Graefes Arch Clin Exp Ophthalmol (2014) 252:1017–1019 DOI 10.1007/s00417-014-2631-5
CASE REPORT
Intraretinal brilliant blue G infiltration during internal limiting membrane peeling Perrine Savary & Laurent Kodjikian
Received: 2 November 2013 / Revised: 27 March 2014 / Accepted: 31 March 2014 / Published online: 3 May 2014 # Springer-Verlag Berlin Heidelberg 2014
Introduction Macular surgery has developed widely during the past decade, simplified by the use of vital dyes such as indocyanine green, trypan blue, or brilliant blue G (BBG) [1, 2]. Brilliant blue G’s safety profile has been studied for both intravitreal and subretinal injections. To our knowledge, the intraretinal injection of BBG has never been tested for safety. We report a case of accidental intraretinal migration of BBG during internal limiting membrane (ILM) staining for epiretinal membrane (ERM) surgery.
Case report A 72-year-old female patient had an idiopathic ERM which caused a decrease in visual acuity (BCVA = 20/30) and metamorphopsia. Pars plana vitrectomy and ERM peeling was proposed and accepted by the patient. The surgeon first performed a near complete 25Ga vitrectomy through a three-port pars plana approach (Constellation, Alcon). A jet stream of BBG (Brilliant Peel, Fluoron/Geuder, Ulm, Germany; 0.25 mg/ml) was used to colour the ILM and was then washed out. The internal limiting membrane was easily peeled using a diamond membrane scraper, with no retinal touch seen or felt by the surgeon. A second injection of BBG administered to check the ILM was entirely removed. An abnormal dying of the retina was observed during the injection, and therefore the staining was stopped. An additional vitrectomy allowed the surgeon to see that the dying persisted but had not reached the foveal area. The ILM had P. Savary (*) : L. Kodjikian Ophthalmology Department, Hopital de la Croix-Rousse, 103 grande rue de la Croix-Rousse, 69004 Lyon, France e-mail: [email protected]
been entirely peeled around the macular area during the first peeling. At day 1, the BBG infiltration was still present: it was located temporal and superior to the fovea, and measured under a disc in diameter (Fig. 1). Optical coherence tomography (OCT) images revealed a defect on the retinal nerve fiber layer that was not present on the preoperative OCT. This defect was unique and focal, located at the higher pole of the infiltration, probably the retinal dying inlet. The infiltration reached all retinal layers up to the retinal pigment epithelium (RPE) without affecting the subretinal area. Over the duration of follow-up, the infiltration disappeared, with progressive local atrophy of inner retinal layers as an after-effect. At 1.5 months after surgery, BCVA had reached 20/25, and the patient had no metamorphopsia. The clinical examination was unchanged 3 years after surgery, and the microperimetry did not show any scotoma (Fig. 2).
Discussion BBG toxicity has been studied for intravitreal and subretinal injection [2, 3]. This case raises the issue of intraretinal BBG toxicity. Indeed, the after-effect of the infiltration was local atrophy of the inner layers directly in contact with the dyed retina. No toxicity was observed outside of the infiltration area, neither in the photoreceptor layer nor the RPE. Consequently, two mechanisms may explain this atrophy: either it is a result of the local chemical toxicity of the intraretinal BBG, or it is simply scarring from the initial local defect which caused the infiltration, with no direct toxicity from the intraretinal BBG. The second point for discussion is the mechanism that created the tiny hole. Its absence before surgery would lead us to suspect an iatrogenic cause. Therefore, it could either have been caused due to a BBG jet stream that was too
1018
Graefes Arch Clin Exp Ophthalmol (2014) 252:1017–1019
Pre operative OCT images 02/16/2011 D+1 04/08/2011
M+1.5 05/23/2011
M+35 03/04/2014
Fig. 1 Fundus ophtalmoscopy and OCT images showing BBG’s infiltration through defect on retinal nerve fiber layer (red asterisk ) and local atrophy of inner layer (orange arrow ) as after-effect
Fig. 2 No scotoma was detected on microperimetry (03/04/2014)
powerful, or have formed during the peeling secondary to retinal traction. A similar case of subretinal migration of BBG was reported in 2009 [4]. The mechanism of infiltration was again not clearly identified, and the subretinal BBG caused damage to the retinal pigment epithelium.
Conflict of interest None. Presentation at a conference EVER 2012, poster Patient consent Obtained
Conclusion
References
This unusual complication to ERM peeling surgery has led us to adapt our technique: supposing the defect was caused by the BBG jet stream, we now allow the BBG to flow gently into the vitreous cavity. Nevertheless, the question of intraretinal BBG toxicity remains unresolved.
1. Burk SE, Da Mata AP, Snyder ME, Rosa RH Jr, Foster RE (2000) Indocyanine green-assisted peeling of the retinal internal limiting membrane. Ophthalmology 107(11):2010–2014 2. Enaida H, Hisatomi T, Goto Y et al (2006) Preclinical investigation of internal limiting membrane staining and peeling using intravitreal brilliant blue. G Retina 26(6):623–30
Graefes Arch Clin Exp Ophthalmol (2014) 252:1017–1019 3. Ueno A, Hisatomi T, Enaida H, Kagimoto T, Mochizuki Y, Goto Y, Kubota T, Hata Y, Ishibashi T (2007) Biocompatibility of brilliant blue G in a rat model of subretinal injection. Retina 27(4):499–504
1019 4. Malerbi FK, Maia M, Farah ME, Rodrigues EB (2009) Subretinal Brilliant Blue G migration during internal limiting membrane peeling. Br J Ophthalmol 93:1687
CASE REPORT
Intraretinal brilliant blue G infiltration during internal limiting membrane peeling Perrine Savary & Laurent Kodjikian
Received: 2 November 2013 / Revised: 27 March 2014 / Accepted: 31 March 2014 / Published online: 3 May 2014 # Springer-Verlag Berlin Heidelberg 2014
Introduction Macular surgery has developed widely during the past decade, simplified by the use of vital dyes such as indocyanine green, trypan blue, or brilliant blue G (BBG) [1, 2]. Brilliant blue G’s safety profile has been studied for both intravitreal and subretinal injections. To our knowledge, the intraretinal injection of BBG has never been tested for safety. We report a case of accidental intraretinal migration of BBG during internal limiting membrane (ILM) staining for epiretinal membrane (ERM) surgery.
