REVIEW ARTICLE
Central Serous Chorioretinopathy:
A Review of the Literature
Gunjan Prakash, MD, Nisha Chauhan, MBBS, Shephali Jain, MBBS,
and Saran Kumar Satsangi, MS
Abstract: Central serous chorioretinopathy (CSCR) is an incompletely
understood multifactorial disease of those who are middle aged charac-
terized by the collection of fluid between the retinal pigment epithelium
and the neurosensory retina. The exact etiology of CSCR and the reason
of its predominance in middle-aged males are still unknown. Many
pharmacologic modalities are suggested for CSCR with no proven effi-
cacy. So this article was written to give a review of the relevant and recent
literature on CSCR and to summarize the etiology, clinical features, and
diagnostic modalities for CSCR with special emphasis on the treatment
options available and those that are still under trial and can be of help in
the future to fasten the recovery and reduce the recurrences.
Key Words: central serous chorioretinopathy, serum cortisol,
autofluorescence, retinal pigment epithelium, micro pulse laser
(Asia Pac J Ophthalmol 2013;2: 104Y110)
n 1866, von Graefe1 first described a disease of the macula with
I recurrent serous detachment and named it recurrent central
retinitis. In 1955, Bennet2 named it central serous retinopathy. At
the same time, Maumenee3 observed, using fluorescein angio-
scopy, that macular detachment resulted from a leak at the level of
retinal pigment epithelium (RPE). In 1967, Gass4Y6 provided the
classic description of the pathogenesis and clinical features of this
condition and termed it idiopathic central serous choroidopathy.
Because the disease involves both the choroid and the retina,
the currently accepted name is central serous chorioretinopathy
(CSCR). Central serous chorioretinopathy is characterized by
collection of fluid between the RPE and the neurosensory retina. It
is incompletely understood with systemic associations, a multi-
factorial etiology, and a complex pathogenesis. From 1866, when
Graefe first described CSCR, to the present, much study and effort
continue to be directed toward the understanding and treatment
for patients with CSCR. We need large, prospective, or even ret-
rospective long-term follow-up studies to decide on 1 or more safe
and effective forms of treatment, which will be generally accepted
by clinicians. Until then, it seems reasonable to suggest laser or
reduced dose/fluence/irradiation time verteporfin photodynamic
therapy (PDT) in recurrent chronic CSCR or in single CSCR
episodes, not resolving for a period of at least 3 months, accom-
panied by signs of chronic CSCR. Ongoing efforts include study
regarding methods of evaluation, understanding of pathogenesis,
and strategies for the treatment and prevention of this disease,
From the Upgraded Department of Ophthalmology, Sarojini Naidu Medical
College, Agra, India.
Received for publication December 24, 2012; accepted March 4, 2013.
The authors have no funding or conflicts of interest to declare.
Reprints: Gunjan Prakash, MD, Upgraded Department of Ophthalmology,
Sarojini Naidu Medical College, Agra, India.
E-mail: gunjan_prakash@rediffmail.com.
Copyright * 2013 by Asia Pacific Academy of Ophthalmology
ISSN: 2162-0989
DOI: 10.1097/APO.0b013e31829069ee
104 www.apjo.org Asia-Pacific Journal of Ophthalmology
Copyright © 2013 Asia Pacific Academy of Ophthalmology. Unauthorized reproduction of this article is prohibited.
which can cause significant short-term and long-term vision loss
in affected individuals.
