Major Review

C Shane Mathew DNB, FRCS

Central Serous Chorioretinopathy

Central serous chorioretinopathy (CSC) is a chorioretinal

disease, incompletely understood with systemic associations,

a multifactorial aetiology, and a complex pathogenesis.

History
Central serous chorioretinopathy (CSC) was first described
by von Graefe in 1866, who named it as relapsing central
luetic retinitis.[1] A variety of names have since been used
to describe this idiopathic detachment of the neurosensory
retina.[2] It was more than 100 years later that Maumenee,
using fluorescein angioscopy, noted that the detachment
of the macula resulted from a leak at the level of the retinal
pigment epithelium (RPE).[5] Subsequently, Gass provided
detailed descriptions of the fluorescein angiographic
characteristics of CSC. In 1965 and 1967, the current terms of
CSC3 and idiopathic central serous choroidopathy[4] (ICSC)
were first introduced to describe the same disease.
Although numerous articles and name changes have
been published in the ophthalmic literature, the cause,
clinical manifestations, natural course, treatment, and the
pathogenesis of this condition remains poorly understood,
little is known about the long-term natural course, and
treatment is based on observational, uncontrolled studies.

Pathogenisis
The pathophysiologic event leading to neurosensory retinal
detachment remains unknown, most researchers believe
that stasis, ischemia, inflammation, or a combination of
the above factors leads to abnormal permeability of the
inner choriocapillaries and eventual elevation of RPE and
serous retinal detachment. Yet the presence of these
pathologic mechanisms in the choroid still cannot replicate
the complete constellation of findings in this disorder. In
the acute form of the disease, many believe that there is a
disruption in the continuity of the detached RPE, leading
to focal leakage beneath an overlying neurosensory retinal
detachment, the signature of the disorder.[6,7,8] This
form of mechanical alteration in the integrity of the RPE,
referred to as a blow-out or micro rip, alters its normally
impermeable state, leading to serous detachment of the
retina.[9,10] In this sense, the retina seems to be affected
only secondarily; whereas the inner choroidal changes
represent the primary abnormality of the disorder, leading
to the current designation of the disease as central serous
chorioretinopathy (CSC).The primary exudative disturbance
in the inner choroid, resulting in a macular detachment, is

thought to be nonvasogenic, that is, not associated with

proliferation of choroidal vessels. The initial avascular
nature of CSC distinguishes it from other forms of macular
detachment associated with neovascularization of the
choroid and eventual disciform scarring.[9,10]
Corticosteroids, either endogenous or exogenous, have
been implicated in this disorder.[11,12] Jampol et al[19]
stated that corticosteroids might sensitise the choroidal
blood vessels or RPE to the effects of endogenous
catecholamines. They also linked the rapid onset of the
non-genomic effects of corticosteroids to the occurrence
of serous retinal detachments after the use of highdose systemic corticosteroids. Carvalho-Recchia et al[20]
published the first report of a consecutive series of patients
with acute CSC studied prospectively for an association
with corticosteroids. They found a statistically significant
difference in corticosteroid exposure between study patients
and controls. In addition, CSC has been described in patients
with endogenously high levels of corticosteroids (Cushings
syndrome, pregnancy, and stress)[21] as well as in patients
with hypercortisolism due to the treatment of ocular (optic
neuritis, ischaemic opticneuropathy, solar retinopathy,
scleritis, anterior uveitis,and chorioretinitis)[19,20] or
systemic diseases. Bouzaset al[22] suggested a category of
systemic diseases that have been associated with CSC only
in cases where glucocorticoids were used (such as asthma,
allergic rhinitis, sinusitis, myasthenia, back pain). They
postulated that glucocorticoid intake in these cases was more
important for the development of CSC than the underlying
disease itself. Many components of the hypothalamus
pituitaryadrenal axis and the autonomic (sympathetic)
nervous system have been implicated in the pathogenesis
ofCSC.[23,24] The other distinguishing characteristic feature
noted clinically is the serous pigment epithelial detachment
,a clinical manifestation in the fundus that is limited to very
few disorders, such as neovascular age-related macular
degeneration, polypoidal choroidal vasculopathy and rarely;
inflammatory and infiltrative choroidal disorders. More
recently, the use of three-dimensional optical coherence
tomography (Fourier/spectral domain OCT) has helped
investigators to study morphological alterations of the RPE
both in symptomatic and asymptomatic eyes of the CSC
patients. Not surprisingly, RPE irregularities, at the site of
leakage, were noted in symptomatic eyes.[13]
Yoshioka etal observed that intravenous epinephrine
produced experimental CSC. They also suggested that
11

