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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 59  |  Issue : 4  |  Page : 376-378

Central serous chorioretinopathy following intravenous steroid therapy for retrobulbar optic neuritis – “Treatment dilemma” – Case report and review of literature


1 Department of Retina and Vitreous, Aravind Eye Hospital, Puducherry, India
2 Department of Neurophthalmology, Aravind Eye Hospital, Puducherry, India

Date of Submission31-Oct-2020
Date of Decision21-Feb-2021
Date of Acceptance04-Aug-2021
Date of Web Publication21-Dec-2021

Correspondence Address:
Dr. Roshni Mohan
Department of Retina and Vitreous, Aravind Eye Hospital, Thavalakuppam, Puducherry - 605 007
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/tjosr.tjosr_163_20

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  Abstract 


The adverse reactions of high-dose exogenous steroid administration are well documented, and central serous chorioretinopathy (CSCR) is one among them. Steroid-induced CSCR has a different clinical profile when compared to idiopathic CSCR and poses a unique clinical challenge, especially when encountered during the management of posterior-segment inflammation such as optic neuritis and posterior uveitis. The clinical course of steroid-induced CSCR is variable and is not dose dependent. Management options include observation, cessation of steroids when permissible, focal laser, photodynamic therapy, and switching to alternative immunosuppressive therapy. We describe a case of steroid-induced recurrent bilateral CSCR during the treatment of unilateral isolated retrobulbar neuritis in a young male, its clinical course, and management. Our case emphasizes the importance of obtaining prior informed consent explaining the possible side effects of high-dose steroid therapy, and documentation is very important for the management of these complex case scenarios.

Keywords: Exogenous steroids, focal laser, optic neuritis, optic neuritis treatment trial, steroid-induced central serous chorioretinopathy


How to cite this article:
Mohan R, Arthi M, Basker A, Sivakumar P. Central serous chorioretinopathy following intravenous steroid therapy for retrobulbar optic neuritis – “Treatment dilemma” – Case report and review of literature. TNOA J Ophthalmic Sci Res 2021;59:376-8

How to cite this URL:
Mohan R, Arthi M, Basker A, Sivakumar P. Central serous chorioretinopathy following intravenous steroid therapy for retrobulbar optic neuritis – “Treatment dilemma” – Case report and review of literature. TNOA J Ophthalmic Sci Res [serial online] 2021 [cited 2022 Aug 12];59:376-8. Available from: https://www.tnoajosr.com/text.asp?2021/59/4/376/333161




  Introduction Top


Central serous chorioretinopathy (CSCR) is characterized by fluid accumulation in the neurosensory retina and may be associated with serous pigment epithelial detachment (PED) and retinal pigment epithelium (RPE) atrophy in long-standing cases.[1] It is widely known to be associated with endogenous and exogenous hypercortisolism including oral, intravenous, intranasal, topical, intra-articular, and intrathecal routes. Steroid-induced CSCR has lesser male preponderance, has bilateral presentation, and may present in atypical variants – diffuse retinal pigment epitheliopathy, acute bullous retinal detachments with or without fibrin, subretinal fibrosis, and multifocal RPE detachments.[2]


