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Central Serous Chorioretinopathy – Case Report

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Title:  Central Serous Chorioretinopathy
Author:  Sravanthi Vegunta, Eileen S. Hwang, Mary E. Hartnett
Photographer:  Mel Chandler
Date:  08/05/2015
Keywords/Main Subjects: Central serous chorioretinopathy; Scotoma; Metamorphopsia; Retinopathy; Corticosteroid use; Smoke stack
Diagnosis: Central serous chorioretinopathy
Brief Description: History of Present Illness: The patient was a 46 year old female with a history of hypothyroidism, depression and seasonal allergies who presented 5 weeks after the sudden onset of a floaters, a paracentral scotoma and distortion in her left eye. At first, her central vision was primarily affected, but shortly before her presentation in our clinic, the affected area spread to include an area to the right as (Figure 1).  She denied visual problems with her right eye.

Her medical history was significant for the use of intranasal steroid spray for seasonal allergies.  She had stopped this a few weeks prior to presentation after a visit to an outside ophthalmologist.

Figure 1: Amsler grid test of the left eye revealed a central grey area and a superior area of distortion.

Figure 1: Amsler grid test of the left eye revealed a central grey area and a superior area of distortion.

Initial examination: The patient’s visual acuity with correction was 20/20 in the right eye and 20/60 in the left eye. Intraocular pressure was 16 mmHg in the right eye and 16 mmHg in the left eye. She did not have a relative afferent pupillary defect. Confrontation visual fields and extraocular motility were intact. Anterior segment slit lamp examination was normal in both eyes. On fundus examination, both optic nerves were normal in appearance with a cup-to-disc ratio of 0.3 in the right eye and 0.2 in the left eye.  The macula of her right eye was normal with a good foveal reflex.  Her left macula had an area of pigment near the fovea (Figure 2) and the retina appeared elevated in the central macula, consistent with subretinal fluid (Figure 3).  The retinal vasculature and periphery were normal in both eyes.

Figure 2: Color fundus photography. A) The right macula and fovea appear normal. B) In the left eye, the foveal reflex appears yellow and blunted. There are parafoveal pigmentary changes. There is an area of retinal elevation consistent with subretinal fluid in the central retina.

Figure 2: Color fundus photography. A) The right macula and fovea appear normal. B) In the left eye, the foveal reflex appears yellow and blunted. There are parafoveal pigmentary changes. There is an area of retinal elevation consistent with subretinal fluid in the central retina.

Clinical Course: Patient underwent optical coherence tomography (OCT; Figures 3 and 4) and fluorescein angiography (FA; Figure 6) of each eye.

Figure 3: Left eye OCT demonstrating subretinal fluid in the central macula.

Figure 3: Left eye OCT demonstrating subretinal fluid in the central macula.

Figure 4: Left eye infrared image showing a hyporeflective area in the central macula corresponding to the area of subretinal fluid.

Figure 4: Left eye infrared image showing a hyporeflective area in the central macula corresponding to the area of subretinal fluid.

Figure 5: Fluorescein angiography of the left eye. There are window defects and late phase leakage from a point in the inferior macula toward the fovea in a smoke stack configuration.

Figure 5: Fluorescein angiography of the left eye. There are window defects and late phase leakage from a point in the inferior macula toward the fovea in a smoke stack configuration.

The patient was diagnosed with central serous chorioretinopathy (CSCR) and informed that her visual changes were likely to improve without intervention. Information was provided to the patient regarding the limited quality data for treatment of CSCR with spironolactone, rifampin, epleronone, and low dose aspirin. Low dose aspirin was recommended to the patient since there was a controlled study supporting its use, and the risks were felt to be relatively benign.

Discussion:

CSCR is characterized by a build up of subretinal fluid in the macula caused by abnormalities of the choroidal circulation.1  Fluid leaks from the choroidal circulation and passes through hyperpermeable areas of the retinal pigment epithelium (RPE), accumulating in the subretinal space. 2

While the specific cause of CSCR is not well understood, some systemic risk factors have been associated with CSCR.  In particular, corticosteroid administration and stressful events (presumably associated with high endogenous corticosteroid levels) are associated with the development of CSCR.2  The patient described in this case report was using intranasal steroids, which have specifically been associated with CSCR in addition to systemic, intraarticular, and topical steroids.

CSCR occurs most often in males between 20 and 50 years of age.  It usually presents with acute onset of unilateral metamorphopsia, blurred vision and a relative scotoma.  Patients can also experience micropsia, impaired dark adaptation, and color desaturation. Presenting visual acuity ranges from 20/15 to 20/200 with an average of 20/30. On fundus examination, there is often an elevation of the neurosensory retina in the central macula due to subretinal fluid.  It is important to perform careful inspection of the fundus to exclude conditions such as optic nerve pit, age-related macular degeneration, polypoidal choroidal vasculopathy, uveitis, and intraocular tumor which can also cause subretinal fluid.  OCT can be used to identify and follow the amount of subretinal fluid.1, 2  FA reveals leakage of dye from a focal choroidal/RPE defect which collects in the subretinal space. This usually occurs in an ink-blot pattern in which the spot of hyperfluorescence secondary to leakage spreads concentrically, but in 10-15% of cases, the dye can spread linearly in a smoke stack configuration, as demonstrated in the imaging from the patient described here.

