AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Background

Central serous chorioretinopathy (CSCR) is a disease in which a serous detachment of the neurosensory retina occurs over an area of leakage from the choriocapillaris through the retinal pigment epithelium (RPE). Other causes for RPE leaks, such as choroidal neovascularization, inflammation, or tumors, should be ruled out to make the diagnosis.

CSCR may be divided into 2 distinct clinical presentations. Classically, CSCR is caused by one or more discrete isolated leaks at the level of the RPE as seen on fluorescein angiography (FA). However, it is now recognized that CSCR may present with diffuse retinal pigment epithelial dysfunction (eg, diffuse retinal pigment epitheliopathy, chronic CSCR, decompensated RPE) characterized by neurosensory retinal detachment overlying areas of RPE atrophy and pigment mottling. During FA, broad areas of granular hyperfluorescence that contain one or many subtle leaks are seen.

Pathophysiology

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

Studies employing multifocal electroretinography have demonstrated bilateral diffuse retinal dysfunction even when CSCR was active only in one eye. These studies support the belief of diffuse systemic effect on the choroidal vasculature.

Type A personalities, systemic hypertension, and obstructive sleep apnea may be associated with CSCR. The pathogenesis here is thought to be elevated circulating cortisol and epinephrine, which affect the autoregulation of the choroidal circulation.  Furthermore, Tewari et al demonstrated that patients with CSCR showed impaired autonomic response with significantly decreased parasympathetic activity and significantly increased sympathetic activity.¹

Corticosteroids have a direct influence on the expression of adrenergic receptor genes and, thus, contribute to the overall effect of catecholamines on the pathogenesis of CSCR. Consequently, multiple studies have conclusively implicated the effect of corticosteroids in the development of CSCR. 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.²

Cotticelli et al showed an association between Helicobacter pylori infection and CSCR.³ The prevalence of H pylori infection was 78% in patients with CSCR compared with a prevalence of 43.5% in the control group.  The authors proposed that H pylori infection may represent a risk factor in CSCR, though no further studies have substantiated this claim.

Mortality/Morbidity

Serous retinal detachments typically resolve spontaneously in most patients, with most patients (80-90%) returning to 20/25 or better vision. Even with return of good central visual acuity, many of these patients still notice dyschromatopsia, loss of contrast sensitivity, metamorphopsia, or, rarely, nyctalopia.

• Patients with classic CSCR (characterized by focal leaks) have a 40-50% risk of recurrence in the same eye.
• Risk of choroidal neovascularization from previous CSCR is considered small (<5%) but has an increasing frequency in older patients diagnosed with CSCR.
• A subset of patients (5-10%) may fail to recover 20/30 or better visual acuity. These patients often have recurrent or chronic serous retinal detachments, resulting in progressive RPE atrophy and permanent visual loss to 20/200 or worse. The final clinical picture represents diffuse retinal pigment epitheliopathy.
• Otsuka et al reviewed a subset of patients who presented with a severe variant of CSCR over a mean follow-up period of 10.6 years.⁴ These patients were characterized by multifocal lesions and bullous retinal detachments with shifting fluid and fibrin deposition. During the follow-up period, 52% of patients experienced recurrences of CSCR ranging from 1-5 episodes. However, 80.4% of eyes (n=46) returned to a visual acuity of better than 20/40 and 52% returned to a visual acuity of 20/20 or better. Eventually, patients reached a state of quiescent disease.

Race

CSCR appears uncommon among African Americans but may be particularly severe among Hispanics and Asians.

Sex

Classically, CSCR is most common in male patients aged 20-55 years with type A personality. This condition affects men 6-10 times more often than it affects women.

Age

Patients may present with a later age of onset (>50 y). Spaide et al reviewed 130 consecutive patients with CSCR and found the age range at first diagnosis to be 22.2-82.9 years, with a mean age of 49.8 years.⁵

• Changes in the presentation and demographics of CSCR are observed with increasing age at first diagnosis. Classically, patients tend to be male and present with focal, isolated RPE leaks in one eye.
• Patients diagnosed at 50 years or older are found to have bilateral disease, demonstrate a decreased male predominance (2.6:1), and show more diffuse RPE changes. Furthermore, these patients are more likely to have systemic hypertension or a history of corticosteroid use.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Patients 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.

Physical

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

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 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.
• 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.
• Recent studies employing 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.
• Systemic associations of CSCR include organ transplantation, exogenous steroid use, endogenous hypercortisolism (Cushing syndrome), systemic hypertension, systemic lupus erythematosus, pregnancy, gastroesophageal reflux disease, use of sildenafil citrate, and use of psychopharmacologic medications.
• • 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.²
  • Haimovici et al evaluated systemic risk factors for CSCR in 312 patients and 312 control subjects.⁶ 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.

