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 Table of Contents  
Year : 2015  |  Volume : 108  |  Issue : 3  |  Page : 136-139

Intravitreal injection of ranibizumab for chronic central serous chorioretinopathy

Department of Ophthalmology, Suez Canal University, Ismailia, Egypt

Date of Submission07-Apr-2015
Date of Acceptance27-Jun-2015
Date of Web Publication30-Oct-2015

Correspondence Address:
Amr Abdel-Fattah Ali Gab-Alla
Department of Ophthalmology, Suez Canal University, Ismailia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2090-0686.168703

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The aim of this study was to evaluate the efficacy of intravitreal injection of ranibizumab for patients with chronic central serous chorioretinopathy (CCSC).
Materials and methods
A prospective interventional noncomparative study was conducted on nine patients with CCSC who were treated with an intravitreal injection of ranibizumab once. Visual acuity with Snellen's chart and the foveal thickness were studied before and after the injection.
The mean age of the patients was 44.3 ± 5.7 years. After 1 month of intravitreal injection, visual acuity improved from 20/120 to 20/30 (P < 0.001). Central retinal thickness improved from 493 ± 76 μm (before injection) to 216 ± 36 μm (1 month after injection) (P < 0.001). None of the cases exhibited relapses.
Intravitreal injection of ranibizumab can be an optional treatment in patients with CCSC as it leads to an anatomic and functional improvement.

Keywords: Central retinal thickness, central serous chorioretinopathy, intravitreal injection, ranibizumab

How to cite this article:
Gab-Alla AA. Intravitreal injection of ranibizumab for chronic central serous chorioretinopathy. J Egypt Ophthalmol Soc 2015;108:136-9

How to cite this URL:
Gab-Alla AA. Intravitreal injection of ranibizumab for chronic central serous chorioretinopathy. J Egypt Ophthalmol Soc [serial online] 2015 [cited 2022 Sep 28];108:136-9. Available from: http://www.jeos.eg.net/text.asp?2015/108/3/136/168703

  Introduction Top

Central serous chorioretinopathy (CSC) is an idiopathic disorder (described by Albrecht von Graefe) that causes serous neurosensory retinal detachment, with active retinal pigment epithelium (RPE) leakage in the macular area [1].

Patients with CSC complain of decreased vision, micropsia, metamorphopsia, color vision changes, and a positive scotoma caused by macular region detachment. The pathogenesis and treatment of CSC are still unclear. It has been reported that the acute form of CSC is usually self-limited and resolves spontaneously in about 4-6 months [2]. Good visual acuity is regained after spontaneous resolution of macular detachment [3]. Infrequently, neurosensory retinal detachment persists and leads to RPE and photoreceptor damage. This form of the disorder is called chronic central serous chorioretinopathy (CCSC) and can result in severe effects on macular function [4].

CSC usually affects young and middle-aged adults, with a higher prevalence in men than in women. The patients' medical history, family history, and general physical examinations are in most cases unremarkable. The pathogenesis of chronic central serous chorio-retinopathy (CCSC) remains indistinct [5].

Medical treatments have no proven effects on the disease. Laser photocoagulation has been widely used. However, the results of different studies on this subject matter are divisive and not conclusive, and laser photocoagulation remains recommended only in selected cases [6],[7],[8].

Ranibizumab is a recombinant humanized antibody fragment that blocks vascular endothelial growth factor (VEGF). It is injected intravitreally as a treatment for exudative age-related macular degeneration [9], diabetic macular edema [10], and macular edema secondary to central and branch retinal vein occlusion [11]. In other retinal pathologies, such as choroidal neovascularization secondary to pathologic myopia or other etiologies and retinopathy of prematurity, its efficacy is under investigations.

  Materials and methods Top

This prospective interventional noncomparative study included nine eyes of nine patients with CCSC (defined as symptoms persisting for more than 6 months). Patients with documented neurosensory detachment on optical coherence tomography (OCT), active leak on fluorescein angiography (FA), and no signs of choroidal neovascularization were included in the study. Patients who had undergone previous treatment with laser photocoagulation, photodynamic therapy (PDT), intravitreal triamcinolone, or bevacizumab in the previous 3 months, glaucoma (intraocular pressure >21 mmHg) patients, those lost to follow-up, and those with previously vitrectomized eyes were excluded from the study.

All eyes were injected with intravitreal ranibizumab (0.5 mg/0.05 ml) once. At baseline and follow-up visits, patients were subjected to best-corrected visual acuity (BCVA), intraocular pressure evaluation, dilated fundus examination, FA, and OCT for measurement of central retinal thickness (CRT).

Outcome was the resolution of neurosensory detachment, improvement in visual symptoms and visual acuity, and resolution of leakage in FA. In all patients, ranibizumab was injected intravitreally in a standard procedure in the operating theater under an operating ophthalmoscope and complete aseptic condition after obtaining informed consent.

Postoperative follow-up included repeated clinical examinations and repeated FA and OCT. Follow-up evaluations were carried out the next day, at 1 week, and then monthly until the 6 months of follow-up. The procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation and the Helsinki Declaration.

