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com/article/1227025-print

emedicine.medscape.com

Central Serous
Chorioretinopathy
Updated: Jun 18, 2019
Author: Kean Theng Oh, MD; Chief Editor: Andrew A Dahl, MD, FACS

Overview

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). It is a self-limited macular disease
marked by distortion, blurry vision, and metamorphopsia. Other causes for RPE leaks, such as choroidal neovascularization,
inflammation, or tumors, should be ruled out to make the diagnosis. Choroidal neovascularization is also an uncommon
complication of CSCR.

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. Broad areas of granular hyperfluorescence that contain one or many subtle leaks are seen using FA.

CSCR most commonly occurs in males and is associated with psychosocial factors such as stress and type A personality
and with corticosteroid exposure. It has a high rate of recurrence.

Treatment consists of observation, focal laser, reduced fluence photodynamic therapy, and mineralocorticoid antagonists.

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.[1, 2]

Studies using multifocal electroretinography have demonstrated bilateral diffuse retinal dysfunction even when CSCR was
active only in one eye.[3] These studies support the belief of diffuse systemic effect on the choroidal vasculature.

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.[4]

Daruich et al examined the role of the mineralocorticoid pathway in the pathophysiology of CSCR. Study in a rodent model
led to the observation that overexpression of a mineralocorticoid receptor expressed in vascular endothelial cells can result
in up-regulation of calcium-dependent potassium channel, which is associated with vasodilation.[5] This association may
suggest the therapeutic mechanism underlying treatment with mineralocorticoid antagonists.

Type A personalities, systemic hypertension, and obstructive sleep apnea may be associated with CSCR.[6] 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.[7]

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Helicobacter pylori infection has also been implicated in the pathogenesis of CSCR. Cotticelli et al showed an association
between H pylori infection and CSCR.[8] 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. While still controversial, other groups have continued to pursue this hypothesis based on case series.[9, 10]
Zavoloka et al also reported that treatment of H pylori infection decreased the duration and symptoms associated with
CSCR.[11] Can et al demonstrated that choroidal thickness increases with H pylori infection and then normalizes after
treatment.[12] However, others have found no association with choroidal thickness and H pylori infection.[13]

Epidemiology
Frequency

United States

Kitzmann et al reviewed the incidence of CSCR in Olmsted County, Minnesota. They evaluated the period from 1980-2002.
They found the mean annual age-adjusted incidence of CSCR to be 9.9 cases per 100,000 population for men and 1.7
cases per 100,000 population for women.[14]

International

Liew et al reviewed the epidemiology of CSCR in Australia. They found an incidence rate of 10 cases per 100,000
population in men. The rate of CSCR in this study was 6-fold higher in men than in women.[10] In the population-based
Beijing Eye Study 2011, the estimated prevalence of CSCR in the Chinese population older than 50 years was 0.14%.[15]

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.[16, 17]

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.[18] 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.

Tsai et al reviewed a population-based cohort of CSCR patients from the Taiwan national health insurance research
database from 2000-2007. They identified CSCR as an independent risk factor for ischemic stroke. After adjusting for age,
sex, and comorbidities, CSCR had a 1.56-fold increased risk of stroke compared with controls.[19] Using this same
database, patients with CSCR were also found to be at increased risk for rhegmatogenous retinal detachment (7.85 times)
and central retinal vein occlusions (3.15 times).[20, 21]

Race

CSCR appears uncommon among African Americans but may be particularly severe among Hispanics and Asians.
However, one study suggests that CSCR is underdiagnosed in African Americans, underestimating its prevalence in this
group of patients.[22]

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. However, as society has shifted, the prevalence of CSCR in women has
increased. Spaide et al reported a male-to-female ratio of 2.6:1.[23]

Age

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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.[23]

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 age 50 years or older are sometimes 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.[24] These older patients are more likely to have choroidal
neovascularization.

Prognosis
The overall prognosis of CSCR is relatively good. Up to 90% of patients return to 20/25 or better vision after a single bout of
CSCR, though with mild residual symptoms. However, with multiple recurrent episodes and RPE decompensation, visual
acuity changes.[18] Development of choroidal neovascularization can also adversely affect the visual prognosis, although
this is rare.[16, 17]

Serous retinal detachments typically resolve spontaneously in most patients, with most patients (80-90%) returning to 20/25
or better vision.[25, 26, 27]

Patients with classic CSCR (characterized by focal leaks) have a 40-50% risk of recurrence in the same eye.[25, 27, 28]

Even with return of good central visual acuity, many of these patients still notice dyschromatopsia, loss of contrast
sensitivity, metamorphopsia, or nyctalopia.[25]

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.[16, 28] These patients can be treated with intravitreal injection of anti-VEGF agents,
including aflibercept, ranibizumab, or bevacizumab.

Patient Education
Because of the concomitant risk of CSCR recurrence of and the small risk of choroidal neovascularization, patients with
CSCR must be educated regarding the risk of choroidal neovascularization, which requires prompt intervention.

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.

