadrant (Top left). FA images in the bottom (left/right) highlight the narrowing of arterioles, blunted end of vessels at the ischemic and non-ischemic zone and complete absence of retino-choroidal angiographic characteristics in the ischemic area.
Discussion Central retinal vein occlusion is one of the most common retinal vascular diseases and often associated with moderate to severe visual loss.3 It has been reported that monthly intravitreal ranibizumab for macular edema from retinal vein occlusion contributes to greater improvement in vision related function compared to sham treated patients through 6 months.1,4 It has also found to be safe and effective with significant impact on visual finction.5 No new safety events were identified with long-term use of ranibizumab and rates of serious adverse events potentially related to treatment were consistent with prior ranibizumab trials.2 All available data, suggest that intravitreal ranibizumab provided an effective treatment for macular edema secondary to central retinal vein occlusion.1–5 Retino-choroidal infarction is an uncommon ophthalmic complication in central retinal vein occlusion. The persistent visual loss in our patient is caused by ischemic damage to the retina and choroid. Reported cases of retinal choroidal ischemia have been caused following intralesional steroid injection,6,7 during the treatment of acute lymphoblastic leukemia8 and in pregnancy induced hypertension and dessiminated intravascular coagulation.9 The risk factors for central retinal vein occlusion are systemic hypertension, diabetes mellitus and open angle glaucoma.9 In women, the risk of occlusion decreased with the use of postmenopausal estrogens and increased with higher erythrocyte sedimentation rates. Cardiovascular disease, electrocardiographic abnormalities, history of treatment of diabetes mellitus, higher blood glucose levels, lower albumin-globulin ratios, and higher alpha-globulin levels were associated with increased risk only for ischemic CRVO.9 Higher total plasma level of homocysteine was also found to be an independent risk factor for central retinal vein occlusion (odds
ratio 13)10 and thrombophilia.11 We do know that progressive retinal vein occlusion can cause extensive ischemia of the retina, however, choroidal ischemia occurs as a result of defective retro-ocular circulation. This can only happen when blood flow to the choroidal perfusion is affected. Choroidal vascular compromise can acutely occur in malignant hypertension and pre-eclampsia.12 Perfusion abnormality depends primarily on the focal effect on choriocapillaries or effect on larger arterioles. Inflammatory conditions like giant cell arteritis and Wegener’s granulomatosis can also cause inflammatory occlusion of choriocapillaries or occlusion of intra-orbital part of ophthalmic artery13 so does vaso-occlusive diseases in a variety of diseases.14–16 This condition results in varieties of choroidal infarction or choroidal ischemia. In the present case, the cause for retino-choroidal ischemia could not be determined. However, it is possible that such an undesirable vascular event could have happened due to occlusion of short posterior ciliary arteries with reasons not known to us. The only risk factor was uncontrolled blood sugar (HbA1c 10.6%) at the time of presentation. This case demonstrates the fluorescein angiographic characteristics of retino-choroidal ischemia occurring after the treatment for central retinal vein occlusion and highlights that such an event can occur in patients with central retinal vein occlusion.
Conflict of interest The authors declared that there is no conflict of interest.
References 1. Varma R, Beassler NM, Suner I, Dolan CM, Ward J, Colman S, et al. Improved vision-related function after ranibizumab for macular
Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
4
2.
3. 4. 5.
6.
7.
N. Hussain, A. Hussain edema after retinal vein occlusion: results from the BRAVO and CRUISE trials: BRAVO and CRUISE study groups. Ophthalmology 2012 Oct;119(10):2108–18. Heier JS, Campochiaro PA, Yau L, Li Z, Saroj N, Rubio RG, et al. Ranibizumab for macular edema due to retinal vein occlusions: longterm follow-up in the HORIZON trial. Ophthalmology 2012;119(4):802–9. Hayreh SS. Classification of central retinal vein occlusion. Ophthalmology 1983;90:458–74. Campochiaro PA, Brown DM, Awh CC, Lee SY, Gray S, Saroj N, et al. Ophthalmology 2011 Oct;118(10):2041–9. Pece A, Isola V, Piermarocchi S, Calori G. Efficacy and safety of antivascular endothelial growth factor (VEGF) therapy with Intravitreal ranibizumab (Lucentis) for naïve retinal vein occlusion: 1 year follow up. Br J Ophthalmol 2011;95:56–68. Amjadi S, Brown TM, Masselos K, Wang LW, Figuiera EC, Francis IC. Anterior segment ischemia and retinochoroidal vascular occlusion after intralesional steroid injection. Reply to Editor. Ophthal Plast Reconstr Surg 2009;25(3):253–4. Yagci A, Palamar M, Egrilmez S, Sahbazov C, Ozbek SS. Anterior segment ischemia and retinochoroidal vascular occlusion after intralesional steroid injection. Ophthal Plast Reconstr Surg 2008;24(1):55–7.
8. Kato Y, Takano Y, Kobayashi M, Ito F, Hara T, Yanagisawa T, et al. Retinochoroidal infarction during treatment of acute lymphoblastic leukemia. Pediatrics Int 2006;48:495–7. 9. Risk factor for central retinal vein occlusion. The eye disease casecontrol study group. Arch Ophthalmol 1996;115(5):545–54. 10. Lahiri KD, Dutta J, Datta H, Das HN. Hyperhomocysteinemia, as an independent risk factor for retinal venous occlusion in an Indian population. Indian J Clin Biochem 2013 Jan;28(1):61–4. 11. Chapin J, Carlson K, Christos PJ, Desancho MT. Risk factors and treatment strategies in patients with retinal vascular occlusions. Clin Appl Thromb Hemost 2013 [Epub ahead of print]. 12. Gaudric A, Coscas G, Bird AC. Choroidal ischemia. Am J Ophthalmol 1982;94:489–98. 13. Iida T, Spaide RF, Kantor J. Retinal and choroidal arterial occlusion in Wegener’s granulomatosis. Am J Ophthalmol 2002;133:151–2. 14. Kinyoun JL, Kalina RE. Visual loss from choroidal ischemia. Am J Ophthalmol 1986;101:650–6. 15. Melton RC, Spaide RF. Visual problems as a presenting sign for thrombotic thrombocytopenic purpura. Retina 1996;16:78–80. 16. Spaide RF, Goldbaum M, Wong DW, Tang KC, Iida T. Serous detachment of the retina. Retina 2003;23:820–46.
Please cite this article in press as: Hussain N., Hussain A. Retino-choroidal ischemia in central retinal vein occlusion. Saudi J Ophthalmol (2014), http:// dx.doi.org/10.1016/j.sjopt.2014.02.004