Case report A 72-year-old female patient had an idiopathic ERM which caused a decrease in visual acuity (BCVA = 20/30) and metamorphopsia. Pars plana vitrectomy and ERM peeling was proposed and accepted by the patient. The surgeon first performed a near complete 25Ga vitrectomy through a three-port pars plana approach (Constellation, Alcon). A jet stream of BBG (Brilliant Peel, Fluoron/Geuder, Ulm, Germany; 0.25 mg/ml) was used to colour the ILM and was then washed out. The internal limiting membrane was easily peeled using a diamond membrane scraper, with no retinal touch seen or felt by the surgeon. A second injection of BBG administered to check the ILM was entirely removed. An abnormal dying of the retina was observed during the injection, and therefore the staining was stopped. An additional vitrectomy allowed the surgeon to see that the dying persisted but had not reached the foveal area. The ILM had P. Savary (*) : L. Kodjikian Ophthalmology Department, Hopital de la Croix-Rousse, 103 grande rue de la Croix-Rousse, 69004 Lyon, France e-mail: [email protected]
been entirely peeled around the macular area during the first peeling. At day 1, the BBG infiltration was still present: it was located temporal and superior to the fovea, and measured under a disc in diameter (Fig. 1). Optical coherence tomography (OCT) images revealed a defect on the retinal nerve fiber layer that was not present on the preoperative OCT. This defect was unique and focal, located at the higher pole of the infiltration, probably the retinal dying inlet. The infiltration reached all retinal layers up to the retinal pigment epithelium (RPE) without affecting the subretinal area. Over the duration of follow-up, the infiltration disappeared, with progressive local atrophy of inner retinal layers as an after-effect. At 1.5 months after surgery, BCVA had reached 20/25, and the patient had no metamorphopsia. The clinical examination was unchanged 3 years after surgery, and the microperimetry did not show any scotoma (Fig. 2).
Discussion BBG toxicity has been studied for intravitreal and subretinal injection [2, 3]. This case raises the issue of intraretinal BBG toxicity. Indeed, the after-effect of the infiltration was local atrophy of the inner layers directly in contact with the dyed retina. No toxicity was observed outside of the infiltration area, neither in the photoreceptor layer nor the RPE. Consequently, two mechanisms may explain this atrophy: either it is a result of the local chemical toxicity of the intraretinal BBG, or it is simply scarring from the initial local defect which caused the infiltration, with no direct toxicity from the intraretinal BBG. The second point for discussion is the mechanism that created the tiny hole. Its absence before surgery would lead us to suspect an iatrogenic cause. Therefore, it could either have been caused due to a BBG jet stream that was too
1018
Graefes Arch Clin Exp Ophthalmol (2014) 252:1017–1019
Pre operative OCT images 02/16/2011 D+1 04/08/2011
M+1.5 05/23/2011
M+35 03/04/2014
Fig. 1 Fundus ophtalmoscopy and OCT images showing BBG’s infiltration through defect on retinal nerve fiber layer (red asterisk ) and local atrophy of inner layer (orange arrow ) as after-effect
Fig. 2 No scotoma was detected on microperimetry (03/04/2014)
powerful, or have formed during the peeling secondary to retinal traction. A similar case of subretinal migration of BBG was reported in 2009 [4]. The mechanism of infiltration was again not clearly identified, and the subretinal BBG caused damage to the retinal pigment epithelium.
Conflict of interest None. Presentation at a conference EVER 2012, poster Patient consent Obtained
Conclusion
References
This unusual complication to ERM peeling surgery has led us to adapt our technique: supposing the defect was caused by the BBG jet stream, we now allow the BBG to flow gently into the vitreous cavity. Nevertheless, the question of intraretinal BBG toxicity remains unresolved.
1. Burk SE, Da Mata AP, Snyder ME, Rosa RH Jr, Foster RE (2000) Indocyanine green-assisted peeling of the retinal internal limiting membrane. Ophthalmology 107(11):2010–2014 2. Enaida H, Hisatomi T, Goto Y et al (2006) Preclinical investigation of internal limiting membrane staining and peeling using intravitreal brilliant blue. G Retina 26(6):623–30
Graefes Arch Clin Exp Ophthalmol (2014) 252:1017–1019 3. Ueno A, Hisatomi T, Enaida H, Kagimoto T, Mochizuki Y, Goto Y, Kubota T, Hata Y, Ishibashi T (2007) Biocompatibility of brilliant blue G in a rat model of subretinal injection. Retina 27(4):499–504
1019 4. Malerbi FK, Maia M, Farah ME, Rodrigues EB (2009) Subretinal Brilliant Blue G migration during internal limiting membrane peeling. Br J Ophthalmol 93:1687