TYPES OF CENTRAL SEROUS
CHORIORETINOPATHY
Acute/Typical/Classic CSCR
This is the commonest, seen in younger patients, character-
ized by acute localized detachment of retina, mild to moderate
loss of visual acuity, 1 or few focal leaks seen in fluorescein an-
giography, and benign self-limiting course.7
Chronic CSCR
This is also known as diffuse retinal pigment epitheliopathy
or decompensated RPE.7 There is chronic presence of shallow
subretinal fluid with widespread alteration of pigmentation of
the RPE. This subtype is associated with older age, chronic
(96 months) detachment of the posterior pole, poorly defined RPE
leakage or ‘‘ooze,’’ multiple pigment epithelial detachments
(PEDs), and poor visual prognosis owing to cystoid macular
edema, foveolar atrophy, subretinal fibrosis, and less commonly,
choroidal neovascularization (CNV).4,8Y12
There is third less common form that causes bullous retinal
detachments usually inferiorly. It is usually associated with shift-
ing fluid and more often seen in patients of organ transplanta-
tion,13,14 patients using corticosteroids,15,16 and patients of Asian
descent.17
PATHOGENESIS OF CENTRAL SEROUS
CHORIORETINOPATHY
Retinal Pigment Epithelium Dysfunction
In fluorescein angiography, focal leakage sites are seen,
which caused detachment of RPE or neurosensory detachment.
This suggests that fluid emanates through the choroid and escapes
into subretinal space through defect in tight junctions between
cells of the RPE.18 According to experimental studies, injury to
RPE speeds the resorption of subretinal fluid.19,20 These studies
pointed out that a simple defect in the RPE integrity alone could
not explain the findings of CSCR.21
One theory suggests that CSCR results from dysfunction of
the RPE. This occurs after an undefined insult. Affected RPE cells
(may be even a single cell) lose their normal polarity and pump
fluid from the choroid toward the retina, causing a neurosensory
detachment.22
All these theories failed to explain why the cells pumped in
the wrong direction, how the pigment epithelium detachments
formed, and how the single isolated disturbance of few RPE cells
may overwhelm the physiologic RPE pump of neighboring nor-
mal RPE. Another factor for limitation of many theories of the
etiology of CSCR is the lack of a suitable animal model to test
hypotheses.
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Choroid Dysfunction
Gass4 suggested that a focal increase in the permeability of
the choriocapillaris was the primary cause of damage to the
overlying RPE in patients with idiopathic central serous chor-
ioretinopathy. Guyer et al23 suggested a potential model for the
pathogenesis of CSCR based on indocyanine green (ICG)Y
videoangiography (ICG-V). They noted diffuse hyperperme-
ability around active leakage sites seen with ICG-V but not with
fluorescein angiography. Therefore, they concluded that hyper-
permeability was at the level of the choroid rather than the RPE.
Excessive tissue hydrostatic pressure within the choroid from
the vascular hyperpermeability may lead to mechanical disrup-
tion of the RPE barrier, damage of RPE cells, and abnormal
egress of fluid under the retina.
Alterations in choroidal circulation may also cause choroidal
ischemia. This was first noted by Hayashi et al,24 who used similar
diagnostic equipment and found areas of choroidal ischemia as
well as leakage of ICG dye from the choriocapillaris. Fluorescein
angiography and ICG angiography (ICG-A) with a scanning laser
ophthalmoscope and a digital imaging system were performed to
evaluate choroidal circulation changes in CSCR by Prunte and
Flammer.25 In their study, segments with late choroidal hyper-
permeability showed delay in filling, which has been attributed to
decreased arterial perfusion or decreased venous outflow. This
may create pressure overload and thus cause choroidal hyperper-
meability. These observations are suggestive of a localized lobular
inflammatory or ischemic choroiditis. However, the cause of the
choroidal abnormality is still unknown. The answer may lie in
changes of the autoregulation in the choroidal blood flow.26 Tittl
et al27 suggested that a persistent abnormal regulatory response
was involved in the pathogenesis of chronic CSCR. They found
that subfoveal choroidal blood flow regulation in patients with
chronic CSCR was impaired. This dysregulation occurred after
substantial functional restoration at least 6 months after the last
