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REVIEW ARTICLE
Year : 2019  |  Volume : 6  |  Issue : 2  |  Page : 27-32

Central serous chorioretinopathy: Recent trends


1 Department of Pediatric Retina and Ocular Oncology, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Coimbatore, Tamil Nadu, India
2 Department of Ophthalmology, JNMC, Belagavi, Karnataka, India

Date of Submission01-Jan-2020
Date of Acceptance27-Jan-2020
Date of Web Publication19-Feb-2020

Correspondence Address:
Dr. Abhishek Das
Department of Pediatric Retina and Ocular Oncology, Aravind Eye Hospital, Avinashi Road, Coimbatore - 641 014, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/erj.erj_1_20

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  Abstract 


Central serous chorioretinopathy (CSCR) belongs to pachychoroid spectrum of diseases, and the pathogenesis is still not fully understood. It is associated with multiple systemic factors. It is characterized by the collection of fluid between the retinal pigment epithelium (RPE) and the neurosensory retina. It mostly affects young men under perceived stress. The involvement of corticosteroids is undisputed although their exact role has not been clarified; other parts of the underlying mechanism of CSCR have been mainly elucidated by imaging techniques, such as fluorescein and indocyanine green angiography. The course is usually self-limiting and in most cases resolves spontaneously within a 3–6-month period, with visual acuity usually recovering to 20/30 or better. However, chronic CSC may develop as a consequence of recurrences or persistent neurosensory detachment and can result in progressive RPE atrophy and permanent visual loss. We used search terms such as “central serous retinopathy,” “central serous chorioretinopathy,” “CSCR,” “management,” and “treatment” and also the keywords of each type of treatment on PubMed and Medline to retrieve articles for this systematic review.

Keywords: Antivascular endothelial growth factor, central serous chorioretinopathy, laser treatment, mineralocorticoid antagonists, photodynamic therapy


How to cite this article:
Das A, Chheda P. Central serous chorioretinopathy: Recent trends. Egypt Retina J 2019;6:27-32

How to cite this URL:
Das A, Chheda P. Central serous chorioretinopathy: Recent trends. Egypt Retina J [serial online] 2019 [cited 2020 Jul 5];6:27-32. Available from: http://www.egyptretinaj.com/text.asp?2019/6/2/27/278674




  Introduction Top


Long back in 1866, von Graefe described central serous chorioretinopathy (CSC) and named it as “relapsing central luetic retinitis.”[1] Maumenee[2] was thefirst to describe a leak at the level of the retinal pigment epithelium (RPE) in 1965 using fluorescein angioscopy (FA). Subsequently, Gass[3],[4],[5],[6],[7] provided detailed descriptions of the fluorescein angiographic characteristics of CSCR.

Central serous chorioretinopathy (CSC) is a condition characterized by a serous retinal detachments frequently involving the macula and usually associated with focal pigment epithelial detachments, choroidal hyperpermeability, and increased choroidal thickness. Spaide et al. defined CSCR as serous elevation of the retina with one or more leaks without evidence of inflammation, infiltration, or choroidal neovascularization. These leaks are often subtle and diffuse in older patients and not necessarily a focal leak. It typically affects young and middle-aged males with Type A personalities between 20 and 45 years of age. Before the onset of symptoms, most patients develop one or more small areas of serous detachment of RPE in the macula or paramacular area. Other risk factors include steroid usage, phosphodiesterase-5 (PDE-5) inhibitor use, obstructive sleep apnea (OSA), Helicobacter pylori infection, pregnancy, and endogenous Cushing's syndrome.

A recent study by Daruich et al. showed that older age, higher subfoveal choroidal thickness, and higher degree of RPE alteration at leakage sites are independent factors of longer acute central serous chorioretinopathy episodes.

Because serous retinal detachments resolve spontaneously within 6 months in most acute CSCR episodes,[8] observation without treatment is generally recommended as initial management.[9] Several treatment options are available for those cases which have persistent serous detachment or severe visual loss.