Address for correspondence: Vasan Eye Care, Kochi

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Kerala Journal of Ophthalmology

the serous detachment of the neurosensory retina in

CSC was biochemically mediated via stimulation of
adrenergic receptors; which resulted in choriocapillary
hyperpermeability and degeneration of the RPE cells above
the damaged endothelial cells.[17]
The first systematic investigation of the relationship
between a type A behaviour pattern (quickness to anger,
competitiveness, and need to be in control) and macular
disease was conducted by Yannuzzi.[2] This was the first
cross-sectional study that employed strict clinical definitions
and matched controls to assess CSC patients to classify them
as a type A behaviour pattern. The latter was statistically
more frequent in CSC patients than in both the control
groups used in this study.
Evidence of familial clustering of CSC has been proposed
by Weenink et al.[25] They reported 27 patients with
characteristic, mostly bilateral, fundus lesions of chronic CSC.
Out of 80 investigated relatives, 35 (44%) had fundus lesions:
22had chronic CSC in one eye, 20 of them had chronic CSC or
RPE atrophy in the fellow eye; 13 relatives had RPE atrophy in
one or both eyes.

Pathogenisis Of Visual Loss

Foveal attenuation, cystoid macular degeneration, secondry
choroidal neovascular membrane and damage of the foveal
photoreceptor layer causes visual loss in CSC.[26,27] Cystoid
macular degeneration, which is generally known as chronic
macular oedema, was defined by Iida et al[26] as cystoid
spaces without intraretinal fluorescein leakage in the fovea.
Posterior cystoid retinal degeneration, generally known
as RPE atrophy or decompensation or depigmentation,
is defined as cystoid retinal degeneration located in the
posterior pole. [28]
One intriguing feature of CSC is the ability of photoreceptors
to continue to function above a serous retinal detachement.
This is in contrast to the profound visual loss associated with
rhegmatogenous retinal detachment.

Natural history of the disease

The natural course of acute CSC is believed to be very good
with primary cases resolving spontaneously in 3 to 4months.
[7,8] Visual acuity usually recovers well in untreated eyes
affected with CSC.[29] However, quality of vision may be
affected.30 Patients with resolved CSC may complain of
metamorphopsia, decrease in brightness, and alteration
in colour vision in the affected eye for several months.
Wong etal[31] concluded that ophthalmologists used to
trivialize the situation as patients sometimes suffer the
consequences following presumed resolution of the disease.
They also found a strong correlation, although statistically
insignificant, of visual acuity and contrast sensitivity in both
normal and ICSC-affected eyes in their long-term follow12

up of resolved ICSC. Koskela et al [32] found a statistically

significant correlation between visual acuity and contrast
sensitivity after resolution of ICSC .Therefore, clinicians need
to be aware that patients may still be visually symptomatic
despite visual acuity returning after an episode of ICSC. Yet,
a small percentage of cases are known to be associated
with recurrent or persistent detachments. In such eyes, the
disorder is referred to as chronic CSC, which is arbitrarily
defined as detachments lasting 6 months or longer.[33]

Management Of CSC
Investigations
A good medical history which include history of duration of
onset, use of steroids in any form, or systemic diseases which
can cause increased catecholamine levels in the circulation
and Type A behaviour pattern etc should be elicited.
Base line investigations such as best corrected visual acuity,
colour vision, amslers grid charting etc should be performed.
Today, current multimode imaging technology is helpful in
the evaluation of a patient with CSC.
Fundus fluoroscene angiogram can demonstrate unifocal or
multifocal areas of smoke stack, ink blot or diffuse pattern
leaks. Subtle Retinal pigment epithelial detachments may
become obvious and retinal pigment anomalies, which may
be far more than clinically detected; can be demonstrated
with this investigation. This also helps physician to locate the
area of leak for treatment.
The use of indocyanine green angiography (ICGA) has
revealed staining of the inner choroidal vessels in the mid
stages of the study, as islands of indocyanine green (ICG)
hyperfluorescence from the posterior pole even to the
peripheral fundus.[41] ICGA findings during the middle phase
about 10 minutes after the ICG injection were classified as
intense or intermediate hyperfluorescence or as having no
hyperfluorescence by sawa etal[43] in chronic csc patients.
Indocyanine green angiogram helps in locating the area of
choriodal hyperpermiability which is the primary pathology,
and helps in accurate localization for treatment. Studies
have shown that areas of choroidal hyperpermiability may
be seen in asymptomatic eyes of patients with CSC and may
not correspond to the area of leak on FA and may be further
away from it.
OCT is traditionally used to quantify the amount and extent
of the subretinal fluid, demonstrate thickening of the neural
retina,RPE detachment, subretinal fibrin and is commonly
used for monitoring during the follow-up and also for
diagnosing the changes in the neurosensory retina that
can cause permanent impairment in vision in such eyes.
Recently, 3D high-speed OCT has shown to facilitate the
understanding of pathophysiologic changes in CSCR. Highresolution optical coherence tomography detects shallow