  Case Report Top


A 37-year-old male presented with sudden-onset defective vision in the left eye (LE) for 1 week with retro-orbital pain. His best-corrected visual acuity (BCVA) was 20/20 and 20/200 in the right eye (RE) and LE, respectively. On examination, LE had grade 3 relative afferent pupillary defect with normal fundus. Color vision was defective with superior field defect in static perimetry (Humphrey's visual field analyzer 30-2 protocol) in the LE. RE was normal. Systemic evaluations including routine blood investigations and magnetic resonance imaging of brain and orbit with contrast were normal. Visual evoked potential was done that showed prolonged latency of P100 in the LE compared to RE. A diagnosis of LE retrobulbar optic neuritis (RBN) was made and the patient was started on intravenous methyl prednisolone (IVMP) 500 mg twice daily for 3 days as per the Optic Neuritis Treatment Trial (ONTT). Post-IVMP, BCVA was 20/20 and 20/80 in the RE and LE, respectively. Fundus examination was normal in the RE with subretinal fluid (SRF) at the fovea in the LE. Optical coherence tomography (OCT) showed small serous PED at the fovea in RE and SRF with fibrin in the LE with pachy vessels in both eyes [Figure 1] and [Figure 2]. Oral steroids were withheld in view of the development of LE CSCR. A week later, BCVA RE had dropped to 20/40 and LE was 20/60. He had developed SRF in both eyes (BE). In view of bilateral CSCR, oral steroids were discontinued. Spectral-domain (SD)-OCT showed neurosensory detachment (NSD) with PED in the RE and persisting fibrinous SRF in the LE [Figure 1] and [Figure 2]. Fundus fluorescein angiography (FFA) showed an inkblot (superior) and a smokestack leak (inferior) in the RE and a single inkblot leak in the LE [Figure 3]. FFA-guided focal laser was done using 532 nm frequency-doubled Nd: YAG laser in BE. One week postlaser, OCT revealed reduction in SRF in BE with flattening of PED in RE. One month postlaser, there was complete resolution of SRF in RE and persistent SRF in LE. We observed the patient, and 2 months postlaser, BCVA was 20/20 in the RE and 20/30 in the LE, RE was dry, and SRF with serous PED persisted in the LE. Since the patient was a young male with high visual demand, we repeated the FFA which revealed window defects in the RE and subfoveal leakage in the LE [Figure 4]. Subthreshold micropulse yellow laser of 577 nm (5% duty cycle) was done in the LE for persistent SRF in view of the leak being subfoveal. The patient showed clinical improvement postmicropulse laser.
Figure 1: Optical coherence tomography images of the right eye. (a) Baseline optical coherence tomography, (b) enhanced depth imaging optical coherence tomography 7 days postintravenous methyl prednisolone, showing neurosensory detachment and subfoveal pachy vessels (denoted by asterisk in white). (c) Resolving neurosensory detachment postlaser therapy, discontinued lines marking the junction of sclera and choroid (denoting pachychoroid), subfoveal choroidal thickness - 635 μ. (d-f) showing macular scan at 1, 2, and 6 months

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Figure 2: Spectal-domain optical coherence tomography of the left eye. (a) Optical coherence tomography showing neurosensory detachment with hyperreflective material in the detachment (fibrin), (b) persisting central serous chorioretinopathy 7 days postintravenous methyl prednisolone (c) resolving neurosensory detachment postlaser therapy, discontinued white lines showing the junction of sclera and choroid denoting pachychoroid, asterisk in white denoting pachy vessel, subfoveal choroidal thickness - 525 μ. (d) Enhanced depth imaging optical coherence tomography postlaser showing clearing of fibrin and small pigment epithelial detachment. (e and f) Enhanced depth imaging optical coherence tomography showing resolving subretinal fluid postsubthreshold laser

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Figure 3: Fundus fluorescein angiography images OD, OS. (a) Early frames of the angiography in OD showing early ink blot leakage in the superior part in between the vascular arcades. (b) showing increasing ink blot leakage in the superior part and smoke stack leak in the inferotemporal aspect. (c) Late frames OD showing typical pattern of leakage as mentioned previously. (d) OS early frames showing early leak in inferotemporal aspect of FAZ. (e) Mid frames OS showing increasing intensity of the leak. (f) Intense leakage in late frames

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Figure 4: Postlaser repeat fundus fluorescein angiography. (a and b) Fundus fluorescein angiography OD showing window defects and no new leaks. (c) Fundus fluorescein angiography OS showing persistent faint leak and few window defects. (d) Persistent faint leak OS in the border of FAZ

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  Discussion Top


The exact role of steroids in the pathophysiology of CSCR is not fully understood. Ambiya et al. showed increased choroidal vascularity index (CVI) in patients with steroid-induced CSCR, which is suggestive of a higher choroidal vascular component compared to stromal component contributing to the pathogenesis.[3] Glucocorticoids suppress synthesis of extracellular matrix elements and inhibits fibroblastic activity inflicting harm to the RPE cells and their tight junctions, increasing the capillary fragility and hyperpermeability with leakage of fluid into the subretinal area. They release catecholamines and also cause platelet aggregation, leading to hypercoagulability, microthrombus formation, and increased blood viscosity, which affect the choroidal microcirculation.[4]

Patients treated with higher doses of steroids were found to be more prone to the development of CSCR.[5] Steroid-induced CSCR is associated with variable individual response instead of dose-dependent results; hence, low doses can also result in CSCR.[6] There is no clear dose-dependency between CSCR incidence and total dosage of steroid administered, and hence, daily dosage may itself have a bigger influence.[7]

Management includes observation, cessation of steroids when needed and alternative immunosuppressive therapy when needed, focal laser to leaks and photodynamic therapy. In patients with leakage treated by laser, there have been no recurrences even with continuation of glucocorticoids at daily doses.[8] Photodynamic therapy is indicated for chronic CSCR and subfoveal leaks and recurrent CSCR. It acts by reducing fluid leakage, SRF accumulation, and serous detachment.[9] These alternative therapeutic approaches help us expedite fluid resorption in patients with high visual demand as in our case.