Fluorescein angiography reveals any presence of a focal or multiple point of leakage under a serous neuroretinal detachment in the form of an “ink blot” pattern progressing to “smoke stack” pattern[10] [Figure 1]. Ink blot is more common than smoke stack pattern. Smoke stack forms due to convection currents, increased protein gradient in the subretinal fluid, and low density of fluorescein dye. Another multi-imaging modality is indocyanine green (ICG) angiography that visualizes changes involving the deeper choroidal vascularization and discloses the presence of any delayed initial filling of arteries and choriocapillaris in the early phase and a remarkable dilation of the large choroidal vein in the following phases, confirming a status of choroidal hyperpermeability [Figure 2]. Spaide et al.[11] in a study found that the ICG-video angiography showed choroidal vascular hyperpermeability with specific patterns and also concluded that older patients with CSCR have a unique temporal and topographic pattern, which can help in establishing diagnosis. Optical coherence tomography is another important tool to visualize the morphologic changes involving the retinal layers and any alterations occurring in the RPE and also to follow up the disease evolution[12],[13] [Figure 3] and [Figure 4]. In particular, deeper penetration with recent SD OCT and swept-source OCT has led to a more detailed evaluation of the alternations of photoreceptor layer and RPE changes, and has especially confirmed the presence of the thickening of the deeper choroidal layers and thinning of the inner choroidal layers using EDI technology.[14],[15] Fundus autofluorescence can show typical tracks of pigment epithelial hypo- and hyper-autofluorescence as a sign of chronic CSCR [Figure 5].
Figure 1: Fundus angiography of the left eye of a 46-year-old male patient with typical inkblot (a) leakage 30 s after fluorescein injection and smoke stack pattern (b) 6 min later. Typical mushroom or umbrella pattern (c) in later stages. (d) Inverted smoke stack pattern in a 40-year-old male patient

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Figure 2: (a) Fundus angiography shows pooling of the dye which is increasing in intensity in later phases. Corresponding indocyanine green angiography shows abnormal dilation of choroidal vessels. (b) Areas of retinal pigment epithelium atrophy showing hyperfluorescence due to window defect

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Figure 3: Spectral-domain optical coherence tomography showing serous retinal detachment with subretinal fluid and pigment epithelial detachment. Source of leakage (*) seen within the subretinal fluid

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Figure 4: Enhanced depth imaging-optical coherence tomography showing subretinal fluid, dome shaped pigment epithelial detachment, diffuse choroidal thickening with dilated outer choroidal vessels (white arrow)

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Figure 5: Fundus autofluorescence of the left eye of a patient suffering from chronic CSCR with typical tracks of pigment epithelial hypo- and hyper-autofluorescence as a sign of chronicity of the disease

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Although a clear and definitive comprehension of the pathophysiology of CSCR is not completely understood, several investigations convey a hypothesis and results that suggest a primary involvement of the RPE and choroidal vascularization.[16]

Spaide et al.[17] concluded in their study that older patients in this study were more likely to have diffuse retinal pigment epitheliopathy (DRPE), bilateral involvement, and lower visual acuity and were more likely to have secondary choroidal neovascular membrane (CNVM). In the same study, few patients with DRPE did not have any history of CSCR, so the hypothesis behind this might be chronic asymptomatic sensory retinal detachments that caused damage to the underlying RPE, leading to DRPE. RPE plays a significant role in the integrity of the barrier function. In acute CSCR, the point of leakage observed on the fluorescein angiography was thought to be the site of fluid flow from the choroidal compartment to the subretinal space. However, some authors demonstrated recently that in the site of the focal RPE defect, an outflow from the subretinal compartment toward the choroidal space can be observed.[18] The pathway that leads to a loss in the activity of RPE functions has not yet been fully understood. The RPE could be susceptible to a loss of activity either as a result of an increase in hydrostatic pressure in the choroidal compartment or in response to a negative effect of ischemic origin, or due to inflammatory or hormonal influences, as has been alternatively hypothesized.

Apart from RPE, choroidal circulation plays an important role in the pathogenesis of CSCR. An increased hyperpermeability of the choroidal lamina is easily observed in the ICG examination, and it is thought to be a consequence of the phenomena of stasis, inflammation, or ischemia.[19] The corresponding increase in hydrostatic pressure within the choroidal compartment could overwhelm the pump functions of the RPE and, in accordance with simple mechanical theory, lead to a progressive fluid accumulation in the subretinal space. The causes responsible for the increased vascular permeability are yet to be determined. The self-regulating mechanisms of the vascular choroidal circulation in CSCR appear to be influenced by the levels and chemical activities of steroid molecules, catecholamines, and sympathomimetic agents.

