CSCR: Diagnosis and Treatment

Central serous chorioretinopathy afflicts working-age patients. While many can be observed, some will require intervention.

John D. Pitcher, III, MD and Jason Hsu, MD, Philadelphia
7/7/2014

Central serous chorioretinopathy (CSCR) is a relatively common cause of visual impairment in the Western world, and is characterized by the accumulation of subretinal fluid in the macula.1,2 The disease classically affects men between the ages of 20 and 50 and has been associated with corticosteroid exposure, phosphodiesterase inhibitor use, obstructive sleep apnea and “type A” personality traits. Patients can present with a variety of visual symptoms including relative central scotoma, metamorphopsia, dyschromatopsia and micropsia.3,4 On examination, the characteristic finding is a posterior neurosensory retinal detachment caused by leakage of fluid from the level of the retinal pigment epithelium. 

Multimodal imaging is useful in making the diagnosis of CSCR. Classically, fluorescein angiography demonstrates an expanding point of fluorescein leakage with late pooling into a serous detachment (See Figure 1). Multiple points of leakage can be seen in some patients.5,6 Indocyanine green angiography may show focal delays and hyperpermeability in the choroidal circulation in many patients with CSCR.7,8 Optical coherence tomography demonstrates subretinal fluid, often associated with a focal pigment epithelial detachment (See Figure 2).9 More recently, enhanced-depth imaging spectral domain OCT has shown increased subfoveal choroidal thickness in some patients with CSCR as compared to normal eyes (See Figure 3).10

The typical natural history of CSCR is complete spontaneous resolution of subretinal fluid with restoration of visual acuity by three months after onset of symptoms. However, up to 20 percent of patients may have persistent serous macular detachment and vision loss past six months, and may be left with some degree of subjective visual impairment such as micropsia or reduced color perception.11-13 If subretinal fluid has not resolved by three months, the patient is defined as having chronic CSCR, and treatment is often considered.
Figure 1. Color fundus photo in a patient with acute central serous chorioretinopathy demonstrating a serous detachment of the neurosensory retina in the macula. Fluorescein angiography revealed early pinpoint hyperfluorescence expanding over the course of the angiogram to pool into the subretinal space. 

Figure 2. SD-OCT showing subretinal fluid associated with a focal pigment epithelial defect (yellow arrow).
 
Figure 3. Enhanced depth imaging SD-OCT in a patient with CSCR demonstrating a thickened choroid (yellow bracket).
 

Treatment Options

There is no gold standard for treatment of persistent CSCR, and a number of therapies have been tried with varying success. Focal laser photocoagulation to pinpoint areas of leakage on FA was the first treatment shown to be of some benefit for CSCR.14 However, photocoagulation is destructive, can lead to symptomatic scotomas, and occasionally formation of secondary choroidal neovascularization. Therefore, this treatment is reserved for focal extrafoveal areas of dye leakage.

Photodynamic therapy more directly targets the choroidal circulation and may be used in patients with sub-foveal and/or multifocal points of leakage. PDT has been used for persistent CSCR with some success. However, it is not approved by the Food and Drug Administration for the treatment of CSCR and has a number of side effects, including photosensitivity to intravenous dye and choroidal hypoperfusion following treatment.15,16 Several recent studies have demonstrated the use of half-fluence and half-dose PDT in acute and chronic CSCR, with the goal of maintaining efficacy while minimizing risk.17-20

Anti-VEGF medications have a number of effects that are theoretically beneficial in CSCR, such as the upregulation of tight junctions between endothelial cells and reduction of vascular fenestrations.21-23 A study by Ji Won Lim, MD, and colleagues suggested that VEGF levels in the aqueous humor of patients with chronic CSCR may be elevated compared to normal eyes.24 Case studies and anecdotal reports of intravitreal anti-VEGF medications in patients with persistent or chronic CSCR have shown improvements in visual acuity, resolution of neurosensory detachments and decreased RPE leakage on FA.25-28 Prospective studies using anti-VEGF medications have shown inconsistent results.29,30 So far, however, the cumulative weight of evidence has failed to show sustained, clinically significant benefits.31 Controlled clinical trials are necessary to determine the tolerability and efficacy of anti-VEGF therapies in CSCR. 

Several small studies have shown mixed results from a variety of systemic medications for CSCR, including carbonic anhydrase inhibitors (acetazolamide),32 adrenergic receptor antagonists (metoprolol, propranolol),33,34 and steroid hormone antagonists (ketoconazole, mifeprestone, finasteride, eplerenone).35-38

Eplerenone, a selective aldosterone-receptor antagonist and potassium-sparing diuretic that was originally approved in 2002 by the FDA for treatment of hypertension, was recently shown in a small series of patients with chronic CSCR to improve visual acuity and significantly decrease central macular thickness.39 The medication is generally well-tolerated but drug interactions must be ruled out prior to initiation and serum potassium and blood pressure must be monitored during treatment. Larger, prospective, placebo-controlled studies are under way to further investigate the efficacy of this treatment option.40 Currently, pharmacologic treatments for CSCR remain investigational and are not considered standard of care. If medically appropriate, systemic corticosteroids should be discontinued in patients with active CSCR. A sleep study may be considered in patients with suspected obstructive sleep apnea.41

Central serous chorioretinopathy is a disease of working-aged patients, many of whom have occupations that demand high levels of visual acuity. Characteristic angiographic and OCT findings are helpful in confirming the diagnosis. While the majority of patients will return to baseline with observation, a subset of patients may be considered for intervention. No therapeutic options are approved by the FDA, but local modalities, both pharmacologic and photic, and systemic medical treatments are under ongoing investigation and may hold promise for future patients diagnosed with CSCR.  REVIEW


Dr. Pitcher is a second year fellow in vitreoretinal surgery at Wills Eye Hospital and a clinical instructor of ophthalmology at Thomas Jefferson University in Philadelphia. He can be reached at johndpitcher@gmail.com.

Dr. Hsu is an assistant professor of ophthalmology on the Retina Service of Wills Eye Hospital and practices at Mid Atlantic Retina. He can be reached at jhsu@midatlanticretina.com.



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