Dr.Namrata Gupta, N19192, Dr.Alok Sen
Purpose:To evaluate the retinal and choroidal changes in steroid induced central serous chorioretinopathy (CSC) in comparison to idiopathic CSC in fellow eyes
Methods: In this retrospective study, spectral domain optical coherence tomography(SD-OCT) of fellow eyes of patients with steroid induced CSC (group A) were compared with the same in idiopathic CSC(group B). Subfoveal changes, retinal pigment epithelial changes and choroidal changes were noted.
Results : There were 25 eyes in group A and 25 eyes in group B. Mean central macular thickness in group A was 452.16 um and group B was 437.24um.
Conclusion: Pachychoroid changes are present in fellow eyes of both groups and these should be followed up closely.
Introduction :
Central serous chorioretinopathy (CSC) is characterized by serous retinal detachment in the posterior pole and is often associated with serous pigment epithelial detachments (PED) and retinal pigment epithelium (RPE) atrophy. CSC was initially thought to originate in the retinal pigment epithelium (RPE) (1) but recently choroidal vascular hyperpermeability has been demonstrated by indocyanine green angiography in CSC(2-5)
Out of many causes , endogenous and exogenous hypercortisolism is associated with CSC(6-8). The common exogenous routes of steroid administration include oral, inhaled, epidural, intra-articular and topical skin ointments(9). However, the exact role of corticosteroids in the pathogenesis of CSC is not fully understood. Choroidal thickness(CT) is increased in both eyes of patients with CSC even if the subretinal fluid is present only in one eye.(10, 11) Thus SD-OCT is a non-invasive tool to evaluate subclinical choroidal abnormalities in CSC (11) and follow up of fellow eyes as they have high chance of developing CSC over a period of time. (12)
Aims and objectives
To evaluate the retinal and choroidal changes in steroid induced central serous chorioretinopathy (CSC) in comparison to idiopathic CSC in fellow eyes
Methods
A retrospective study was done at a tertiary eye care centre, to compare fellow eyes of patients with steroid induced CSC (Group A) versus idiopathic CSC (group B). The study duration was from January 2016 to December 2017.
The inclusion criteria were:
(1) Age ≥ 18 years
(2) Acute or chronic CSC diagnosed by the presence of subretinal fluid at fovea, verified by OCT
(3) Group A: who were exposed to corticosteroids within 12 months prior to the development of CSC and Group B: who did not have a history of current or prior exposure to any type of corticosteroids or any other risk factor
(4) Treatment naive patients
The exclusion criteria were:
(1)Tobacco use
(2) Vitreoretinal/macular disorders other than CSC currently or in the past
(3) Evidence of glaucoma
(4) Alcohol intake
(5) Cataract surgery in the past 6 months
(6) Any mediaopacity likely to cause attenuation of signal strength in OCT
(7) History of malignant hypertension
(8) Pregnancy
(9) Hypermetropia >4 diopter
(10) Type A personality
(11) Collagen vascular disorder
(12) Obstructive Sleep Apnea
(13) Helicobacter Pylori infection
(14) Bilateral CSC
A detailed ocular history (onset of symptoms, previous treatment), the demography (age, gender), laterality, systemic comorbidities (diabetes and hypertension) were recorded. A detailed history of the duration and route of steroid exposure was taken.
The clinical examination included assessment of the best corrected visual acuity (BCVA) in Snellen, refraction , slit lamp biomicroscopy, indirect ophthalmoscopy, and digital fundus fluorescein angiography (FFA). All eyes underwent spectral-domain OCT (SD-OCT) to obtain central macular thickness (CMT), and the Subfoveal Choroidal Thickness (SFCT). The SFCT was measured at subfoveal location as the vertical distance between the hyperreflective line of Bruch’s membrane and the innermost hyperreflective line of the chorio–scleral interface. Other features noted in OCT included presence of subretinal deposits, RPE irregularities and PED
Statistical Analysis—Sample size was calculated using a prevalence of 10 per 100000 men (13)
The Snellen BCVA was converted to logarithm of the minimum angle of resolution (logMAR) equivalent for statistical analysis.