We used search terms such as “central serous retinopathy,” “central serous chorioretinopathy,” “CSCR,” “management,” and “treatment” and also the keywords of each type of treatment on PubMed and Medline to retrieve articles for this systematic review.

The aim of this current review is to provide an overview on the current treatment options for acute and chronic CSCR, including observation, retinal laser treatment, photodynamic therapy (PDT) with verteporfin, intravitreal anti-vascular endothelial growth factor (VEGF) therapy, and mineralocorticoid receptor (MR) antagonists.


  Treatment Options Top


Observation

Patient coming withfirst episode of acute CSCR can be observed. The patient should be monitored periodically to observe the progression or resolution of the neurosensory detachment (NSD) that normally takes place within a period of 3–6 months.[19] Any form of corticosteroid therapy with any route of administration should be advised to discontinue.[20]

In addition, OSA, the use of PDE-5 inhibitors or sympathomimetic drugs, pregnancy, signs or symptoms related to Cushing's syndrome, and the presence of a “Type A” personality pattern should be determined in the general clinical assessment because of the possible associations reported in some case series.[21],[22]

Laser photocoagulation

Laser photocoagulation delivery has been a standard treatment for acute and chronic CSCR. The treatment attempts to produce a sealing effect of the RPE defect as identified through fluorescein angiography. An additional effect of the retinal laser photocoagulation is a promoting effect on the pump function of the RPE through stimulation of the closer RPE cells.[9],[22]

There are several controlled studies comparing laser photocoagulation to simple observation or sham laser treatment, and they have provided evidence of the beneficial effects of laser treatment. Patients receiving laser treatment showed a faster flattening of the NSD measured in a mean period of 8–10 weeks.[23],[24] Burumcek et al.[25] demonstrated a lack of recurrence in the laser photocoagulation group, which compared with seven eyes in the control group that showed one or more recurrences during the mean follow-up period of 4.8 years.[9],[26]

Among complications, choroidal neovascularization may occur in the site of laser application in <10% of the treated cases. The delivery of laser spot in the juxtafoveal area should consider the residual paracentral scotoma, which could negatively affect reading ability.[26]

Subthreshold retinal laser treatment

To avoid various complications of laser photocoagulation including paracentral scotoma and CNVM, experts tried laser application in a subthreshold setting. Various studies have disclosed that when we use short-duration diode laser pulses the RPE is almost solely affected, with little histopathological effect on the inner retina.[24]

In a study by Bandello et al.,[27] five patients with chronic CSCR with a disease duration lasting more than 3 months were initially included and treated with multiple laser spots applied over and adjacent to the area of RPE leakage or decompensation. Within 1 month, all patients had experienced a complete resolution of their NSD.

A study by Chen et al. showed (26 eyes) that a gain of visual acuity of three lines or more was achieved in 58% and a gain of between one and three lines was achieved in 23% of the treated eyes.[28]

Verma et al.[29] randomized acute CSCR patients in a control study with a single focal leak to diode laser or argon photocoagulation. 30 eyes had resolution of fluid and similar final visual acuities at 12 weeks, but the diode group had significantly better final contrast sensitivity.

Therefore, subthreshold retinal laser photocoagulation appears to be a safe form of treatment in chronic CSCR. Results however are not superior to PDT. Furthermore, it seems unsuitable for diffuse leakage and DRPE decompensation. Hence, more randomized trials are required to determine the safety and efficacy of subthreshold micropulse diode laser in the treatment of CSCR.

Transpupillary thermotherapy

In a study by Shukla et al.,[30] where they performed transpupillary thermotherapy (TTT) in long-standing CSCR, it resulted in the resolution of CSCR with subfoveal angiographic leaks and significant improvement in visual outcome, in comparison with the natural history of persistent CSCR. Still, more evidence is required to establish the efficacy of TTT.

Photodynamic therapy with verteporfin

Many authors suggested a possible direct action on the choriocapillaris endothelium along with the choriocapillaris occlusion that is able to achieve both a blood flow stasis and a reduction of vascular permeability.

A study by Yannuzzi et al.[31] reported outcomes obtained from 20 eyes of 15 patients who received standard PDT for chronic CSCR with laser treatment targeting the area of choroidal hyperpermeability recognized by ICG angiography. A complete resolution of NSD was detected in 12 patients (60%), and vision improvement was noticed in six eyes.