Presentation

History
Patients with central serous chorioretinopathy (CSCR) typically present with acute symptoms of visual loss and
metamorphopsia (especially micropsia) in one eye. 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.[28]

Pigment epithelial detachments, RPE mottling and atrophy, subretinal fibrin, and, rarely, subretinal lipid or lipofuscinoid
flecks also may be seen.[29] Choroidal neovascularization may develop after multiple episodes of CSCR.

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.[30]

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.[31, 32]

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.[33] Fraunfelder and Fraunfelder further evaluated the
association of CSCR with sildenafil.[34] 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.

Another hypothesis involves activation of the mineralocorticoid pathway. Inappropriate or over-activation of mineralocorticoid
pathways in ocular tissues could lead to vasodilation in the choroid. This pathway would also link CSCR to co-morbidities
such as systemic hypertension and psychological stress. Animal models stimulated by aldosterone demonstrate clinical
findings similar to acute CSCR.[35]

The complement cascade has also been implicated in chronic CSCR. Certain polymorphisms of complement factor H and
variants in the C4B have been associated with chronic CSCR in certain populations.[36, 37]

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.[38, 39, 32, 40, 6, 41] 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.[4] Haimovici et al evaluated systemic risk factors for CSCR in 312 patients and 312 control subjects.[42]
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.

DDx

Diagnostic Considerations
CSCR may have a broad range of manifestations considering its presentation from acute to chronic CSCR. Sahoo et al
described CSCR as a "great mimicker and...one of the commonest causes of referral."[43, 44, 45, 46]

Ozkaya et al found that, in a series of patients with suspected pattern dystrophy, 55% of eyes were misdiagnosed and
actually had age-related macular degeneration or CSCR as the underlying disease.[46]

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Differential Diagnoses
Best Disease

Choroidal hemangioma

Choroidal Neovascularization (CNV)

Exudative (Wet) Age-Related Macular Degeneration (AMD)

Exudative Retinal Detachment

Macular Hole

Nonexudative (Dry) Age-Related Macular Degeneration (AMD)

Pattern dystrophy of the retinal pigment epithelium

Pseudophakic (Irvine-Gass) Macular Edema

Rhegmatogenous Retinal Detachment

Choroidal Neovascular Membranes

Tuberculous choroiditis

Vogt-Koyanagi-Harada (VKH) Disease

Workup

Workup

Laboratory Studies
Laboratory tests, in general, are not helpful in the diagnosis of central serous chorioretinopathy (CSCR), 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.[47] OCT showed accumulation of this material on the outer surface of
the retina in neurosensory detachments.

A 45-year-old man presented with micropsia and blurry vision OS. His visual acuity was 20/15 OD and 20/30 OS. The
OCT shows subretinal fluid localized under the foveal center. Six weeks later, the subretinal fluid had resolved and his
vision had recovered to 20/15 OU.

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

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hyperfluorescence corresponding to window defects and blockage caused by RPE atrophy and clumping with one or more
areas of subtle continued leakage.[28]

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.

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.

Newer technology to evaluate the retina is available. Ooto et al showed that adaptive optics scanning laser ophthalmoscopy
is useful in evaluating cone abnormalities associated with visual acuity loss in eyes with CSCR.[48]

Other Tests
Multifocal electroretinography has been used to identify focal regions of decreased retinal function, even in asymptomatic or
clinically inactive eyes. Chappelow and Marmor first described the persistently reduced focal electrical responses on
multifocal electroretinography in eyes with resolved CSCR.[49] 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.[50]
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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. Ojima et al showed that areas of reduced
sensitivity were typically focal and localized to clinically apparent regions of irregular RPE. Fixation studies showed stability
of central fixation.[51, 52]

Treatment

Medical Care
Efficacy of tranquilizers or beta-blockers is unknown. Furthermore, an evaluation of 230 consecutive patients with central
serous chorioretinopathy (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.[53] 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.[54]

Forooghian et al evaluated the safety and efficacy of finasteride, an inhibitor of dihydrotestosterone synthesis, in 5 patients
for chronic CSCR. Macular thickness and subretinal fluid decreased while treated and recurred immediately upon planned
cessation of the medication.[55]

Steinle et al reported a single patient successfully treated with oral rifampin after having chronic subretinal fluid for more
than 2 years’ duration. The fluid resorbed after 1 month of rifampin therapy.[56] Shulman et al conducted a prospective pilot
study on 12 patients with chronic CSCR and concluded that oral rifampin may be a treatment option in patients with
longstanding chronic CSCR.[57] However, a case of rifampin-induced hepatotoxicity has also been reported during
treatment of CSCR.[58]

Kurup et al reported a retrospective series of 9 patients who were treated with low-dose oral methotrexate with resolution of
subretinal fluid without any apparent complications.[59]

Chin et al reported a series of 120 patients who had some response to mineralocorticoid antagonists, eplerenone or
spironolactone. They specifically evaluated patients with recalcitrant disease and found a positive effect in half of the
patients treated.[60] Other authors have also demonstrated the potential for mineralocorticoid antagonists in the treatment of
CSCR.[61, 62]