Statistical analysis

Collected data were coded, entered, and analyzed using Microsoft Excel software. Data were then imported into Statistical Package for the Social Sciences (SPSS version 10.0) software for analysis. Descriptive statistics were presented as mean ± SD for quantitative data and as n (%) for qualitative data. Statistical significance was determined at 95% level of confidence (P < 0.05).

  Results Top

The study included nine eyes of nine male patients who received intravitreal ranibizumab injection for CCSC (defined as symptoms present for longer than 6 months). The mean age of patients was 44.3 ± 5.7 years. No one had a history of recent corticosteroid therapy. The mean follow-up period was 6 months.

The mean baseline visual acuity was 20/120 and improved to 20/30 at the last follow-up, with statistically significant difference (P < 0.001). All eyes had visual improvement; 80% of patients had gained two or more lines. None of the eyes had decreased vision compared with the baseline BCVA. There was a significant decrease in the mean of CRT throughout the study, which was correlated with the improvement in both of BCVA and FA leakage.

The mean baseline CRT for all patients was 493 ± 76 μm and decreased to 216 ± 36 μm after 1 month, with statistically significant difference (P < 0.001); at the last follow-up at sixth month, there was a statistically significant difference from the baseline (P < 0.001). None of the cases exhibited relapses [Figure 1] and [Figure 2].
Figure 1: (a) Fluorescein angiogram of right chronic central serous chorioretinopathy; (b) optical coherence tomography (OCT) of the macula at baseline, central retinal thickness (CRT) = 480 μm; (c) OCT of the same patient after 1 month of intravitreal injection of ranibizumab, CRT = 232 μm.

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Figure 2: (a) Fluorescein angiogram of left chronic central serous chorioretinopathy; (b) optical coherence tomography (OCT) of the macula at baseline, central retinal thickness (CRT) = 656 μm; (c) OCT of the same patient after 1 month of intravitreal injection of ranibizumab, CRT = 207 μm.

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  Discussion Top

CSC is a condition in which detachment of the neurosensory retina occurs over an area of leakage from the choriocapillaris through the RPE. CCSC is characterized by neurosensory retinal detachment overlying areas of RPE atrophy and pigment mottling [12]. Prior hypotheses for the pathophysiology have incorporated abnormal ion transport across the RPE and focal choroidal vasculopathy. Indocyanine green angiography has confirmed both multifocal choroidal hyperpermeability and hypofluorescent areas indicative of focal choroidal vascular compromise. A number of investigators suppose that initial choroidal vascular compromise leads to secondary dysfunction of the overlying RPE [12].

Stewart [13] mentioned that laser damages the RPE with a risk of developing choroidal neovascularization, which has left clinicians looking for new treatments that are both more effective and less toxic. Researchers have also used the 810 nm laser, as in transpupillary thermotherapy. However, Penha et al. [14] described severe retinal thermal injury in a 31-year-old man following this treatment and recommended caution for this adverse complications.

Cardillo Piccolino et al. [15] stated that PDT guided by indocyanine green angiography seems to treat macular detachment and serous exudation and preserve visual acuity in patients with CCSC. PDT may possibly decrease choriocapillaris blood flow and choroidal exudation in the areas of subretinal fluid production. However, there are undesired effects such as pigmentary changes in the treatment zone and persistent hypoperfusion of the choriocapillaris. Chan et al. [16] stated that development of choroidal neovascularization within the photodynamic region was due to localized ischemia in the choriocapillaris resulting from PDT in CCSC.

Shams and Ianchulev [17] stated that VEGF is a regulator of ocular angiogenesis and vascular permeability. When increased choroidal hyperpermeability claimed to be one of the main causes of CSC, it seemed logic to treat such cases with anti-VEGF such as ranibizumab.

Kim et al. [18] studied the effectiveness of intravitreal ranibizumab injection for acute CSC (symptomatic for less than 3 months) on 20 patients (0.5 mg/0.05 ml) who were followed up for 6 months. All patients had increased BCVA, decreased CRT, and resolution of the neurosensory detachment.

In this study, an intravitreal injection of ranibizumab was used for the treatment of CCSC, which showed good results; however, there is no straight evidence as regards the role of VEGF in inducing CSC.

The overall mean of BCVA in our study improved from 20/120 at baseline to 20/30 after 1 month and stayed stationary for 6 months after the intravitreal injection of ranibizumab (0.5 mg/0.05 ml) due to complete resolution of all cases after one intravitreal injection. Improvement in vision relies on the duration of the disease and the amount of photoreceptor damage. However, all eyes had visual improvement and 80% of patients gained two or more lines improvement compared with the baseline.

Torres-Soriano et al. [19] reported in a study of six eyes (five chronic and one recurrent CSC) that visual acuity improved in all cases by 1 month after bevacizumab injection and remained stable up to the third month; they reported BCVA improvement from 20/200 at baseline to 20/100 at 1 month and 20/50 at 3 months, as well as a decrease in neurosensory detachment on OCT. Two eyes (1/3 of patients) required a second injection of bevacizumab with a higher concentration dose of 2.5 mg.

