Ophthalmology Volume 120, Number 12, December 2013 Financial Disclosure(s): Supported by Research to Prevent Blindness, New York, New York.
References 1. Bunt TJ. The clinical significance of the asymptomatic Hollenhorst plaque. J Vasc Surg 1986;4:559–62. 2. Chawluk JB, Kushner MJ, Bank WJ, et al. Atherosclerotic carotid artery disease in patients with retinal ischemic syndromes. Neurology 1988;38:858–63. 3. Bull DA, Fante RG, Hunter GC, et al. Correlation of ophthalmic findings with carotid artery stenosis. J Cardiovasc Surg (Torino) 1992;33:401–6. 4. Wakefield MC, O’Donnell SD, Goff JM. Re-evaluation of carotid duplex for visual complaints: who really needs to be studied? Ann Vasc Surg 2003;17:635–40. 5. McCullough HK, Reinert CG, Hynan LS, et al. Ocular findings as predictors of carotid artery occlusive disease: is carotid imaging justified? J Vasc Surg 2004;40: 279–86.
Dexamethasone Intravitreal Implant Trapped at the Macula in a Silicone Oil-filled Eye The Ozurdex (dexamethasone 0.7 mg) sustained-release intravitreal implant (Allergan Inc., Irvine, CA) is approved by the US Food and Drug Administration for treatment of adults with macular edema after retinal vein occlusions and with noninfectious posterior uveitis. It has been used off-label to treat diabetic macular edema, persistent cystoid macular edema (CME) after complicated cataract extraction, and retinitis pigmentosaassociated refractory CME.1-3 We describe an unusual retinal finding that developed when the implant became trapped at the macular surface under silicone oil. A 67-year-old man presented with a macula-on rhegmatogenous retinal detachment of the left eye in the setting of hemorrhagic posterior vitreous detachment after cataract surgery 2 months prior. Vision was count fingers at 3 inches through the vitreous hemorrhage. He underwent retinal detachment repair with combined scleral buckle and pars plana vitrectomy with gas injection (14% C3F8). Six weeks postoperatively, the macula remained attached; however, the retina had redetached inferotemporally from proliferative vitreoretinopathy. The patient underwent repeat vitrectomy with membrane peeling and silicone oil (5000-centistoke) injection. Six weeks after the second repair, the macula was still attached under oil, with a small, 2-discearea sized traction detachment inferonasally. Vision was 20/100 with pinhole correction, and spectral-domain optical coherence tomography (SDOCT) revealed the presence of CME. No retinal breaks were identified. Prednisolone acetate 1% was given 4 times per day. At 12 weeks after the second surgery, CME persisted, and the patient had vision of 20/80 with pinhole correction. The small inferonasal detachment was unchanged. The patient elected to undergo silicone oil removal and dexamethasone implant injection several weeks later, leaving the small inferonasal traction detachment undisturbed. At postoperative week 1, best-corrected vision had improved to 20/40, and the CME was mostly resolved. Two weeks later, the patient presented with a limited macula-on superior retinal detachment. He underwent repeat
2748
vitrectomy with membrane peeling and silicone oil (5000centistoke) injection. The dexamethasone implant was left in the eye. On postoperative day 1, the implant had migrated to the macula, resting near the fovea. (Fig 1A). Its position beneath the oil in apposition to the retina was confirmed on SD-OCT (Fig 1B). The patient described a scotoma associated with the implant. One month later, vision was 20/80 with pinhole correction, and the CME had resolved (Fig 1C). The implant had shifted orientation but remained trapped beneath the silicone oil at the macula. After an additional month, the vision had improved to 20/50, the CME had not recurred, and the implant had moved inferiorly, away from the macula. An area of pigmented epiretinal membrane (ERM) matching the shape of the dexamethasone implant and corresponding with the location of previous implant-retinal contact was visible in the macula (Fig 2A). The patient reported that he could still perceive a linear scotoma from this area, although this resolved over the next several months. At 3 months after the final surgical repair, with stable vision and no CME, the