Shane Mathew - Central Serous Chorioretinopathy

elevations of the retina, and not surprisingly, a thickening

of the choroid.[42] Studies have demonstrated micro rips in
RPE; thus throwing light to pathogenic mechanisms. Gupta
et al[14] studied three-dimensional single-layer RPE scans
and found that the majority of asymptomatic eyes of CSC
patients also showed an uneven RPE surface. This finding was
not present in control eyes of healthy volunteers. The authors
postulated that accumulation of sub-RPE fluid along with RPE
dysfunction, which results in the formation of RPE bumps,
visible on spectral-domain OCT, may represent a preclinical
or subclinical stage of the disease. Previous studies showed
that mERG changes and choroidal permeability changes are
present in both affected and fellow eyes of CSC patients.
[15,16]
Fundus auto florescence abnormalities in CSC show multiple
distinct patterns and seem to provide functional information.
Yutaka etal[44] in their study of 475 eyes with CSC revealed
that confluent hypoautofluorescence of the macula, granular
hypoautofluorescence of the macula, and increasing age all
were independent predictors of decreased visual acuity.

and pregnancy have been reported to be associated with this

form of CSC. It has been described however as an idiopathic
CSC form as well.[37,38,39] In the largest case series of ICSC
with spontaneous bullous exudative RD, visual prognosis
was good without any treatment.[40]
Photoreceptor atrophy at the fovea, despite successful
reattachment, occurs after duration of symptoms of
approximately 4 months.[45] Thus treatment should be
considered in recurrent chronic CSC or a single CSC episode,
of greater than 3 months duration, with some signs of
chronic CSC.
Previous permanent visual loss in the fellow eye caused by a
similar procedure would also indicate that treatment should
be instituted even in the absence of chronic CSC signs or even
if foveal photoreceptors were not immediately threatened.

Types of CSC and treatment criteria

It may be important to distinguish CSC into acute and chronic
disease even though literature does not give clear cut
definitions; as this may correlate with long term prognosis,
to decide on the time of initiation of treatment or to wait
and watch.
Acute form of the disease is usually self limiting over time
with minimal residual changes on imaging. Spade etal[34 ]
defined chonic CSC as meaning a serous macular elevation,
visible biomicroscopically or detected by OCT, that is
associated with RPE atrophic areas and subtle leaks or illdefined staining by Fundus fluorescene angiogram(Fig 1).
The major difference between the two entities as suggested
by Pollock etal[35] where chronic disease is associated with
wide spred RPE disturbance without overt detachment in
most cases . Chronic detachments and geographic zones of
atrophy, produced by antecedent exudative detachments,
including those gravitating into the inferior fundus forming
RPE tracks(Fig2) , and the acute pigment epithelial leak at
the edge of a pigment epithelial detachment, have been
noted . In acute cases one may see focal RPE disturbances
with marked detachment. Diffuse RPE or sick RPE syndrome
is a term that has been defined in literature as chronic CSC
by some investigators[35] or as a form of chronic CSC by
others. It has been reported as an idiopathic condition or as
a complication of systemic corticosteroid treatment.[35] Its
natural course is favourable despite the remaining problems
in colour vision and some degree of metamorphopsia.
Bullous serofibrinous exudative retinal detachment occurs in
some patients with CSC which may pose diagnostic dilemma .
Corticosteroid therapy, organ transplantation, haemodialysis,

Fig 1. Patient with recurrent Central Serous Choroidopathy

associated with depigmentation of the RPE in the macular area. FFA
of the above patient showing window defect and a focal RPE leak

Fig 2 Chronic CSC showing RPE track seen on fundus photograph

which is better delineated and seen on FFA as linear area of window
defect extending to the inferior fundus

Therapeutic Approaches
Before the development of other treatments, psychotherapy
was suggested as a therapy. Corticosteroids were presented
as the only treatment choice in CSC several years ago.
Adrenocorticotropic hormone, anti-inflammatory drugs,
retrobulbar tolazoline injections, subconjuctival injections
of milk, albumin and salt solutions, anti-syphilitic and anti13

Vol. XXIV, No.1, Mar. 2012

Kerala Journal of Ophthalmology

tubercular drugs, insulin-free pancreatic extract, and thyroid

comparison with the natural history of persistent CSC. Long-

extract have all also been suggested in the past. The role of

term results are unknown.

stimulation of adrenergic receptors in the pathogenesis of

CSC led some investigators to suggest that b- or a-adrenergic

Discontinuation of corticosteroids

blockade could be utilised in the treatment of CSC.