Diffuse application of PDT for CSCR led to evidence of adverse events which included pigmentary changes in the treated area, RPE atrophy, choriocapillaris nonperfusion, and iatrogenic choroidal neovascularization.[32],[33]

Chan et al.[34] compared the efficacy of half-dose PDT with placebo in acute CSCR. Sixty-three eyes that had CSC for 3 months were randomized to ICG-guided half-dose PDT (3 mg/m2) or to placebo. At 12 months, 94.9% of the PDT group compared to 57.9% of the placebo group showed complete resolution of the NSD (P = 0.001), and similarly, the best-corrected visual acuity (BCVA) was significantly better in the PDT group.

Another study by Lim et al.,[23] where they compared half-dose PDT with focal laser photocoagulation, found that of 26 eyes, a greater proportion of eyes in the PDT group (14 eyes) showed a complete absorption of subretinal fluid compared with the laser group (12 eyes) (P = 0.022). No significant variation was measured in visual acuity or in the parameters of multifocal electroretinography between the two during the 6-month follow-up period.

Zhao et al.[35] randomized 131 patients and compared the efficacy and safety of a 50% dose of PDT with the efficacy and safety of a 30% dose for acute CSCR. During the 1-year follow-up, half-dose PDT was superior to 30% dose PDT.

Reibaldi et al.[36] recruited 42 eyes and compared standard-fluence PDT with half-fluence PDT (HFPDT) in chronic CSCR in a prospective nonrandomized clinical trial and found that greater proportion of moderate choriocapillaris nonperfusion was seen in eight eyes receiving standard-fluence PDT compared with no cases in the group receiving half-fluence. Rest findings were not significant.

There are still many horizons to be explored, including the settings of PDT protocol such as HFPDT, low-fluence PDT, or reduced-fluence PDT; effects of PDT on chorioretinal atrophy; the role of PDT for patients showing no or minimal choroidal hyperpermeability; and the action of PDT on the rate of recurrences.

Antivascular endothelial growth factor therapy

Anti-VEGF drugs have been a choice in the treatment of acute and chronic CSCR with a hypothesis that it reduces choroidal vascular hyperpermeability, even in the absence of clear evidence of an increased intraocular concentration of VEGF levels.[37]

Chung et al.[38] evaluated the efficacy of bevacizumab for acute or chronic CSCR in a recent meta-analysis. However, the results showed no positive effects of the drug.

Bae et al.[39],[40] carried out a randomized controlled trial comparing ranibizumab with half-fluence PDT in chronic CSCR in a cohort of 32 patients with 1 year of follow-up. The authors demonstrated the overall superiority of PDT compared with ranibizumab considering the percentage of patients with complete resolution of the subretinal fluid (88.9% vs. 12.5%) and the reduction in choroidal hyperpermeability.

More number of randomized control trials with long-term follow-up is required to prove the efficacy of anti-VEGF in the treatment of CSCR.

Mineralocorticoid antagonists

An excess of endogenous (cortisol) or exogenous glucocorticoids is associated with CSCR and that glucocorticoids also show to some extent an affinity for the MRs. The mechanism linking the subretinal fluid accumulation and the activity of glucocorticoids seems to involve the overactivation of the ocular MR through an overexpression of the MR or an increased stimulation.

Spironolactone and eplerenone are currently in use. Eplerenone shows increased selectivity and fewer side effects secondary to the activation of progesterone receptors.

Herold et al.[41] treated CSCR with spironolactone 25 mg and showed that subretinal fluid and total central retinal decreased. Statistically significant improvement in the BCVA was noted.

Bousquet et al.[42] showed a statistically significant reduction in NSD in the group receiving spironolactone in comparison with the placebo group.

Efficacy of eplerenone for the treatment of chronic CSCR was investigated in some case series, each with a short-term follow-up. Salz et al.[43] and Singh et al.[44] showed beneficial effects of eplerenone. Still, long-term control studies are required.


  Conclusion Top


Identification of the numerous risk factors associated with CSCR is of utmost importance. We have seen a number of treatment options over the past decade; still, timings of the available options remain debatable. Till date, PDT remains the best option to treat CSCR at any stage especially subfoveally, which is largely supported by evidence. Further large, prospective, or even retrospective long-term follow-up studies are required to decide on one or more safe and effective forms of treatment, which will be generally accepted by clinicians in the near future.

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 interes



 
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