Schaal et al. [12] treated 12 eyes with CCSC in which patients received 2 ± 1 intravitreal injections of bevacizumab (2.5 mg) on average during a follow-up of 24 ± 14 weeks. Mean BCVA increased by 2 ± 2 lines; the change in BCVA was significant (P < 0.02). Mean CRT improved significantly over follow-up (P < 0.05), with six patients (50%) showing complete resolution of subretinal fluid.

  Conclusion Top

The anatomic and functional improvement after intravitreal ranibizumab injection suggests that VEGF may be implicated in fluid leakage in patients with CCSC. The study also suggests a potential role for anti-VEGF agents in the treatment of CCSC. Further assessment of intravitreal ranibizumab for CCSC in controlled randomized large number of patients with longer follow-up period is required to confirm the efficacy of ranibizumab and to determine the ideal protocol for this new hopeful treatment option.

  Acknowledgements Top

Conflicts of interest

There are no conflicts of interest.

  References Top

Gass JD. Pathogenesis of disciform detachment of the neuroepithelium: II. Idiopathic central serous chorio-retinopathy. Am J Ophthalmol 1967; 63 :587-615.  Back to cited text no. 1
Hussain D, Gass JD. Idiopathic central serous chorio-retinopathy. Indian J Ophthalmol 1998; 46 :131-137.  Back to cited text no. 2
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Bird AC. Pathogenesis of serous detachment of retina and pigment epithelium. In: Ryan SJ, editor Retina. 3rd ed. St Louis: Mosby Inc: 2001;995-1002.  Back to cited text no. 5
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De Laey JJ. Central serous chorio-retinopathy: to treat or not to treat?. Doc Ophthalmol 1986; 61 :367-372.  Back to cited text no. 7
Ficker L, Vafidis G, While A, Leaver P. Long-term follow-up of a prospective trial of argon laser photocoagulation in the treatment of central serous retinopathy. Br J Ophthalmol 1988; 72 :829-834.  Back to cited text no. 8
Rosenfeld PJ, Brown DM, Heier JS, Boyer DS, Kaiser PK, Chung CY, et al. Ranibizumab for neovascular age-related macular degeneration. N Engl J Med 2006; 355 :1419-1431.  Back to cited text no. 9
Mitchell P, Bandello F, Schmidt-Erfurth U, Lang GE, Massin P, Schlingemann RO, et al. The RESTORE study: ranibizumab monotherapy or combined with laser versus laser monotherapy for diabetic macular edema. Ophthalmology 2011; 118 :615-625.  Back to cited text no. 10
Brown DM, Campochiaro PA, Singh RP, Li Z, Grav S, Saroi N, et al. Ranibizumab for macular edema following central retinal vein occlusion: six-month primary end point results of a phase III study. Ophthalmology 2010; 117 :1124-1133.  Back to cited text no. 11
Schaal KB, Hoeh AE, Scheuerle A, Schuett F, Dithmar S. Intravitreal bevacizumab for treatment of chronic central serous chorio-retinopathy. Eur J Ophthalmol 2009; 19 :613-617.  Back to cited text no. 12
Stewart JM. Central serous chorio-retinopathy half dose verteporfin PDT for central serous chorio-retinopathy. Br J Ophthalmol 2006; 90 :805-806.  Back to cited text no. 13
Penha FM, Aggio FB, Bonomo PP. Severe retinal thermal injury after indocyanine green-mediated photothrombosis for central serous chorio-retinopathy. Am J Ophthalmol 2007; 143 :887-889.  Back to cited text no. 14
Cardillo Piccolino F, Eandi CM, Ventre L, Rigaultde de la Longrais RC, Grignolo FM. Photodynamic therapy for chronic central serous chorio-retinopathy. Retina 2003; 23 :752-763.  Back to cited text no. 15
Chan WM, Lam DS, Lai TY. Choroidal vascular remodeling in central serous chorio-retinopathy after indocyanine green guided photodynamic therapy with verteporfin: a novel treatment at primary disease level. Br J Ophthalmol 2003; 87 :1453-1458.  Back to cited text no. 16
Shams N, Ianchulev T. Role of vascular endothelial growth factor in ocular angiogenesis. Ophthalmol Clin North Am 2006; 19 :335-344.  Back to cited text no. 17
Kim M, Lee S, Lee S. Intravitreal ranibizumab for acute central serous chorio-retinopathy. Ophthalmologica 2013; 229 :152-157.  Back to cited text no. 18
Torres-Soriano ME, Garcia-Aguirre G, Kon-Jara, V, Ustariz-Gonzales O, Abraham-Marin M, Ober MD, et al. A pilot study of intra-vitreal bevacizumab for the treatment of central serous chorio-retinopathy (case reports). Graefe′s Arch Clin Exp Ophthalmol 2008; 246 :1235-1239.  Back to cited text no. 19


  [Figure 1], [Figure 2]


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