episode. Measurements of ocular fundus pulsation in patients with
newly diagnosed active CSCR have previously provided evi-
dence that choroidal perfusion in the macular region might be
abnormal.28
Combined RPE and Choroid Dysfunction
It has been shown that leaks at the levels of the RPE seen
on the fluorescein angiography were contiguous with the areas
of vascular hyperpermeability in ICG-A.23 However, all the
areas of choroidal hyperpermeability are not associated with
actual fluorescein leaks. These areas may be clinically silent and
could affect the ability of overlying RPE to pump fluid from
retina to the choroid.26
ETIOLOGY OF CENTRAL SEROUS
CHORIORETINOPATHY
Central serous chorioretinopathy is a disease that usually
affects men between the age of 20 and 50 years. However, the
youngest patient with CSCR ever described is a 7-year-old
girl.29 Men are affected approximately 8 or 9 times more often
than women.30 When CSCR occurs in women, it is more likely
to occur between age 30 and 40 years. Idiopathic CSCR has been
associated with type A31 personality and elevated endogenous
cortisol.32 Cortisol is a hormone secreted by the adrenal cortex,
which assists the body to deal with various forms of stress. It
reduces inflammation and immune system function and triggers
the breakdown of protein into sugars. The association of objec-
tive and subjective stress with CSCR also points to cortisol be-
cause stress raises cortisol levels. In addition, a high level of
corticotrophin-releasing factor, the hypothalamic hormone that
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Central Serous Chorioretinopathy
drives cortisol levels, causes a subjective experience of stress-
fulness. Patients with CSCR have high levels of cortisol made by
their own adrenal gland (50%Y80% higher than the average and
outside the reference range).32
This condition, predominantly, affects young males and its
incidence declines with advancing age. Because plasma testos-
terone levels also decline with age,33 there might be some relation
of CSCR with testosterone levels. Central serous chorioretino-
pathy has been associated with the use of corticosteroids34 and
also with vasoconstrictive agents. There have been several cases
where CSCR has recurred during each of several courses of
treatment with cortisone drugs and gone away each time the
treatment was stopped. It can be produced in animals by injection
of intravenous epinephrine.25
Haimovici et al35 evaluated systemic risk factors for
CSCR. Systemic steroid use and pregnancy were most strongly
associated with CSCR according to their study. Other risk fac-
tors included antibiotic use, alcohol use, untreated hyperten-
sion, and allergic respiratory disorders.
There is study that showed an association between Helico-
bacter pylori infection and CSCR. The prevalence of H. pylori
infection was 78% in patients with CSCR compared with a
prevalence of 43.5% in the control group in that study. The
authors proposed that H. pylori infection may represent a risk
factor in CSCR, although no further studies have substantiated
this claim.36
There are also studies that suggest that CSCR may be caused
or modulated to some degree by psychological factors. Personal-
ity tests administered to patients with CSCR and a matched con-
trolled group showed higher values on the hyperchondria and
hysteria scale in the group with CSCR.37 The association with
migraine headache in some cases and the association with corti-
costeroids and epinephrine also imply a possible connection with
stress. Central serous chorioretinopathy is also associated with
pregnancy, but the underlying mechanism of CSCR in pregnancy
remains unclear. It is believed that raised levels of endogenous
steroid cortisol could set off a chain of events that alter the blood
retinal barrier, choriocapillaris, and RPE, resulting in focal areas
of increased permeability and thus leading to CSCR.38
SYMPTOMS OF CENTRAL SEROUS
CHORIORETINOPATHY
Mild blurring of vision with visual acuity ranging from 6/6
to 6/60, usually correctable with hyperopic correction,39,40 with
varying degrees of central scotoma (due to detached retina),
metamorphosia (owing to irregular retinal plane), micropsia41
(due to increased distance between photoreceptors in the de-
tached retina), dyschromatopsia (due to anatomic derangements),
FIGURE 1. Fundus photograph of the left eye of a patient having
CSCR showing transparent detachment of neurosensory retina.