Sharma et al[52] reported an observational case series of

Acetazolamide has also been tried as a means of treatment

atypical severe CSC treated with corticosteroids for their

of the chronic macular oedema caused by CSC or other

ocular condition. Discontinuation of corticosteroids resulted

chorioretinal diseases with short-term encouraging results

in reattachment of the retina in 88% of affected eyes. They

but no evidence of long-term benefit. However, there is no

concluded that discontinuation of corticosteroids in atypical

significant proof to support such therapeutic approaches

CSC could lead to obliteration of RPE leaks and retinal

Current and future treatment options for CSC

reattachment without laser treatment.

Laser photocoagulation

Photodynamic Therapy

Robertson and Ilstrup46 suggested a reduction in CSC

Chan et al[53] postulated that PDT could be beneficial for the

recurrences and shortening of the duration of detachment

with direct laser photocoagulation compared with sham or
indirect (away from the site of leakage) photocoagulation

treatment of CSC by its effect on the structure of choroidal

vasculature, causing alterations in choroidal permeability.
Both Fluorescein and ICG-A-guided PDT have been

within a follow-up period of 18 months. Dellaporta[47]

recommended for treatment of CSC.

concluded that untreated eyes were 3.3 times more likely to

Choroidal hypoperfusion, which is the main mechanism of

develop recurrence than treated eyes. Gilbert et al[48] found

no difference either in final visual acuity or in recurrence rate
between eyes treated with argon laser photocoagulation
and untreated eyes in their retrospective long-term followup study of CSC patients. They also explained discrepancies
in recurrence rates in various studies by the different followup durations and different treatment techniques (laser spot
size).
In the study, with the longest follow-up (612 years), argon
laser photocoagulation treatment was not shown to reduce
the incidence of recurrent disease or of chronic CSC. This study
also showed that the role of argon laser photocoagulation
in CSC with good visual acuity is limited to hastening relief
of symptoms by achieving speedier resolution of serous

action of PDT in CSC, can also lead to complications, especially

if conventional PDT is performed. This led investigators to
reconsider PDT parameters for the treatment of CSC. Lai et
al54 reduced the dosage of verteporfin and shortened the
interval between infusion and laser application to induce
choroidal vascular remodelling and they also found that it is
safe and effective in acute and chronic cases.
Reibaldi et al[55] described two cases of long-standing
CSC treated with ICG-A-guided low-fluence PDT with
god anatomical and functional results. The anatomic and
functional outcomes were encouraging. They also studied
the efficacy of ICG-guided low-fluence PDT compared with
standard PDT in a prospective non-randomised clinical

detachment.[49]

trial which showed equal efficacy. They postulated that

Thus with the current level of evidence one may conclude

by low-fluence PDT.[56] Recently, Inoue et al[57] shortened

that treatment is mainly effective in acute csc with focal

leaks seen on FFA; in faster resolution of subretinal fluid
and symptoms when compared to the natural history of
the disease. However, if the area of leakage is subfoveal
or juxtafoveal, photocoagulation may induce secondary

choroidal hypoperfusion related to PDT could be reduced

the irradiation time and reduced the total energy using the
same light intensity and the same verteporfin dosage as the
standard protocol.
Maruko et al,[58] showed that the choroidal thickness and

choroidal neovascularisation (CNV) and/or of damage foveal

hyperpermeability seen during ICG-A was reduced after PDT.

photoreceptors.[50] Therefore other treatment options

They suggested that PDT reduces the choroidal vascular

appear safer.

hyperpermeability seen in CSC and it may act by a different

Transpupillary thermotherapy
Shukla et al [51] performed TTT in long-standing CSC, which
resulted in the resolution of CSC with subfoveal angiographic
leaks and significant improvement in visual outcome, in
14

mechanism than laser photocoagulation Most published

studies suggest PDT with verteporfin is a safe and efficacious
treatment even in chronic CSC and that complications
are rare. Unlike argon laser photocoagulation, it can be
performed for subfoveal leakage too. (Figure 3a and b).

Shane Mathew - Central Serous Chorioretinopathy

Fig 3 a . Pre Low fluence Photodynamic therapy Colour fundus and FFA images of a case of chronic CSC with multifocal areas of leaks
including sub foveal leaks .