Visual disturbances often resolve spontaneously in a few months, although recurrence is common and chronic CSCR can occur.  Some patients experience permanent visual changes.  If the subretinal fluid fails to resolve with observation alone, photodynamic therapy (PDT) may be performed to hasten subretinal fluid resorption.  There is no evidence that PDT improves final visual outcomes, but since photoreceptor atrophy begins as early as 4 months after onset, there may be a theoretical a long term benefit to treatment if the fluid persists for more than 3 months.  However, PDT is not without significant risk of vision loss and secondary CNV.  The use of half-dose verteporfin and a 10 minute time interval between infusion and laser application may reduce these risks while still providing efficacious treatment of the abnormal choroidal vasculature.

In additional to PDT, several other treatment options for CSCR have been studied. However, studies with large sample sizes and prospective, controlled design are lacking. Studies of the efficacy of bevacizumab and ranibizumab therapies have shown significantly improved retinal thickness and visual acuity in the first 3 months following treatment, but this improvement is not sustained beyond 6 months.3-7

Medications that inhibit mineralocorticoid production or antagonize the mineralocorticoid receptor have recently been studied as potential treatments for CSCR. Zhao et al.8 demonstrated efficacy of eplerenone in a CSCR animal model, and a small pilot study of 13 human patients showed promise.9.  There are a handful of ongoing clinical trials for eplerenone, which is an FDA-approved medication used in the treatment of congestive heart failure.

Caccavale et al.10 studied the efficacy of aspirin for CSCR treatment with the rationale that aspirin may correct abnormalities of the choroidal vasculature and reduce serum levels of plasminogen activator inhibitor 1 (PAI-1), elevated levels of which have been found in patients with CSCR.11, 12 Caccavale et al. conducted a prospective trial in which patients treated with six months of 100 mg aspirin demonstrated improved visual acuity compared to historic controls.  Significant improvements in visual acuity were present at one month and three months, and persisted to twelve months.

In the case of the patient described in this case report, she was eagerly seeking some kind of treatment.  PDT was not recommended because at one month after onset, the risk of vision loss from PDT was not justified in a disease with a 90% spontaneous resolution rate.  Eplerenone was considered, but excluded because of the need for monitoring serum potassium.  The patient was started on low dose aspirin since there was some evidence supporting its efficacy, and the risks of this treatment were relatively low.
Series: Case Report 2015
References:

  1. Kanski J, Bowling B. Clinical Ophthalmology, 7 ed. United Kingdom: Elsevier Health Sciences, 2011.
  2. Ryan S, Schachat A, Wilkinson C, Hinton D, Sadda S, Wiedemann P. Retina, 5 ed. United Kingdom: Elsevier Health Sciences, 2013.
  3. A randomized trial comparing intravitreal triamcinolone acetonide and focal/grid photocoagulation for diabetic macular edema. Ophthalmology 2008;2008 Sep;115:1447-9.
  4. Aydin E. The efficacy of intravitreal bevacizumab for acute central serous chorioretinopathy. J Ocul Pharmacol Ther 2013;29:10-3. doi: 10.1089/jop.2012.0072. Epub 2012 Aug 27.
  5. Lim JW, Ryu SJ, Shin MC. The effect of intravitreal bevacizumab in patients with acute central serous chorioretinopathy. Korean J Ophthalmol 2010;24:155-8. doi: 10.3341/kjo.2010.24.3.155. Epub 2010 Jun 5.
  6. Artunay O, Yuzbasioglu E, Rasier R, Sengul A, Bahcecioglu H. Intravitreal bevacizumab in treatment of idiopathic persistent central serous chorioretinopathy: a prospective, controlled clinical study. Curr Eye Res 2010;35:91-8. doi: 10.3109/02713680903428306.
  7. Park SU, Lee SJ, Kim M. Intravitreal anti-vascular endothelial growth factor versus observation in acute central serous chorioretinopathy: one-year results. Korean J Ophthalmol 2014;28:306-13. doi: 10.3341/kjo.2014.28.4.306. Epub 2014 Jul 22.
  8. Zhao M, Celerier I, Bousquet E, et al. Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy. J Clin Invest 2012;122:2672-9. doi: 10.1172/JCI61427. Epub 2012 Jun 11.
  9. Bousquet E, Beydoun T, Zhao M, Hassan L, Offret O, Behar-Cohen F. Mineralocorticoid receptor antagonism in the treatment of chronic central serous chorioretinopathy: a pilot study. Retina 2013;33:2096-102.
  10. Caccavale A, Romanazzi F, Imparato M, Negri A, Morano A, Ferentini F. Low-dose aspirin as treatment for central serous chorioretinopathy. Clin Ophthalmol 2010;4:899-903.
  11. Yamada R, Yamada S, Ishii A, Tane S. [Evaluation of tissue plasminogen activator and plasminogen activator inhibitor-1 in blood obtained from patients of idiopathic central serous chorioretinopathy]. Nihon Ganka Gakkai Zasshi 1993;97:955-60.
  12. Iijima H, Iida T, Murayama K, Imai M, Gohdo T. Plasminogen activator inhibitor 1 in central serous chorioretinopathy. Am J Ophthalmol 1999;127:477-8.

Identifier: Moran_CORE_21271
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