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Prakash et al Asia-Pacific Journal of Ophthalmology
hypermetropization42 (due to anterior displacement of retinal
plane), and migraine-like headaches.6
SIGNS OF CENTRAL SEROUS
CHORIORETINOPATHY
Biomicroscopic examination reveals transparent detach-
ment of neurosensory retina with a halo delimiting the elevated
area (Fig. 1). There is absence of foveal light reflex. Sometimes
there is yellowish discoloration of fovea due to increased visi-
bility of retinal xanthophylls. Sometimes yellowish white deposits
are seen covering the posterior surface of detached retina. Mul-
tiple yellowish white dotlike deposits covering the posterior
surface of the detached retina can be seen.43,44
Usually, PED is present in patients with CSCR, and it has a
round or oval shape with a pink halo owing to shallow separation
of retina at the edge of the PED. Subretinal fluid is usually clear,
thus details of RPE and choroid are visible but may be grayish or
cloudy.4,7 Histopathologic studies show fibrin in subretinal fluid,
which may polymerize and cause opacification.18
Peripheral dependent bullous neurosensory detachments
have been described in patients with CSCR.45
IMAGING TECHNIQUES
Fundus Fluorescein Angiography
A typical finding is one or more hyperfluorescent leaks at the
level of RPE.46 In most (approximately 90%) cases, inkblot pat-
tern is seen (Fig. 2), and the dye spreads symmetrically to all sides
and slowly and evenly stains the subretinal detachment. In ap-
proximately 10% of the cases, smokestack pattern is seen (Fig. 3),
that is,, the dye rises within the detachment and then expands
laterally in a mushroom- or umbrella-like fashion along the upper
limits of the detachment. This occurs because of the convection
currents and a protein gradient with increased protein within the
subretinal fluid.47 Focal leaks are more common nasally and su-
periorly than temporally and inferiorly.46,48 Most leaking points
are in a ring 1 mm wide starting 0.5 mm from the center of the
fovea maybe because of the absence of rod cells in the foveal area
resulting in weaker adhesions between RPE and neurosensory
retina.45 In some cases, the leakage point is not seen either be-
cause the leak has healed or because of other mimicking condi-
tions such as exudative age-related macular degeneration or
unilateral acute idiopathic maculopathy.
Fundus autofluorescence (FAF) imaging is recently used as
diagnostic modality because it is noninvasive, unlike FFA. In
FAF, images of normal fundus, retinal vessels, and optic disc are
dark because of lack of autofluorescence. In cases of CSCR,
there are patches of autofluorescence in macular area because of
intraretinal and subretinal precipitates. Spaide and Klancnik 49
FIGURE 2. Inkblot appearance on FFA of a patient having CSCR.
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& Volume 2, Number 2, March/April 2013
FIGURE 3. Classic smoke stack appearance seen on FFA of a
patient having CSCR.
believe that the origin of FAF in CSCR is due to either the ac-
cumulated photoreceptor outer segments (these cells contain
lipofuscin that has the property of autofluorescence) that are not
phagocytized by the RPE or macrophages with phagocytized
outer segments.
Indocyanine Green
This demonstrates multifocal areas of choroidal vascular
hyperpermeability (unifying feature of all CSCRs irrespective
of demography or etiology)50 representing occult PEDs.25,51,52
These areas are best seen in the mid phases of angiogram; in the
later phases, choroidal hyperfluorescence becomes less prominent
with silhouetting or negative staining of the larger choroidal ves-
sels. Sometimes in quiescent phase of CSCR, there is no fluo-
rescein leakage, but still there are areas of choroidal vascular
hyperpermeability in ICG, which serves as a marker of the
disease.
