|LETTER TO THE EDITOR
|Year : 2011 | Volume
| Issue : 4 | Page : 338-339
Intravitreal bevacizumab for subfoveal choroidal neovascularization complicating active central serous chorioretinopathy
Subrata Mandal, Subijay Sinha, Zahir Abbas, Pradeep Venkatesh
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS, New Delhi - 110 029, India
|Date of Web Publication||11-Jun-2011|
CN 5, Sector V, Saltlake, Kolkata-700091
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mandal S, Sinha S, Abbas Z, Venkatesh P. Intravitreal bevacizumab for subfoveal choroidal neovascularization complicating active central serous chorioretinopathy. Indian J Ophthalmol 2011;59:338-9
|How to cite this URL:|
Mandal S, Sinha S, Abbas Z, Venkatesh P. Intravitreal bevacizumab for subfoveal choroidal neovascularization complicating active central serous chorioretinopathy. Indian J Ophthalmol [serial online] 2011 [cited 2020 Feb 27];59:338-9. Available from: http://www.ijo.in/text.asp?2011/59/4/338/82021
Idiopathic central serous chorioretinopathy (CSCR) usually affects middle-aged men and is characterized by a serous neurosensory retinal detachment in the macular region. Visual disturbances are usually mild and spontaneous recovery occurs over a few months. Some eyes with CSCR may however have a poor visual outcome due to retinal pigment epithelium atrophy, persistent pigment epithelial detachment, subretinal fluid, recurrences, and submacular choroidal neovascularization (CNV).  Probable reasons for development of CNV following CSCR are decompensation of the pigment epithelium/Bruch's membrane complex by disease process itself, or puncture of Bruch's membrane by laser burns used to treat the disease. 
The reported treatment options for CNV secondary to CSCR are laser photocoagulation, photodynamic therapy (PDT) 
and transpupillary thermotherapy (TTT). As intravitreal bevacizumab (IVBe) has shown encouraging results in CNV from different etiologies, we tried it as a treatment for CNV secondary to CSCR in the patient described herein.
A 36-year-old man presented with sudden blurring of vision in the right eye (RE). Patient also revealed that he had suffered from a similar episode nine months earlier from which he had recovered spontaneously. At presentation he had a best corrected vision acuity (BCVA) of 20/200 RE and 20/20 in left eye (LE). Fundus examination indicated the presence of CSCR and subfoveal CNV in the RE. Existence of both pathologies concurrently were confirmed on fundus fluorescein angiography (FFA) and optical coherence tomography (OCT) [Stratus OCT]. FFA demonstrated subfoveal early hyperfluorescence with increasing leakage in the late phase suggestive of CNV. It also showed an ink-blot hyper-fluorescence superior to the fovea gradually increasing in size and intensity [Figure 1] indicative of active CSCR. OCT revealed subfoveal CNV, subretinal fluid and cystoid retinal edema [Figure 2].
|Figure 1: Fundus photographs and fundus fluorescein angiography. First row: Fundus photograph and angiogram showing active central serous chorioretinopathy with ink-blot leakage superior to the fovea and subfoveal classic choroidal neovascularisation. Second row: Follow-up photograph and angiogram one month after intravitreal bevacizumab (1.25 mg/0.05 ml) show absence of ink-blot leakage and resolution of the neovascular membrane|
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|Figure 2: Optical coherence tomography. Horizontal and vertical 6-mm line scan Optical coherence tomography images show subfoveal choroidal neovascular membrane associated with subretinal fluid and cystoid macular edema at baseline (first row). Repeat Optical coherence tomography scans show disappearance of cystoid edema and complete resolution of subretinal fluid at one-month follow-up (second row)|
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After obtaining informed consent, off-label IVBe (1.25 mg/0.05 ml) was administered. One month after injection repeat FFA showed absence of ink-blot leakage and decreased leakage from CNV. OCT demonstrated resolution of both subretinal fluid and cystoid edema [Figure 2]. His BCVA improved to 20/25 RE at one month and was maintained till one year follow-up. No recurrence in CSCR or CNV was seen.
It is well recognized that CNV requires mediators of angiogenesis. The most widely studied mediator has been vascular endothelial growth factor (VEGF), which plays a central role in the complex cascade of vessel growth, proliferation, and hyper-permeability. Intravitreal injections of bevacizumab, a humanized anti-VEGF antibody which inhibits VEGF-A protein has been reported to produce favorable results in CNV from various etiologies. Our patient had active CSCR along with classic subfoveal CNV. The role of VEGF and anti-VEGF agents in CSCR has not been studied widely. Some reports suggest favorable results of bevacizumab in CSCR. , In our case we found prompt resolution of ink-blot leak and CNV exudation.
In conclusion, the anatomic and visual result in the eye with CNV associated with active CSCR after IVBe is encouraging. Further studies are required to confirm the efficacy and safety of bevacizumab in the management of concurrent CSCR and CNV.
| References|| |
Loo RH, Scott IU, Flynn HW Jr, Gass JD, Murray TG, Lewis ML, et al
. Factors associated with reduced visual acuity during long-term follow-up of patients with idiopathic central serous chorioretinopathy. Retina 2002;22:19-24.
Gomolin JE. Choroidal neovascularization and central serous chorioretinopathy. Can J Ophthalmol 1989;24:20-3.
Chan WM, Lam DS, Lai TY, Yuen KS, Liu DT, Chan CK, Treatment of Choroidal Neovascularization in Central Serous Chorioretinopathy by Photodynamic Therapy With Verteporfin. Am J Ophthalmol 2003;136:836-45.
Chan WM, Lai TY, Liu DT, Lam DS. Intravitreal bevacizumab (avastin) for choroidal neovascularization secondary to central serous chorioretinopathy, secondary to punctate inner choroidopathy, or of idiopathic origin. Am J Ophthalmol 2007;143:977-83.
Schaal KB, Hoeh AE, Scheuerle A, Schuett F, Dithmar S Intravitreal bevacizumab for treatment of chronic central serous chorioretinopathy. Eur J Ophthalmol 2009;19:613-7.
[Figure 1], [Figure 2]