Pre PDT OCT BCVA 4/60 <N 36

Post PDT 7 Days

Post PDT 14 DAYS

Post PDT 30 days BCVA 6/18 N12

Fig 3b .Pre and serial post low fluence PDT Oct images showing complete resolution of sub retinal fluid in 4 weeks
15

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Kerala Journal of Ophthalmology

Micropulse diode laser photocoagulation

Sub threshold micropulse diode laser (810 nm) has recently
been assessed for the treatment of chronic CSC [59,60].
It scores over conventional laser in having minimal or no
collateral damage. It has been used in chronic disease with
definite leak or diffuse leak. In the largest series reported;
visual gain of 2 to 3 lines were observed in 58 % of the patients.
ICG assisted subthreshold micropulse photocoagulation was
assessed by Ricci et al[60] in chronic CSC and they found
beneficial effect from this treatment but with incomplete
recovery in 1 year. It was found not superior to PDT.
Thus to conclude; subthreshold micropulse laser is found to
be safe and effective in chronic CSC and may be considered as
an alternative to PDT is cases with well defined or focal areas
of leak .They seem to be ineffective in diffuse area of leakage
and sick RPE syndrome. Larger, controlled, randomised
clinical trials are needed to establish their definitive role.

VEGF Antagonists
The hypothesis that VEGF inhibitors can reduce choroidal
vascular permeability and ischemia has led some
investigators to use intravitreal bevacizumab in acute
and chronic CSC.[61,62] However, all of the related reports
are small, uncontrolled case series with a short duration of
follow-up; larger, controlled trials are still needed to evaluate
the efficacy and safety of anti-VEGF agents for this disease.

Corticosteroid antagonists
The role of corticosteroid antagonists in treating CSC
was first proposed by Jampol etal .[63] This was based on
endogenous hypercortisolism in patients with CSC. The
potential treatment of CSC episodes using antiglucocorticoid
agents includes RU486(mifepristone) and ketoconazole.
It was first tested as a potential treatment for CSC by
Golshahiet al,[64] in a prospective, case-controlled study
which they did not show any conclusive benefit. Meyerle
et al65 found a delayed therapeutic response at 8 weeks
after initiation of treatment with increasing the dose of
ketoconazole.

Asprin
Diseases,associated with CSC, plasminogen activator
inhibitor-1(PAI-1) was increased and that aspirin is effective
in lowering PAI-1 levels and platelet aggregation made some
physicians to evaluate its role in this disease. Caccavale et
al[66] evaluated low-dose acetyl salicylic acid (aspirin) in 107
CSC patients with a mean follow-up time of 20 months. They
found a rapid recovery of visual acuity and a reduced number
of recurrences in their patients.

Conclusions
CSC definitely seems to be a multifactorial disease with
16

systemic association and multiple etiopathogenisis which

ultimately lead to bilateral disease. As for today we need
large, prospective or even retrospective long term follow-up
studies to decide on one or more safe and effective forms
of treatment, which will be generally accepted by clinicians.
Until then, it seems reasonable to suggest reduced dose/
fluence/irradiation time verteporfin PDT in recurrent chronic
CSC or in single CSC episodes, not resolving for a period of
at least 3 months, accompanied by signs of chronic CSC. In
both of which there is active leakage involving the fovea or a
juxtafoveal area. The success seen in treating islands of active
or intense staining in the inner choroid with ICGA-guided PDT
has also led clinicians to treat focal RPE leaks near the fovea
with fluorescein guidance. These leaks are known to occur in
association with ICG inner choroidal staining and will respond
well to PDT without leaving the photocoagulative legacy of
photoreceptor and RPE degeneration and the accompanying
visual scotoma. Caution in treating such leaks near the fovea
is appropriate when there is accompanying fibrin visible
on clinical examination because of the potential for an
exaggerated response. ICGA-guided therapy remains the best
approach for clinicians to consider for eyes with chronic CSC,
particularly if they demonstrate intense or intermediate ICGA
hyperfluorescence patterns in the choroid and persistent
or progressive detachment with associated degenerative
changes in the RPE and photoreceptors accompanied by
vision loss. Micropulse diode laser treatment, applied on well
defined leaking sites, can be considered as an alternative. The
use of corticosteroid antagonists, possibly after evaluation
of patients cortisol profile (for example, urine cortisol or
tetrahydroaldosterone levels), is an interesting future option
that merits further investigation. In addition, counselling
about discontinuation of steroid treatment in any form for
systemic or ocular conditions and explanation of the relation
of the disease to stress is helpful in the management of CSC
patients.

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Dr C Shane Mathew completed his Ophthalmology residency from Joseph Eye Hospital, Trichi and then did his retina
fellowship at Sankara Netralaya. Presently, he is the Vitreo Retinal Consultant at Vasan Eye Care Hospital

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