patient underwent silicone oil removal. When CME recurred, the patient opted for another Ozurdex injection 2 months later. At last follow-up 3 months after silicone oil removal, his bestcorrected vision was 20/40 in his left eye. The patient complained of some residual distortion centrally in his left eye. The pigmented ERM was partially regressed but remained thicker than the more diffuse ERM that had now formed over the entire macula (Fig 2B). Loss of the foveal contour owing to ERM was seen on SD-OCT (Fig 2C). To our knowledge, this is the first report of an injectable intravitreal implant being trapped against the retinal surface by silicone oil. Remarkably, the implant remained relatively immobile over the course of >1 month, suggesting that in an eye with a complete oil fill, the intersection between the oil and the potential fluid-filled space at the retinal surface is not a dynamic environment. We expect that, as the use of injectable therapeutics grows and the indications for their use broaden, this phenomenon may be observed more commonly in eyes containing vitreous substitutes such as silicone oil. The development of a pigmented macular ERM, in a shape matching the implant and corresponding exactly to its area of retinal contact, could reflect a toxic effect from elevated local concentrations of dexamethasone or degradable vehicle material diffusing into the fluid phase between the oil and the retina, or it could be a response to microtrauma from the implant abrading the retinal surface. It is noteworthy that this pigmented and thickened ERM formed in addition to a more subtle epiretinal proliferation more typical of a postretinal detachment eye, in this case seen elsewhere in the fundus (Fig 2B, C; nasal and superior macula). Future reports could help investigators to deduce the mechanism if similar findings occur in association with other injectable implants held against the retinal surface by silicone oil. Based on our experience with this patient, we recommend that if a dexamethasone implant remains trapped at the central macula, the treating physician consider removal of the implant or the oil if possible, to avoid an increased stimulus for ERM formation with its associated impact on vision. Alternatively, an office maneuver to try to displace the implant, not attempted in our case, could entail placing the patient in a supine position and then slowly sitting up or rolling to the side. Of note, despite the apparent lack of movement at the margin of the oil bubble, the CME was adequately treated, presumably by the dexamethasone drug diffusing from the implant. Although in this case an adequate
Reports therapeutic effect was achieved with regard to the CME, additional studies are necessary to provide a better understanding of the pharmacodynamics of sustained-release medications from devices implanted or inserted into eyes filled with a vitreous substitute such as silicone oil.4,5
ARMIN R. AFSHAR, MD, MBA ALLISON R. LOH, MD PEAR PONGSACHAREONNONT, MD DANIEL M. SCHWARTZ, MD JAY M. STEWART, MD University of California, San Francisco, Department of Ophthalmology, San Francisco, California Financial Support: That Man May See, Inc., and Research to Prevent Blindness.
References 1. Boyer DS, Faber D, Gupta Set al; ; Ozurdex CHAMPLAIN Study Group. 2. Dexamethasone intravitreal implant for treatment of diabetic macular edema in vitrectomized patients. Retina 2011;31:915–23. 2. Meyer LM, Schönfeld CL. Cystoid macular edema after complicated cataract surgery resolved by an intravitreal dexamethasone 0.7-mg implant. Case Rep Ophthalmol 2011;2:319–22. 3. Srour M, Querques G, Leveziel N, et al. Intravitreal dexamethasone implant (Ozurdex) for macular edema secondary to retinitis pigmentosa. Graefes Arch Clin Exp Ophthalmol 2013;251: 1501–6. 4. Kim JT, Yoon YH, Lee DH, et al. Dexamethasone intravitreal implant in the silicone oil-filled eye for the treatment for recurrent macular oedema associated with ankylosing spondylitis: a case report. Acta Ophthalmol 2013;91:331–2. 5. Spitzer MS, Kaczmarek RT, Yoeruek E, et al. The distribution, release kinetics, and biocompatibility of triamcinolone injected and dispersed in silicone oil. Invest Ophthalmol Vis Sci 2009;50:2337–43.