ONTT, the benchmark for treatment of patients with acute monosymptomatic optic neuritis, states that the use of oral steroids alone may increase the chances of recurrences of optic neuritis and recommends high-dose IVMP or dexamethasone as pulse therapy for treatment.[10] Hence, the incidence of CSCR in predisposed individuals may be much more than documented in literature.

Our patient developed bilateral CSCR when treated with high-dose IVMP for LE RBN. Our treatment dilemma included continuing oral steroid therapy as per ONTT versus the necessity to discontinue steroids due to concomitant CSCR. Our patient had first episode of RBN with normal neuroimaging and a bilateral sequential visual loss due to CSCR; hence, we decided to stop steroids. We might need to restart steroid therapy or start an adjunct immunomodulatory therapy in case of recurrences of optic neuritis or lesions in MRI.

Development of CSCR during the management of ocular inflammation with glucocorticoids is not uncommon. Choosing the right treatment and weighing the risks and benefits of stopping or continuing steroid therapy are important in these cases. The importance of informed written consent explaining the development of CSCR and other potential side effects while instituting high-dose steroid therapy cannot be underestimated. Proper documentation and baseline SD-OCT are very useful in the management of these complicated case scenarios.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Manayath GJ, Ranjan R, Shah VS, Karandikar SS, Saravanan VR, Narendran V. Central serous chorioretinopathy: Current update on pathophysiology and multimodal imaging. Oman J Ophthalmol 2018;11:103-12.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Raimundo M, Fonseca C, Lemos J, Fonseca P. Central serous chorioretinopathy as a cause of vision loss in chronic relapsing inflammatory optic neuropathy. Am J Ophthalmol Case Rep 2018;11:131-4.  Back to cited text no. 2
    
3.
Ambiya V, Goud A, Rasheed MA, Gangakhedkar S, Vupparaboina KK, Chhablani J. Retinal and choroidal changes in steroid-associated central serous chorioretinopathy. Int J Retina Vitreous 2018;4:11.  Back to cited text no. 3
    
4.
Loo JL, Lee SY, Ang CL. Can long-term corticosteriods lead to blindness? A case series of central serous chorioretinopathy induced by corticosteroids. Ann Acad Med Singap 2006;35:496-9.  Back to cited text no. 4
    
5.
Majumder PD, Menia N, Sudharshan S, Rao C, Ganesh SK, Biswas J. Clinical profile of uveitis patients developing central serous chorioretinopathy: An experience at a tertiary eye care center in India. Indian J Ophthalmol 2019;67:247-51.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Chang YS, Weng SF, Chang C, Wang JJ, Wang JY, Jan RL. Associations between topical ophthalmic corticosteroids and central serous chorioretinopathy: A Taiwanese population-based study. Invest Ophthalmol Vis Sci 2015;56:4083-9.  Back to cited text no. 6
    
7.
Wakakura M, Song E, Ishikawa S. Corticosteroid-induced central serous chorioretinopathy. Jpn J Ophthalmol 1997;41:180-5.  Back to cited text no. 7
    
8.
Khairallah M, Kahloun R, Tugal-Tutkun I. Central serous chorioretinopathy, corticosteroids, and uveitis. Ocul Immunol Inflamm 2012;20:76-85.  Back to cited text no. 8
    
9.
Shibata A, Ohkuma Y, Hayashi T, Tsuneoka H. Efficacy of reduced-fluence photodynamic therapy for serous retinal pigment epithelial detachment with choroidal hyperpermeability. Clin Ophthalmol 2013;7:2123-6.  Back to cited text no. 9
    
10.
Beck RW, Cleary PA, Anderson MM Jr., Keltner JL, Shults WT, Kaufman DI, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med 1992;326:581-8.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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