DIFFERENTIALS

Section 4 of 11  

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• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Idiopathic polypoidal choroidal vasculopathy
Pattern dystrophy (adult foveomacular dystrophy)
Retinal angiomatous proliferation

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Laboratory tests, in general, are not helpful in the diagnosis, although a recent case report identified an elevated level of plasminogen activator inhibitor 1 in the serum of patients with CSCR.

Imaging Studies

• Optical coherence tomography (OCT) reveals many aspects of the pathophysiology of CSCR, ranging from subretinal fluid, pigment epithelial detachments, and retinal atrophy following chronic disease. OCT is especially helpful in identifying subtle, even subclinical, neurosensory macular detachments. Spaide correlated lipofuscinoid deposition of material in CSCR that might mimic vitelliform lesions in pattern dystrophies.⁷ OCT showed accumulation of this material on the outer surface of the retina in neurosensory detachments.
• FA of classic CSCR shows one or more focal leaks at the level of the RPE. The classic "smokestack" appearance of the fluorescein leak is seen only in 10-15% of cases. FA of diffuse retinal pigment epitheliopathy demonstrates focal granular hyperfluorescence corresponding to window defects and blockage caused by RPE atrophy and clumping with one or more areas of subtle continued leakage.
• ICG angiography has shown hypofluorescent areas early in the angiogram followed by late hyperfluorescence and leakage in choroidal vasculature. Often, multiple areas of leakage are seen on ICG angiography that are not evident clinically or on FA. According to some researchers, characteristic mid phase findings on ICG angiography allow differentiation from occult choroidal neovascularization in older individuals. Multiple patches of hyperfluorescence presumably are due to choroidal hyperpermeability, which, in later phases, results in silhouetting or negative staining of larger choroidal vessels.

Other Tests

• Multifocal electroretinography has been used to identify focal regions of decreased retinal function, even in asymptomatic or clinically inactive eyes. Furthermore, investigators, including Lai et al, are using multifocal electroretinography as a means of assessing the efficacy and safety of new treatment modalities for CSCR.⁸ 
• Microperimetry (using the Nidek MP-1 microperimeter) has also shown that, despite clinical resolution of CSCR, there is lower retinal sensitivity in the macula even once visual acuity returned to 20/20. Fixation studies showed stability of central fixation.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• Efficacy of tranquilizers or beta-blockers is unknown. Furthermore, an evaluation of 230 consecutive patients with CSCR found that use of psychopharmacologic agents (eg, anxiolytics, antidepressants) was a risk factor for CSCR. Use of corticosteroids in the treatment of CSCR should be avoided because it may result in exacerbation of serous detachments already present.
• Tatham and Macfarlane described a case series of patients who were treated with propranolol for CSCR.⁹ They suggested that beta-blockade had a hypothetical mechanism in treating CSCR. Further evidence is needed to substantiate this potential treatment.
• Nielsen et al proposed the use of mifepristone in the treatment of chronic CSCR in a case report.¹⁰
• Intravitreal bevacizumab (Avastin) has been used to successfully treat the rare complication of choroidal neovascularization following CSCR.

Surgical Care

Laser photocoagulation should be considered under the following circumstances: (1) persistence of a serous retinal detachment for more than 4 months, (2) recurrence in an eye with visual deficit from previous CSCR, (3) presence of visual deficits in opposite eye from previous episodes of CSCR, and (4) occupational or other patient need requiring prompt recovery of vision.

• Laser treatment also may be considered in patients with recurrent episodes of serous detachment with a leak located more than 300 µm from the center of the fovea.
• Laser treatment shortens the course of the disease and decreases the risk of recurrence for CSCR, but it does not appear to improve the final visual prognosis.
• Some evidence suggests that patients with chronic CSCR (diffuse retinal pigment epitheliopathy) may have better prognosis with laser treatment.
• Photodynamic therapy
• • Photodynamic therapy (PDT) has growing support in the literature as a treatment of chronic CSCR and, most recently, acute phases of this condition.  PDT is known to have a direct effect on the choroidal circulation but was limited by potential adverse effects, such as macular ischemia. Authors, such as Lai et al, are now describing reduced dosing of verteporfin, while the use of reduced fluence has been shown to be therapeutically effective in age-related macular degeneration.⁸ The rates of adverse events have decreased significantly with these modifications.
  • Use of verteporfin and PDT was first reported in 2003 in the setting of CSCR. 
  • Yannuzzi et al described using ICG angiography to first identify areas of choroidal hyperpermeability that were then targeted with PDT.¹¹ 
  • Subsequent studies, using PDT protocols established by the Treatment of Age-Related Macular Degeneration With Photodynamic Therapy (TAP) Study, have reported case series that support the use of PDT, especially in the setting of chronic CSCR with neurosensory detachments. 
  • PDT is believed to hasten both fluid resorption and visual recovery. 
  • Lai et al described the use of half dose verteporfin in the treatment of CSCR.⁸ They proposed 3 mg/m² of verteporfin infused over 8 minutes, followed 2 minutes later with ICG guided PDT. Of the eyes treated, 85% showed complete resolution of the neurosensory retinal detachment and/or pigment epithelial detachment by 1 month after treatment.
  • Multiple authors have also begun to use PDT as a first-line therapy for acute focal leaks from CSCR with reported success. Most papers describe resolution of subretinal fluid within 1 month of treatment. 
  • Chan et al demonstrated that there is evidence of choroidal vascular changes on ICG with regard to choroidal permeability and vascular remodeling.¹²
• ICG mediated photothrombosis is a technique using a low-intensity laser combined with ICG dye infusion to treat focal areas of hyperpermeability in the choroid.  Like PDT, it addresses treatment to the level of the choroidal vasculature.
• • An 810-nm laser is applied after infusion of ICG dye.
  • Without prior ICG dye, investigators have also used the 810-nm laser as transpupillary thermotherapy (TTT) with moderate anecdotal success.
  • However, Penha et al (2007) described severe retinal thermal injury in a 31-year-old man following this treatment modality and recommended caution for this adverse event following ICG mediated TTT treatment.¹³