Subfoveal Choroidal Thickness in Retinal Vein Occlusion Since Spaide et al1 described the enhanced depth imaging mode of optical coherence tomography to visualize the choroid, an increasing number of studies have examined choroidal thickness and its associated factors in normal eyes and eyes with various retinal and retinochoroidal disorders. The studies revealed that the mean subfoveal choroidal thickness (SFCT) in normal eyes is approximately 250 mm at age 65 years; that SFCT shows a marked interindividual variability with values as low as 8 mm and values as great as 854 mm; that SFCT decreases by about 4 mm per year of age and by 15 mm per diopter of myopia; and that SFCT is additionally associated with male gender, a deeper anterior chamber, and thicker lens.2 Clinical studies showed that eyes affected by central serous chorioretinopathy and their contralateral eyes as well as eyes with polypoidal vascular choroidopathy have an abnormally thick subfoveal choroid.3 Because retinal vein occlusions (RVOs) as retinal vascular diseases may have an association with abnormalities of the choroidal vasculature, we conducted this study to assess the choroidal thickness in patients with RVOs.
The Beijing Eye Study 2011 is a population-based, cross-sectional study in Northern China.2 The Medical Ethics Committee of the Beijing Tongren Hospital approved the study protocol and all participants gave informed consent. Out of 4403 individuals aged 50 years, 3468 (78.8%) participated. The RVOs defined were defined as described previously.4 Their presence and locations were examined on fundus photographs. We measured SFCT using a spectral domain optical coherence tomography (OCT; Spectralis, Heidelberg Engineering Co., Heidelberg, Germany) with enhanced depth imaging (OCT) modality after pupil dilation. The technique was described in detail recently.1,2 Measurements of SFCT and assessments of RVOs were available for 3222 (92.9%) subjects (1811 women [56.2%]) with a mean age of 64.29.6 years (range, 50e93). The RVOs were detected in 85 eyes (48 right eyes) of 81 subjects (45 women). Ophthalmoscopically, all these RVOs did not seem to have a recent onset. There was no marked cystoid macular edema, neither upon ophthalmoscopy nor detected on the macular OCT images. On univariate analysis, SFCT was significantly (P ¼ 0.002) thinner in the RVO study group than in the remaining study population of subjects without RVOs (218104 mm; range, 55e513) versus 255107 mm (range, 8e854). After adjustment for age, gender, axial length, anterior chamber depth, and lens thickness, SFCT was no longer associated with the presence of an RVO (P ¼ 0.22; standardized coefficient beta, 0.02; correlation coefficient B, 17.2; 95% confidence interval, 44.7 to 10.1). In binary regression analysis with RVO presence as dependent variable, and age, systolic blood pressure, and SFCT as independent variables, RVO presence was not associated with SFCT (P ¼ 0.25). The SFCT did not vary significantly between 59 eyes contralateral to eyes affected by RVOs and the ipsilateral eyes with RVOs (22399 mm [range, 65e517] vs 223110 mm [range, 55e513]; P ¼ 0.98) nor did refractive error (P ¼ 0.59) or axial length (P ¼ 0.41). Eyes with a branch RVO (75 eyes) and eyes with a central RVO (10 eyes) did not differ significantly in SFCT (218105 mm [range, 55e513] vs 220105 mm [range, 65e431]; P ¼ 0.96) nor in age (P ¼ 0.28) and axial length (P ¼ 0.79). On multivariate analysis, with adjustment for age, gender, axial length, anterior chamber depth, and lens thickness, SFCT was not associated with the presence of branch RVOs (P ¼ 0.15; beta, 0.02; B, 21.4; 95% confidence interval, 50.7 to 7.8) nor presence of central RVOs (P ¼ 0.76; beta, 0.01; B, 12.0; 95% confidence interval, 65.8 to 89.8). In our population-based study on a relatively large study population, we found that that there was no association of SFCT with either longstanding branch or central RVO after adjustment for age, axial length, gender, anterior chamber depth, and lens thickness. Correspondingly, affected eyes and contralateral unaffected eyes in patients with unilateral RVOs did not differ in SFCT, nor varied the contralateral unaffected eyes from eyes of subjects without RVOs. Our findings seem to be in contrast with the results of a recent, retrospective, hospital-based study by Tsuiki et al,5 who examined 36 patients with unilateral central RVO.5 They found that SFCT was significantly thicker in eyes affected by central RVO than in the fellow unaffected eyes (25783 mm vs 22368 mm; P < 0.01). Tsuiki et al additionally detected that after treatment with intravitreal bevacizumab, SFCT significantly decreased to 22865 mm (P < 0.01). The discrepancy between Tsuiki’s study and our investigation may be explained by the difference in the study design; Tsuiki et al examined patients with a recently developed central RVO, whereas our population-based study
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Ophthalmology Volume 120, Number 12, December 2013
Figure 1. A, Dexamethasone implant trapped at the macula 1 day after silicone oil injection. B, Spectral-domain optical coherence tomography (SD-OCT) showing dexamethasone implant at the macula, 1 week after silicone oil injection. C, Shift in position of the dexamethasone implant shown on SD-OCT 1 month after silicone oil injection.
Figure 2. A, Pigmented epiretinal membrane (large arrows), matching the shape of the dexamethasone implant, in the macula where the implant was trapped under oil. A small fragment of implant material incorporated into the membrane is visualized as a bright white spot (small arrow). B, Fundus photograph at last follow-up. Pigmented epiretinal membrane has regressed (large arrow). The small fragment of incorporated implant material remains unchanged (small arrow). C, Spectral-domain optical coherence tomography at last visit showing loss of foveal contour from the epiretinal membrane.
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References 1. Bunt TJ. The clinical significance of the asymptomatic Hollenhorst plaque. J Vasc Surg 1986;4:559–62. 2. Chawluk JB, Kushner MJ, Bank WJ, et al. Atherosclerotic carotid artery disease in patients with retinal ischemic syndromes. Neurology 1988;38:858–63. 3. Bull DA, Fante RG, Hunter GC, et al. Correlation of ophthalmic findings with carotid artery stenosis. J Cardiovasc Surg (Torino) 1992;33:401–6. 4. Wakefield MC, O’Donnell SD, Goff JM. Re-evaluation of carotid duplex for visual complaints: who really needs to be studied? Ann Vasc Surg 2003;17:635–40. 5. McCullough HK, Reinert CG, Hynan LS, et al. Ocular findings as predictors of carotid artery occlusive disease: is carotid imaging justified? J Vasc Surg 2004;40: 279–86.