Optical Coherence Tomography
This is an effective and noninvasive method for quantify-
ing serous detachments of retina and RPE (Fig. 4). Patterns seen
are optically empty vaulted area representing neurosensory de-
tachment, small bulges from RPE related to leaking spots, or
semicircular space under the RPE with overlying thinned retina
related to PEDs53,54 (Fig. 4, white arrow). Longitudinal mea-
surements help to track the resolution of subretinal fluid and
provide an objective measure of the clinical course, thus re-
ducing need for angiograms in each follow-up visit.55
TREATMENT OF CENTRAL SEROUS
CHORIORETINOPATHY
Most of the CSCR cases resolve spontaneously within few
months with final visual acuity of 6/9 or better.2,56,57 Only 5% of
all CSCR cases experience severe permanent visual loss.5 Al-
though CSCR has been described as a benign and self-limiting
disease, it has a tendency to reoccur in about half of the cases,
with decreased visual function. The need for early treatment
emerges from clinical evidence that stresses that if the resolution
of the neuroepithelial detachment occurs within 4 months after
onset of symptoms, it is possible to reduce the incidence of ret-
inal atrophy and the consequent decrease in visual acuity.58 In
the largest case series of CSCR with exudative bullous retinal
detachments, no significant difference was noted in the resolu-
tion of subretinal exudation, detachment, or final visual acuity in
lasered versus nonlasered CSCR with exudative bullous retinal
detachment patients.59 However, because their sample size was
small and cases were not randomized for laser or nonlaser
treatment, a prospective randomized study in future with a large
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Asia-Pacific Journal of Ophthalmology & Volume 2, Number 2, March/April 2013
FIGURE 4. OCT image of a patient with CSCR showing serous
detachment of RPE and retina. White arrow shows PED.
number of patients could possibly establish the efficacy of laser
or some other alternative treatment.
Pharmacologic Treatment
Earlier psychotherapy was suggested as a therapy60 but was
abandoned when the pathogenesis became clear. Several years
ago, corticosteroids were presented as only pharmacologic treat-
ment of CSCR, but its use was stopped once steroids were
established as causative agents in CSCR. All the proposed phar-
macologic therapies are based on pathologic mechanisms. Effi-
cacy of barbiturates or tranquilizers in reducing the psychogenic
component of this disorder is unknown. Because CSCR may be
related to the abnormal circulating levels of epinephrine, the use
of A-blockers has been suggested.61,62
Adrenocorticotropic hormone, anti-inflammatory drugs, ret-
robulbar tolazoline injections, subconjunctival injections of milk,
albumin and salt solutions, antisyphilitic and antitubercular
drugs, insulin-free pancreatic extract, and thyroid extract have all
also been suggested in the past. The use of the aforementioned
agents was not proven to be effective by any clinical trials.63 The
use of acetazolamide has been suggested with short-term en-
couraging results but no evidence of long-term benefit.64
The use of low-dose aspirin results in more rapid visual
rehabilitation and less recurrences in patients with CSCR ac-
cording to a large case series. Its beneficial effect supports the
hypothesis of impaired fibrinolysis and platelet aggregation in
choriocapillaris in CSCR.65
Intravitreal bevacizumab (Avastin, F. Hoffmann-La Roche
Ltd, Switzerland) has been used to successfully treat the rare com-
plication of CNV after CSCR by reducing the choroidal hyperper-
meability and choroidal ischemia.66Y69 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-vascular endothelial growth factor agents
for this indication.
Discontinuation of corticosteroids in atypical CSCR could
lead to obliteration of RPE leaks and retinal reattachment without
laser treatment.70
Argon Laser Treatment
It is the most commonly used treatment modality. It redu-
ces the leakage through the RPE and thus resolution of sub-
retinal fluid. When applied at the site of leakage seen during
FFA, it shortens the duration of macular detachment but does
not affect the final visual acuity.71Y76
According to some studies, laser reduces the rate of recur-
rence,75,76 and according to others, it does not.71,72,74 Robertson
and Ilstrup77 suggested a reduction in CSCR recurrences and
shortening of the duration of detachment with direct laser photo-
coagulation compared with sham or indirect (away from the
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Central Serous Chorioretinopathy
site of leakage) photocoagulation within a follow-up period of
18 months. Dellaporta78 concluded that untreated eyes were
3.3 times more likely to develop a recurrence than treated eyes.
