Central Serous Chorioretinopathy Clinical Presentation

  • Author: Kean Theng Oh, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Nov 2, 2011
 

History

  • Patients with central serous chorioretinopathy typically present with acute symptoms of visual loss and metamorphopsia (especially micropsia). Other symptoms include decreased central vision and a positive scotoma.
  • The decreased vision usually is improved by a small hyperopic correction.
  • Other clinical signs include a delayed retinal recovery time following photostress, loss of color saturation, and loss of contrast sensitivity.
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Physical

  • Clinical examination shows a serous retinal detachment but no subretinal blood. The neurosensory retinal detachment may be very subtle, requiring contact lens examination for detection.[13]
  • Pigment epithelial detachments, RPE mottling and atrophy, subretinal fibrin, and, rarely, subretinal lipid or lipofuscinoid flecks also may be seen.[14]
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Causes

Previous hypotheses for the pathophysiology have included abnormal ion transport across the RPE and focal choroidal vasculopathy. The advent of ICG angiography has highlighted the importance of the choroidal circulation to the pathogenesis of central serous chorioretinopathy (CSCR).

  • ICG angiography has demonstrated both multifocal choroidal hyperpermeability and hypofluorescent areas suggestive of focal choroidal vascular compromise. Some investigators believe that initial choroidal vascular compromise subsequently leads to secondary dysfunction of the overlying RPE.[15]
  • Type A personalities and systemic hypertension may be associated with CSCR, presumably because of elevated circulating cortisol and epinephrine, which affect the autoregulation of the choroidal circulation.[16, 17]
  • Recent studies using multifocal electroretinography have demonstrated bilateral diffuse retinal dysfunction even when CSCR was active only in one eye. This supports the belief of diffuse systemic effect on the choroidal vasculature.[3]
  • Allibhai et al reported an association with sildenafil citrate and CSCR.[18] Fraunfelder and Fraunfelder further evaluated the association of CSCR with sildenafil.[19] The authors reviewed 1500 cases of sildenafil associated ocular side effects. Eleven of these cases described men with CSCR. The symptoms resolved following cessation of sildenafil in 8 of 11 patients but recurred in 3 of these patients upon restarting sildenafil. They determined that a causal relationship could not be determined as a result of the cyclic nature of CSCR though patients with refractory CSCR should consider cessation of sildenafil use.
  • Systemic associations of CSCR include organ transplantation, exogenous steroid use, endogenous hypercortisolism (Cushing syndrome), systemic hypertension, sleep apnea, systemic lupus erythematosus, pregnancy, gastroesophageal reflux disease, and use of psychopharmacologic medications.[20, 21, 17, 22, 4, 23]
    • Carvalho-Recchia et al showed in a series that 52% of patients with CSCR had used exogenous steroids within 1 month of presentation as compared with 18% of control subjects.[6]
    • Haimovici et al evaluated systemic risk factors for CSCR in 312 patients and 312 control subjects.[24] Systemic steroid use (odds ratio [OR], 37.1) and pregnancy (OR, 7.1) were most strongly associated with CSCR. Other risk factors included antibiotic use, alcohol use, untreated hypertension, and allergic respiratory disorders.
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Contributor Information and Disclosures
Author

Kean Theng Oh, MD  Consulting Staff, Associated Retinal Consultants, PC

Kean Theng Oh, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Brian A Phillpotts, MD  Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine

Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, James C Folk, MD, to the development and writing of this article.

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Fluorescein angiography in the early recirculation phase of a patient with a localized neurosensory detachment in the macula from central serous chorioretinopathy. Note the focal hyperfluorescence.
Fluorescein angiography in the late recirculation phase of the same patient as in the image above. Note the distribution of leakage of fluorescein dye within the neurosensory detachment.
 
 
 
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