Dexamethasone Intravitreal Implant Trapped at the Macula in a Silicone Oil-filled Eye The Ozurdex (dexamethasone 0.7 mg) sustained-release intravitreal implant (Allergan Inc., Irvine, CA) is approved by the US Food and Drug Administration for treatment of adults with macular edema after retinal vein occlusions and with noninfectious posterior uveitis. It has been used off-label to treat diabetic macular edema, persistent cystoid macular edema (CME) after complicated cataract extraction, and retinitis pigmentosaassociated refractory CME.1-3 We describe an unusual retinal finding that developed when the implant became trapped at the macular surface under silicone oil. A 67-year-old man presented with a macula-on rhegmatogenous retinal detachment of the left eye in the setting of hemorrhagic posterior vitreous detachment after cataract surgery 2 months prior. Vision was count fingers at 3 inches through the vitreous hemorrhage. He underwent retinal detachment repair with combined scleral buckle and pars plana vitrectomy with gas injection (14% C3F8). Six weeks postoperatively, the macula remained attached; however, the retina had redetached inferotemporally from proliferative vitreoretinopathy. The patient underwent repeat vitrectomy with membrane peeling and silicone oil (5000-centistoke) injection. Six weeks after the second repair, the macula was still attached under oil, with a small, 2-discearea sized traction detachment inferonasally. Vision was 20/100 with pinhole correction, and spectral-domain optical coherence tomography (SDOCT) revealed the presence of CME. No retinal breaks were identified. Prednisolone acetate 1% was given 4 times per day. At 12 weeks after the second surgery, CME persisted, and the patient had vision of 20/80 with pinhole correction. The small inferonasal detachment was unchanged. The patient elected to undergo silicone oil removal and dexamethasone implant injection several weeks later, leaving the small inferonasal traction detachment undisturbed. At postoperative week 1, best-corrected vision had improved to 20/40, and the CME was mostly resolved. Two weeks later, the patient presented with a limited macula-on superior retinal detachment. He underwent repeat
2748
vitrectomy with membrane peeling and silicone oil (5000centistoke) injection. The dexamethasone implant was left in the eye. On postoperative day 1, the implant had migrated to the macula, resting near the fovea. (Fig 1A). Its position beneath the oil in apposition to the retina was confirmed on SD-OCT (Fig 1B). The patient described a scotoma associated with the implant. One month later, vision was 20/80 with pinhole correction, and the CME had resolved (Fig 1C). The implant had shifted orientation but remained trapped beneath the silicone oil at the macula. After an additional month, the vision had improved to 20/50, the CME had not recurred, and the implant had moved inferiorly, away from the macula. An area of pigmented epiretinal membrane (ERM) matching the shape of the dexamethasone implant and corresponding with the location of previous implant-retinal contact was visible in the macula (Fig 2A). The patient reported that he could still perceive a linear scotoma from this area, although this resolved over the next several months. At 3 months after the final surgical repair, with stable vision and no CME, the patient underwent silicone oil removal. When CME recurred, the patient opted for another Ozurdex injection 2 months later. At last follow-up 3 months after silicone oil removal, his bestcorrected vision was 20/40 in his left eye. The patient complained of some residual distortion centrally in his left eye. The pigmented ERM was partially regressed but remained thicker than the more diffuse ERM that had now formed over the entire macula (Fig 2B). Loss of the foveal contour owing to ERM was seen on SD-OCT (Fig 2C). To our knowledge, this is the first report of an injectable intravitreal implant being trapped against the retinal surface by silicone oil. Remarkably, the implant remained relatively immobile over the course of >1 month, suggesting that in an eye with a complete oil fill, the intersection between the oil and the potential fluid-filled space at the retinal surface is not a dynamic environment. We expect that, as the use of injectable therapeutics grows and the indications for their use broaden, this phenomenon may be observed more commonly in eyes containing vitreous substitutes such as silicone oil. The development of a pigmented macular ERM, in a shape matching the implant and corresponding exactly to its area of retinal contact, could reflect a toxic effect from elevated local concentrations of dexamethasone or degradable vehicle material diffusing into the fluid phase between the oil and the retina, or it could be a response to microtrauma from the implant abrading the retinal surface. It is noteworthy that this pigmented and thickened ERM formed in addition to a more subtle epiretinal proliferation more typical of a postretinal detachment eye, in this case seen elsewhere in the fundus (Fig 2B, C; nasal and superior macula). Future reports could help investigators to deduce the mechanism if similar findings occur in association with other injectable implants held against the retinal surface by silicone oil. Based on our experience with this patient, we recommend that if a dexamethasone implant remains trapped at the central macula, the treating physician consider removal of the implant or the oil if possible, to avoid an increased stimulus for ERM formation with its associated impact on vision. Alternatively, an office maneuver to try to displace the implant, not attempted in our case, could entail placing the patient in a supine position and then slowly sitting up or rolling to the side. Of note, despite the apparent lack of movement at the margin of the oil bubble, the CME was adequately treated, presumably by the dexamethasone drug diffusing from the implant. Although in this case an adequate
Reports therapeutic effect was achieved with regard to the CME, additional studies are necessary to provide a better understanding of the pharmacodynamics of sustained-release medications from devices implanted or inserted into eyes filled with a vitreous substitute such as silicone oil.4,5
ARMIN R. AFSHAR, MD, MBA ALLISON R. LOH, MD PEAR PONGSACHAREONNONT, MD DANIEL M. SCHWARTZ, MD JAY M. STEWART, MD University of California, San Francisco, Department of Ophthalmology, San Francisco, California Financial Support: That Man May See, Inc., and Research to Prevent Blindness.