The worst complication of laser treatment is photocoagu-
lation of fovea, which leads to persistent scotoma,30 others be-
ing secondary choroidal neovascular membrane especially when
excessive laser intensity is used, but this may also occur in un-
treated eyes.71,79Y81
Because CSCR is a self-limiting disease and also the litera-
ture on argon laser suggests that there is only a speedy resolution
with no effect on final visual acuity and there are possible com-
plications of laser especially when applied very close to fovea,
thus there are only specific indications for photocoagulation: it is a
general recommendation to observe a new-onset acute serous
macular detachment for the first 3 months unless there are special
occupational needs that require rapid resolution or in cases of
uniocular patients. If macular detachment has not resolved in
3 months and leakage is remote from fovea, it is reasonable to do
a laser treatment in a symptomatic patient. If the leakage is
within 500 Km of fovea, it is recommended to observe for
6 months. Other indications for laser are history of CSCR in
fellow eye with unfavorable outcome and recurrent macular de-
tachment in the eye of a patient who has experienced permanent
visual loss from initial episode. It is also indicated in severe forms
of CSCR with poor prognosis if left untreated such as multiple
serous detachments of RPE, bullous sensory retinal detachments,
dependent neurosensory detachment, epithelial tracts, diffuse RPE
decompensation, subretinal deposits of fibrin and lipids, and
CSCRs associated with CNV. With a recent angiogram as a guide,
more peripheral leaks are treated first, only up to the point of dull
gray coagulation to avoid risk of secondary CNV.
After laser application at leakage point, resolution of macular
detachment generally takes 2 weeks in uncomplicated cases or may
be up to 6 weeks in long-standing cases with turbid subretinal
fluid. Complete visual recovery requires twice that time. The pa-
tient should be monitored carefully for CNV in follow-up visits
with repeat FFA if hemorrhage, increased turbidity of subretinal
fluid, or thickening at the level of RPE in, at, or adjacent to the
area of laser application is noted.
Transpupillary Thermotherapy
According to a study, it leads to resolution of CSCR with
subfoveal angiographic leaks and significant improvement in
visual outcome, in comparison with the natural history of per-
sistent CSCR.82 Long-term results are unknown.
Photodynamic Therapy
Photodynamic therapy with verteporfin is a treatment mo-
dality with a rationale of reducing the blood flow in hyper-
permeable choriocapillaris. Indocyanine greenYguided PDT
has shown promising results especially in cases of diffuse de-
compensation of RPE, which was earlier a challenge to treat
because of multiple indistinct leaks.46 It causes the reduction
of subretinal fluid; recurrences do occur but are responsive to
retreatment.
Both fluorescein-guided (as it tightens the blood retinal
barrier at the level of RPE) and ICG-AYguided (as it decreases
choroidal hyperpermeability) PDT have been recommended for
treatment of idiopathic CSCR. Fluorescein angiographyYguided
PDT83 can be used for typical acute leaks, but because of high
cost, its use is limited to focal leaks near the center of the fovea
where laser photocoagulation may cause excessive harm. In
chronic CSCR, location of laser spot is based on regions of cho-
roidal hyperpermeability seen on ICG.84
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Prakash et al Asia-Pacific Journal of Ophthalmology
Choroidal hypoperfusion, which is the main mechanism of
action of PDT in CSCR, can also lead to complications, especially
if conventional PDT is performed, according to the Treatment of
Age-Related Macular Degeneration with Photodynamic Therapy
Study guidelines.85 Lee et al86 described 3 cases of abrupt visual
loss due to severe choroidal ischemia after using standard PDT in
patients with CSCR. Retinal pigment epithelium atrophy, juxta-
foveal CNV, and transient reduction in macular function demon-
strated by multifocal electro-retinogram led investigators to
reconsider PDT parameters for the treatment of CSCR.46,87,88
Lai et al89 reduced the dosage of verteporfin and shortened
the interval between infusion and laser application to induce
choroidal vascular remodeling and minimize any collateral dam-
age to adjacent retinal structures. The safe and beneficial effect of
‘‘safety enhanced’’ (half-dose verteporfin) PDT was demonstrated
in both acute and chronic CSCR by the same investigators.90,91
Zhao et al92 suggested that 30% of verteporfin full dose was
the effective lowest dose in the treatment of their patients with
acute CSCR. Reibaldi et al93 described 2 cases of long-standing
CSCR treated with ICG-AYguided low-fluence PDT. The ana-
tomical and functional outcomes were encouraging. They con-
cluded that ICG-AYguided low-fluence PDT seemed effective
and safe for treating long-standing chronic CSCR. The same
investigators studied the efficacy of ICG-guided low-fluence
PDT compared with standard PDT in a prospective nonrandomized
clinical trial; both standard-fluence PDT and low-fluence PDT
resulted in complete subretinal fluid reabsorption with visual
acuity improvement. They postulated that choroidal hypoperfu-
sion related to PDT could be reduced by low-fluence PDT.94
Recently, Inoue et al95 shortened the irradiation time and reduced
the total energy using the same light intensity and the same ver-
teporfin dosage as the standard protocol. They reported that the
success rate of PDT for CSCR depends on the degree of hyper-
fluorescence seen on ICG-A. Photodynamic therapy is not effec-
tive or the recurrence rate is predicted to be high in eyes without
intense hyperfluorescence.
