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Central Serous

Chorioretinopathy

Definition
Central serous chorioretinopathy
(CSCR) is often a straightforward
clinical diagnosis when it presents as
a typical serous neurosensory retinal
detachment in a middle-aged male.
However, atypical presentations or
chronic cases are more of a
challenge. CSCR is a diagnosis of
exclusion. Care must also be taken to
ensure that corticosteroid

Etiology
Despite observations using
indocyanine green angiography
(ICGA) that suggest that CSCR is
primarily a choroidopathy, debate
continues over whether the primary
underlying pathology is at the level
of the choroid, the retinal pigment
epithelium (RPE) or both.

Corticosteroids have long been described as an


exacerbating or precipitating factor in CSCR. The
ophthalmologist should carefully question a patient with
CSCR to determine any recent corticosteroid use. Affected
individuals may have forgotten previous intraarticular
corticosteroid injections or may not realize that their
inhaler, nose spray or skin cream contains corticosteroids.
The ophthalmologist may need to communicate with the
other physicians coman-aging the patients care to ensure
that only corticosteroid-sparing medications are being
used. This is particularly crucial in chronic or recurrent
cases because the lack of resolution may be due to
unrecognized corticosteroid use.

Risk factor
Demographically, CSCR is believed to be predominantly
a disease of men 20 to 45 years of age; however, in
women and older patients (> 50 years) CSCR may be
more common than initially reported. CSCR diagnosed
after age 50 should raise a high suspicion of
neovascular age-related macular degeneration instead.
CSCR is more common in Cauca-sians, Hispanics and
Asians, and less common in those of African descent.
Persons with CSCR have a reported higher prevalence of
migrainelike headaches or psychiatric conditions,
including hypochondria, hysteria and conversion
disorder. High-stress occupations or lifestyles also have
been associated with CSCR.

A patient with CSCR usually presents


with visual acuity in the range of
20/20 to 20/200, with an average
presenting visual acuity of 20/30.
Visual acuity can often be improved
with a small hyperopic correction
given the associated shallow
neurosensory detachment.

Symptoms
Patients with CSCR may complain of
decreased visual acuity, micropsia,
metamorphopsia, abnormal color vision
and scotomas. Patients may be
asymptomatic if the fovea is uninvolved.
Other clinical signs include a delayed
retinal recovery time following
photostress, loss of color saturation, and
loss of contrast sensitivity.

Pathophisiology
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 using 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.

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.

Diagnosis examination
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.
Pigment epithelial detachments, RPE
mottling and atrophy, subretinal fibrin,
and rarely subretinal lipid or lipofuscinoid
flecks also may be seen.

Imaging
Optical coherence tomography (OCT) reveals
many aspects of the pathophysiology of central
serous chorioretinopathy (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. OCT showed
accumulation of this material on the outer surface
of the retina in neurosensory detachments.

FA (Fluorescein angiography) 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

Hallo Macula

Treatment
No medical treatment has proven effective for CSCR;
however, acetazolamide has been suggested to hasten
the resolution of subretinal fluid. Corticosteroids are
contraindicated and have no therapeutic role in CSCR.
Direct focal laser photocoagulation, with low-intensity
laser burns to the leakage site, abbreviates the disease
course but has no effect on final visual acuity or
recurrence rate. Because of the generally good prognosis
of CSCR and the tangible risks associated with laser
photocoagulation to the macula, including scarring and
secondary CNV formation, laser treatment is seldom
indicated for CSCR.

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.
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.

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