References 1. Boyer DS, Faber D, Gupta Set al; ; Ozurdex CHAMPLAIN Study Group. 2. Dexamethasone intravitreal implant for treatment of diabetic macular edema in vitrectomized patients. Retina 2011;31:915–23. 2. Meyer LM, Schönfeld CL. Cystoid macular edema after complicated cataract surgery resolved by an intravitreal dexamethasone 0.7-mg implant. Case Rep Ophthalmol 2011;2:319–22. 3. Srour M, Querques G, Leveziel N, et al. Intravitreal dexamethasone implant (Ozurdex) for macular edema secondary to retinitis pigmentosa. Graefes Arch Clin Exp Ophthalmol 2013;251: 1501–6. 4. Kim JT, Yoon YH, Lee DH, et al. Dexamethasone intravitreal implant in the silicone oil-filled eye for the treatment for recurrent macular oedema associated with ankylosing spondylitis: a case report. Acta Ophthalmol 2013;91:331–2. 5. Spitzer MS, Kaczmarek RT, Yoeruek E, et al. The distribution, release kinetics, and biocompatibility of triamcinolone injected and dispersed in silicone oil. Invest Ophthalmol Vis Sci 2009;50:2337–43.
Subfoveal Choroidal Thickness in Retinal Vein Occlusion Since Spaide et al1 described the enhanced depth imaging mode of optical coherence tomography to visualize the choroid, an increasing number of studies have examined choroidal thickness and its associated factors in normal eyes and eyes with various retinal and retinochoroidal disorders. The studies revealed that the mean subfoveal choroidal thickness (SFCT) in normal eyes is approximately 250 mm at age 65 years; that SFCT shows a marked interindividual variability with values as low as 8 mm and values as great as 854 mm; that SFCT decreases by about 4 mm per year of age and by 15 mm per diopter of myopia; and that SFCT is additionally associated with male gender, a deeper anterior chamber, and thicker lens.2 Clinical studies showed that eyes affected by central serous chorioretinopathy and their contralateral eyes as well as eyes with polypoidal vascular choroidopathy have an abnormally thick subfoveal choroid.3 Because retinal vein occlusions (RVOs) as retinal vascular diseases may have an association with abnormalities of the choroidal vasculature, we conducted this study to assess the choroidal thickness in patients with RVOs.
