Central Serous Chorioretinopathy (Grand Rounds)

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Original article contributed by: Jesse L. Berry, MD
All contributors: Jesse L. Berry, MD
Assigned editor:
Review: Assigned status Up to Date by Jesse L. Berry, MD on March 23, 2017.


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History

  • 40-year-old male presents with 10 days of dim central vision in the right eye
  • Associated with metamorphopsia and paracentral scotoma
  • Denies previous ocular history, floaters, flashes, pain, trauma
  • Post-doctoral research fellow who states he is under a great deal of pressure at work lately

Exam Findings

  • VA: 20/25, 20/20
  • IOP: 14, 16
  • Pupils: Round and reactive, no rAPD
  • Brightness sense: 80%, 100%
  • Color plates: 8/8, 8/8
  • EOM full OU
  • Anterior segment: within normal limits
  • Dilated fundus exam: subretinal fluid extending from the superior arcade to the fovea
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Differential Diagnosis

  • Central serous chorioretinopathy
  • Optic pit
  • Age-related macular degeneration
  • Polypoidal choroidal vasculopathy
  • Choroidal hemangioma
  • Rhegmatogenous retinal detachment
  • Vogt-Koyanagi-Harada disease

Additional Investigations

  • Subretinal fluid in the right eye spontaneously resolved. However nine months later, the patient represented with bilateral subretinal fluid after increase in life stressors
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  • Subretinal fluid did not improve with Eplerenone 50mg daily. We then proceeded with verteporfin PDT for the left eye.
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Diagnosis

  • Central serous chorioretinopathy

Pathophysiology

  • Central serous chorioretinopathy is characterized by development of well-circumscribed, serous detachment of the neurosensory retina. The etiology is unclear, however a combination of altered RPE barrier and choroidal hyperpermeability are postulated.

Treatment

  • Observation
  • Systemic drugs of mifepristone, ketoconazole, spironolactone, rifampin, eplerenone (use these drugs because of their impact on steroid metabolism)
  • Thermal laser photocoagulation
  • Verteporfin photodynamic therapy
    • Two step process:
      • IV verteporfin (Visudyne) localized to endothelial cells of vessels
      • Local activation of the drug by a laser preferentially absorbed by the drug
  • Photochemical reaction creates reactive oxygen species and free radicals
  • Causes endothelial cell damage, platelet adherence, vascular thrombosis and capillary closure

Prognosis and Future Directions

  • Natural course
    • 80 to 90 percent with spontaneous resorption within three to four months
    • VA recovery can take up to one year
    • Mild metamorphopsia, faint scotoma, abnormalities in contrast sensitivity and color vision frequently persist
    • 40 to 50 percent experience recurrence

References

  • Ryan S, et al. Retina, 5th Edition. Saunders, December 7, 2012.
  • Kitzmann AS, Pulido JS, Diehl NN, et al. The incidence of central serous chorioretinopathy in Olmsted County, Minnesota, 1980-2002. Ophthalmology. 2008 Jan;115(1):169-73.
  • Lim JW, Kim MU, Shin M-C. Aqueous humor and plasma levels of vascular endothelial growth factor and interleukin-8 in patients with central serous chorioretinopathy. Retina. 2010 Oct;30(9):1465-71.
  • Reibaldi M, et al. Standard-fluence versus low-fluence photodynamic therapy in chronic central serous chorioretinopathy: a nonrandomized clinical trial. Am J Ophthalmol. 2010 Feb;149(2):307-315.e2.
  • Kim H-S, Lee JH. The short-term effect of intravitreal bevacizumab for treatment of central serous chorioretinopathy. J Korean Ophthalmol Soc 2010;51:860-864.
  • Bae SH, et al. Low-fluence photodynamic therapy versus ranibizumab for chronic central serous chorioretinopathy: one-year results of a randomized trial. Ophthalmology. 2014 Feb;121(2):558-65.
  • Artunay O, et al. Intravitreal bevacizumab in treatment of idiopathic persistent central serous chorioretinopathy: A prospective, controlled clinical study. Curr Eye Res 2010;35:91-98.

Contact

  • Andrew Moshfeghi, MD, MBA, Associate Professor of Clinical Ophthalmology, andrew.moshfeghi@med.usc.edu
  • Ramon Lee, MD, PGY-2 Ophthalmology resident, ramon.lee@med.usc.edu