Activity

Patient participation in stress-reducing activities (eg, exercise, meditation, yoga) is recommended.

MEDICATION

Section 7 of 11  

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• References

No medical therapy is indicated for CSCR.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Most patients receive follow-up care for 2 months to determine whether the fluid resolves spontaneously.

In/Out Patient Meds

• Tatham and Macfarlane described a case series of patients who were treated with propranolol for CSCR.⁹ They suggested that beta-blockade had a hypothetical mechanism in treating CSCR. Further evidence is needed to substantiate this potential treatment.
• Nielsen et al proposed the use of mifepristone in the treatment of chronic CSCR in a case report.¹⁰
• Intravitreal bevacizumab (Avastin) has been used to successfully treat the rare complication of choroidal neovascularization following CSCR.

Complications

• A small minority of patients develops choroidal neovascularization at the site of leakage and laser treatments. A retrospective review of cases shows that one half of these patients may have had signs of occult choroidal neovascularization at the time of treatment. In the other patients, the risk of choroidal neovascularization may have been increased by the laser treatment.
• Acute bullous retinal detachment may occur in otherwise healthy patients with CSCR. This appearance may mimic Vogt-Koyanagi-Harada disease, rhegmatogenous retinal detachment, or uveal effusion. A case report also has implicated the use of corticosteroids in CSCR as a factor increasing the likelihood of subretinal fibrin formation. Reducing the corticosteroid dose frequently will lead to resolution of the serous retinal detachment.
• RPE decompensation from recurrent attacks leads to RPE atrophy and subsequent retinal atrophy. RPE decompensation is a manifestation of CSCR but may also be considered as a long-term complication.

Prognosis

• Serous retinal detachments typically resolve spontaneously in most patients, with most patients (80-90%) returning to 20/25 or better vision.
• Patients with classic CSCR (characterized by focal leaks) have a 40-50% risk of recurrence in the same eye.
• Even with return of good central visual acuity, many of these patients still notice dyschromatopsia, loss of contrast sensitivity, metamorphopsia, or nyctalopia.
• A subset of patients (5-10%) may fail to recover 20/30 or better visual acuity. These patients often have recurrent or chronic serous retinal detachments, resulting in progressive RPE atrophy and permanent visual loss to 20/200 or worse. The final clinical picture represents diffuse retinal pigment epitheliopathy.
• Risk of choroidal neovascularization from previous CSCR is considered small (<5%) but has an increasing frequency in older patients diagnosed with CSCR.

Patient Education

• If possible, patients should avoid stressful situations. Patient participation in stress-reducing activities (eg, exercise, meditation, yoga) is recommended.
• Recent evidence associates systemic hypertension with CSCR, but it is unknown as to whether careful control of systemic hypertension will reduce the incidence of CSCR.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Misdiagnosis of CSCR (very difficult to do given appropriate studies)
• Inappropriate treatment using a laser with subsequent development of choroidal neovascular membranes and improperly placed laser burns inducing central scotomas. Keep in mind that laser treatment often is appropriate and that these complications may occur even with proper application of laser.
• Inappropriate use of steroids in the patient with CSCR
• Inadequate counseling of a patient regarding expectations for full recovery and no recurrences

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  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.
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Media type:  Photo

Media file 2:  Fluorescein angiography in the late recirculation phase of the same patient as in Media file 1. Note the distribution of leakage of fluorescein dye within the neurosensory detachment.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
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• Follow-up
• Miscellaneous
• Multimedia
• References

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Article Last Updated: Jul 16, 2007