Appropriate statistical tests were used using SPSS software
Results:
The study included 25 eyes of 25 patients in group A (steroid associated CSC) and 25 eyes of 25 patients in group B (no history of exposure to steroids or any other risk factor). Out of 25 patients in group A, there was history of exposure to oral steroids in nine (36%) cases, parenteral steroids in one (4%) cases, inhalational steroids in two (8%) cases, skin ointment in 10 (40%) and topical steroids in three (12%) case. The mean age was (group A: 41.53 years; group B: 45.67 years ), mean duration of symptoms was (group A: mean, 79 days ; group B: mean, 195 days), and the mean baseline best corrected visual acuity was (group A: 20/20 Snellen ± 0.447 logMAR; group B: 20/33 Snellen ± 0.34 logMAR). None of the participants had bilateral CSC. The CMT was lower in group A (Group A: mean, 452.16 μm, 95% CI; Group B: mean, 437.24μm, 95% CI) Between the two groups, there was no significant difference in the proportion of cases having subretinal deposits , RPE irregularities and PEDs.
Discussion:
Our study found a higher CMT in idiopathic CSC as compared to steroid associated CSC similar to a study done by Arora et al(13). However, there was no significant difference in the SFCT. Only few studies have compared choroidal features of steroid-associated CSC with those of idiopathic CSC (12,14) which found that eyes with steroid-associated CSC have a thinner central choroid, lesser choroidal vessel dilatation, and a lesser choroidal vessel hyperpermeability as compared to eyes with idiopathic CSC. Further to this, even the fellow eyes in case of the steroid-associated CSC had a thinner central choroid as compared to those in case of idiopathic CSC.
Conclusion:
Choroidal permeability is increased in both eyes of patients with CSC. The changes in anatomicalparameters of the fellow eye can be used as a guide for monitoring disease occurrence in the fellow eye.
References:
- Gass JD. Pathogenesis of disciform detachment of the neuroepithelium. II. Idiopathic central serous choroidopathy. Am J Ophthalmol 1967;63:587–615.
- Scheider A, Nasemann JE, Lund OE. Fluorescein and indocyanine green angiographies of central serous choroidopathy by scanning laser ophthalmoscopy. Am J Ophthalmol 1993;115:50–56.
- Guyer DR, Yannuzzi LA, Slakter JS, et al. Digital indocyaninegreen videoangiography of central serous chorioretinopathy. Arch Ophthalmol 1994;112:1057–1062.
- Piccolino FC, Borgia L. Central serous chorioretinopathy and indocyanine green angiography. Retina 1994;14:231–242.
- Pru¨nte C. Indocyanine green angiographic findings in central serous chorioretinopathy. Int Ophthalmol 1995;19:77–82.
- Abu el-Asrar AM. Central serous chorioretinopathy complicating systemic corticosteroid therapy. Eur J Ophthalmol. 1997;7(3):297–300.
- Chaine G, Haouat M, Menard-Molcard C, Favard C, Vignal-Clermont C, Campinchi-Tardy F, et al. Central serous chorioretinopathy and systemic steroid therapy. J Fr Ophtalmol. 2001;24(2):139–146.
- Gass JD, Little H. Bilateral bullous exudative retinal detachment complicating idiopathic central serous chorioretinopathy during systemic corticosteroid therapy. Ophthalmology. 1995;102(5):737–747.
- Tsai DC, Chen SJ, Huang CC, Chou P, Chung CM, Huang PH, et al. Epidemiology of idiopathic central serous chorioretinopathy in Taiwan, 2001–2006: a population-based study. PLoS ONE. 2013;8(6):e66858
- Maruko I, Iida T, Sugano Y, Ojima A, Sekiryu T. Subfoveal choroidal thickness in fellow eyes of patients with central serous chorioretinopathy. Retina 2011;31:1603‑8.
- Imamura Y, Fujiwara T, Margolis R, Spaide RF. Enhanced depth imaging optical coherence tomography of the choroid in central serous chorioretinopathy. Retina 2009;29:1469‑73
- Arora S, Pyare R, Sridharan P, Arora T, Thakar M, Ghosh B. Choroidal thickness evaluation of healthy eyes, central serous chorioretinopathy, and fellow eyes using spectral domain optical coherence tomography in Indian population. Indian Journal of ophthalmology ,2016Jan1;64(10):747.
- Liew G, Quin G, Gillies M, Fraser-Bell S. Central serous chorioretinopathy: a review of epidemiology and pathophysiology. Clinical and Experimental ophthalmology, 2013Jan.1;41(2):201-14
- Honda S, Miki A, Kusuhara S, Imai H, Nakamura M. Choroidal thickness of central serous chorioretinopathy secondary to corticosteroid use. Retina. 2017;37(8):1562–1567.


Leave a Comment