The Beijing Eye Study 2011 is a population-based, cross-sectional study in Northern China.2 The Medical Ethics Committee of the Beijing Tongren Hospital approved the study protocol and all participants gave informed consent. Out of 4403 individuals aged 50 years, 3468 (78.8%) participated. The RVOs defined were defined as described previously.4 Their presence and locations were examined on fundus photographs. We measured SFCT using a spectral domain optical coherence tomography (OCT; Spectralis, Heidelberg Engineering Co., Heidelberg, Germany) with enhanced depth imaging (OCT) modality after pupil dilation. The technique was described in detail recently.1,2 Measurements of SFCT and assessments of RVOs were available for 3222 (92.9%) subjects (1811 women [56.2%]) with a mean age of 64.29.6 years (range, 50e93). The RVOs were detected in 85 eyes (48 right eyes) of 81 subjects (45 women). Ophthalmoscopically, all these RVOs did not seem to have a recent onset. There was no marked cystoid macular edema, neither upon ophthalmoscopy nor detected on the macular OCT images. On univariate analysis, SFCT was significantly (P ¼ 0.002) thinner in the RVO study group than in the remaining study population of subjects without RVOs (218104 mm; range, 55e513) versus 255107 mm (range, 8e854). After adjustment for age, gender, axial length, anterior chamber depth, and lens thickness, SFCT was no longer associated with the presence of an RVO (P ¼ 0.22; standardized coefficient beta, 0.02; correlation coefficient B, 17.2; 95% confidence interval, 44.7 to 10.1). In binary regression analysis with RVO presence as dependent variable, and age, systolic blood pressure, and SFCT as independent variables, RVO presence was not associated with SFCT (P ¼ 0.25). The SFCT did not vary significantly between 59 eyes contralateral to eyes affected by RVOs and the ipsilateral eyes with RVOs (22399 mm [range, 65e517] vs 223110 mm [range, 55e513]; P ¼ 0.98) nor did refractive error (P ¼ 0.59) or axial length (P ¼ 0.41). Eyes with a branch RVO (75 eyes) and eyes with a central RVO (10 eyes) did not differ significantly in SFCT (218105 mm [range, 55e513] vs 220105 mm [range, 65e431]; P ¼ 0.96) nor in age (P ¼ 0.28) and axial length (P ¼ 0.79). On multivariate analysis, with adjustment for age, gender, axial length, anterior chamber depth, and lens thickness, SFCT was not associated with the presence of branch RVOs (P ¼ 0.15; beta, 0.02; B, 21.4; 95% confidence interval, 50.7 to 7.8) nor presence of central RVOs (P ¼ 0.76; beta, 0.01; B, 12.0; 95% confidence interval, 65.8 to 89.8). In our population-based study on a relatively large study population, we found that that there was no association of SFCT with either longstanding branch or central RVO after adjustment for age, axial length, gender, anterior chamber depth, and lens thickness. Correspondingly, affected eyes and contralateral unaffected eyes in patients with unilateral RVOs did not differ in SFCT, nor varied the contralateral unaffected eyes from eyes of subjects without RVOs. Our findings seem to be in contrast with the results of a recent, retrospective, hospital-based study by Tsuiki et al,5 who examined 36 patients with unilateral central RVO.5 They found that SFCT was significantly thicker in eyes affected by central RVO than in the fellow unaffected eyes (25783 mm vs 22368 mm; P < 0.01). Tsuiki et al additionally detected that after treatment with intravitreal bevacizumab, SFCT significantly decreased to 22865 mm (P < 0.01). The discrepancy between Tsuiki’s study and our investigation may be explained by the difference in the study design; Tsuiki et al examined patients with a recently developed central RVO, whereas our population-based study
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Ophthalmology Volume 120, Number 12, December 2013
Figure 1. A, Dexamethasone implant trapped at the macula 1 day after silicone oil injection. B, Spectral-domain optical coherence tomography (SD-OCT) showing dexamethasone implant at the macula, 1 week after silicone oil injection. C, Shift in position of the dexamethasone implant shown on SD-OCT 1 month after silicone oil injection.
Figure 2. A, Pigmented epiretinal membrane (large arrows), matching the shape of the dexamethasone implant, in the macula where the implant was trapped under oil. A small fragment of implant material incorporated into the membrane is visualized as a bright white spot (small arrow). B, Fundus photograph at last follow-up. Pigmented epiretinal membrane has regressed (large arrow). The small fragment of incorporated implant material remains unchanged (small arrow). C, Spectral-domain optical coherence tomography at last visit showing loss of foveal contour from the epiretinal membrane.
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