Long-term efficacy from this form of treatment is unknown.
In addition, the number of patients in most of the relevant studies
is limited, and often there is no dramatic improvement in terms of
the functional outcome of the treatment despite impressive ana-
tomical outcomes observed with OCT. In addition, using con-
ventional PDT, visual improvement may be limited in patients
with prolonged symptom duration and in those who have baseline
confluent RPE atrophy and disintegrity of the junction between
foveal outer and inner photoreceptor layer or progression of RPE
atrophy after PDT. The risk of PDT-induced foveal injury in these
patients should also be considered.96 As far as direct comparison
of laser photocoagulation with PDT treatment is concerned, we
now have some results coming from the study by Maruko et al,97
in which authors showed that the choroidal thickness and hyper-
permeability seen during ICG-A was reduced after PDT. They
suggested that PDT reduces the choroidal vascular hyperperme-
ability seen in CSCR and it may act by a different mechanism than
laser photocoagulation. Most published studies suggest that PDT
with verteporfin is a safe and efficacious treatment even in chronic
CSCR and that complications are rare. This is especially true
when PDT parameters are changed to minimize potential damage.
However, conventional laser is still the choice because of
its low cost and good efficacy as compared with PDT.
Micropulse Laser Photocoagulation
IQ 577 laser have been successfully used in few patients of
chronic CSCR.98 The 577-nm yellow wavelength is ideal for
CSCR and other retinal applications because it is highly selective
for the RPE. Oxyhemoglobin in the RPE absorbs yellow light
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& Volume 2, Number 2, March/April 2013
better than any other wavelength, whereas xanthophylls have
negligible uptake of yellow light, localizing the effects to the RPE
and further protecting the fovea. Yellow micropulse laser appears
to be effective for chronic CSCR. In every case treated in 1 series,
the improvement after treatment was significant. No retinal dam-
age was seen in any of the eyes, except for minimal hyper-
fluorescence in 1 immunocompromised patient with RPE changes
in both eyes before treatment. Although most patients in the series
responded well within 30 days of treatment, some may need more
than 1 laser treatment. Long-term, prospective studies are needed
to confirm the safety and efficacy of this approach.
CONCLUSIONS
Central serous chorioretinopathy is an incompletely under-
stood multifactorial disease of those in middle age characterized
by the collection of fluid between RPE and neurosensory retina
owing to RPE dysfunction and choroidal hyperpermeability.
There is a proven association of CSCR with endogenous hyper-
cortisolism and stress. It causes variable visual loss. Diagnosis
can be aided with OCT, FFA, and ICG. Recently, there has been
an increase in FAF imaging for CSCR owing to its noninvasive
nature. There is no proven medical treatment for CSCR to date
although trials are going on to test the efficacy of drugs antago-
nistic to the suggested causative factors. Conventional laser is
still considered the choice because of its low cost and good ef-
ficacy compared with PDT. Trials are going on to establish the
safety and efficacy of micropulse laser because it is selective to
RPE and thus will protect the fovea, unlike laser, which can cause
foveal scarring.
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