Intravitreal bevacizumab (Avastin) has been used to successfully treat the complication of choroidal neovascularization
following CSCR.[63, 64, 65] Multiple studies have evaluated intravitreal bevacizumab in the treatment of CSCR
uncomplicated by choroidal neovascularization. Despite multiple studies suggesting a trend toward benefit, other studies
show that bevacizumab does not significantly affect the course of CSCR.[66, 67]

Other anti-VEGF agents such as aflibercept (Eylea) and ranibizumab (Lucentis) are also being used to treat the
neurosensory detachment of CSCR, both in the presence and in the absence of choroidal neovascularization. Bae et al
conducted a prospective randomized study comparing intravitreal ranibizumab to low-fluence photodynamic therapy in
chronic CSCR. At 6 months, they concluded that the anatomic outcomes with ranibizumab injections were “not promising”
compared with low-fluence photodynamic therapy.[68] Semeraro et al compared intravitreal bevacizumab to low-fluence
photodynamic therapy for treatment of chronic CSCR. The series was limited to 22 patients total and no statistical significant
difference could be identified between the two groups.[69]

Surgical Care
Laser photocoagulation

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.[70, 71] 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.[72, 73] Some
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evidence suggests that patients with chronic CSCR (diffuse retinal pigment epitheliopathy) may have better prognosis with
laser treatment.

Photodynamic therapy

Photodynamic therapy (PDT) in the treatment of chronic CSCR was first reported in 2003. 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. The rates of adverse events have decreased significantly with
these modifications.[74, 50, 75] 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. Yannuzzi et al described using ICG angiography to first identify areas of choroidal hyperpermeability
that were then targeted with PDT.[75]

Lai et al described the use of half-dose verteporfin in the treatment of CSCR.[50] Of the eyes treated, 85% showed
complete resolution of the neurosensory retinal detachment and/or pigment epithelial detachment by 1 month after
treatment. Reibaldi et al evaluated the treatment efficacy of standard-fluence PDT versus low-fluence PDT using
microperimetry. The study found improvement of macular sensitivity following treatment along with greater efficacy in
treatment overall using low-fluence PDT.[76] Bae et al compared low fluence PDT to intravitreal ranibizumab in a
prospective randomized trial. Although only 8 eyes were randomized to each group, ranibizumab did not appear promising
when compared with low fluence PDT. After a single treatment, 6 of the 8 eyes in the PDT group had resolution of subretinal
fluid whereas 4 of the 8 eyes in the ranibizumab group ultimately required PDT rescue treatment.[77] 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.[78] 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.[79] 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.[80, 81] However,
Penha et al 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.[82]

Activity
At one time, stress reduction was considered a mainstay of controlling recurrences and duration of CSCR. Potentially,
patient participation in stress-reducing activities (eg, exercise, meditation, yoga) can still be recommended.

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.[17, 73]

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.[26]

Long-Term Monitoring

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Most patients with CSCR receive follow-up care for 2 months to determine whether the fluid resolves spontaneously. Even
following resolution of symptoms, patients should be cautioned about the high likelihood of recurrence and the potential for
development of choroidal neovascularization.

Medication

Medication Summary
Currently, the use of mineralocorticoid antagonists such as aldosterone or eplerenone for the treatment of chronic and
recurrent central serous chorioretinopathy (CSCR) is rising among retinal specialists worldwide. Eplerenone is administered
at 25-50 mg orally each day. Multiple clinical trials have evaluated and supported the efficacy of mineralocorticoid antagonist
use. Coordination with the patient's primary care provider is recommended, and, in many instances, the primary care
provider will substitute one of the patient's existing antihypertensive medications with the mineralocorticoid antagonist. Other
case reports and series have evaluated a range of potential medical treatments for CSCR, such as rifampin. Currently, only
case series and reports support the use of other medications.

Tatham and Macfarlane described a case series of patients who were treated with propranolol for CSCR.[53] 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.[54]

Intravitreal bevacizumab (Avastin) has been used to successfully treat the rare complication of choroidal neovascularization
following CSCR.[63, 64, 65]

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: Alpha Omega Alpha, American Academy of
Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Michigan
Society of Eye Physicians & Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department 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,
Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Steve Charles, MD Founder and CEO of Charles Retina Institute; Clinical Professor, Department of Ophthalmology,
University of Tennessee College of Medicine

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Andrew A Dahl, MD, FACS Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM);
Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency
Program; Staff Ophthalmologist, Telluride Medical Center

Andrew A Dahl, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American
College of Surgeons, American Intraocular Lens Society, American Medical Association, American Society of Cataract and
Refractive Surgery, Contact Lens Association of Ophthalmologists, Medical Society of the State of New York, New York
State Ophthalmological Society, Outpatient Ophthalmic Surgery Society

Disclosure: Nothing to disclose.

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Additional Contributors

Brian A Phillpotts, MD

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

Disclosure: Nothing to disclose.

Acknowledgements

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

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