Download A Case of Bilateral Chronic Central Serous Chorioretinopathy

A Case of Bilateral Chronic Central Serous Chorioretinopathy
Thomas Walent, O.D.
Optometric Resident, VHMC Wilkes-Barre, PA
ABSTRACT
Central serous chorioretinopathy (CSCR) is a chorioretinopathy characterized by an exudative
neurosenosory retinal detachment with or without an associated detachment of the retinal pigment
epithelium. CSCR has several recognized risk factors, and can manifest in several different categories of
disease. Pateints’ symptoms vary greatly from mild disturbance to severe visual significance. CSCR
usually is self limiting and resolves spontaneously in 4 to 8 weeks. If the patient’s symptoms continue
for more than 3 months without resolution, introduction of other therapies should be considered.
Much is still no known regarding the pathophysiology of the disease, however with the advent of new
imaging technology and techniques designed to further understand the structure and function of the
retina, a better understanding has been established regarding the pathophysiology of CSCR. A wide
variety of treatment strategies have been postulated targeted towards pathophysiological defects
within the retina causing CSCR.
CASE REPORT
In March 2005, a 41 year old white male reported to the Wilkes-Barre VHMC Eye Clinic with complaints
of having a visual distortion in his right eye. Patient describes this distortion to be more evident at near.
Patient had no ocular history, and a systemic medical history positive for allergic rhinitis and joint pain.
Visual acuity testing revealed distance and near VA of 20/20 OU, with complaints of visual distortion in
the central vision OD. Amsler grid testing revealed positive metamorphopsia OD, without scotoma.
Entrance testing, slit lamp examination and IOP were unremarkable. Dilated fundus exam revealed
healthy optic nerves OU, with pigmentary changes within the central macula OD, without retinal fluid or
thickening. All other aspects of retinal vasculature, posterior pole, and peripheral retina were
unremarkable. The patient was referred to a retinal specialist for retinal evaluation with FA and OCT.
The retinal specialist confirmed the diagnosis of a previous episode of Central Serous Chorioretinopathy
OD, based on the macular pigmentation.
In March 2007, the patient returned to clinic with a new onset distortion in his right eye at distance and
near following a heated argument that he engaged in over the weekend. All aspects of examination
were unremarkable with the exception of having a large area of metamorphopsia OD with Amsler grid
testing. OCT revealed a serous retinal detachment beneath the fovea. The patient was referred to a
retinal specialist who confirmed an old CSCR which is now active in nature. The specialist chose
observation as the best course of action for this case.
In March 2009, the patient again returns to the clinic with new onset changes in his vision, complaining
of having difficulty with his near vision. The patient reports that he has recently returned to school, and
has been under a tremendous amount of stress and anxiety. The examination revealed mild presbyopia
OU, with no signs of active CSCR OU. Dilated fundus exam did reveal new pigmentation OS, which may
have indicated a small previous episode of CSCR that was asymptomatic to the patient. OCT confirmed
this diagnosis, showing no active CSCR, but mild thickening of both maculae.
In April 2011, patient reports new onset distortion OS at near, with a central blind spot. This is
particularly bothersome to the patient because his school work had intensified, and must read several
hours per day. He admits that he was having great difficulty balancing the stress of school and his
personal life, and has great levels of anxiety. Amsler grid testing revealed stable central
metamorphopsia OD, and new onset central metamorphopsia with a temp wedge shaped scotoma OS.
OCT revealed thickening of the central macula OD with a serous retinal detachment OS. Patient was
referred to a retinal specialist who confirmed the new onset serous retinal detachment OS and again
advised observation and management of stress levels. The retinal specialist inquired about use of
steroids for his systemic conditions, which the patient denied. The following month the patient
returned with similar symptoms, which he believed were worsening. OCT revealed serous retinal
detachments OU, and dilated fundus exam confirmed these findings, with macular pigmentation
OD>OS. The patient’s systemic medical history was again questioned, in which the patient revealed that
not only does he use a steroid inhaler for his asthma, but also receives multiple cortisone injection is his
shoulders for several years. The patient did not understand that these medications were steroid based.
Observation was again suggested, and he was encouraged to speak to his primary care doctor and
orthopedist regarding the use of these medications, which were clearly exacerbating his CSCR.
Over the following months and up to this current point the patient’s symptoms continue, however the
serous detachment in his left eye has subsided, and he continues to have a chronic serous RD in his right
eye that is not improving. The patient has become increasingly frustrated with his condition and stated,
“This needs to stop happening, isn’t there something else you can do?”
INTRODUCTION
Central serous chorioretinopathy (CSCR) is a chorioretinopathy characterized by an exudative
neurosenosory retinal detachment with or without an associated detachment of the retinal pigment
epithelium. The disease was first described by Albrect von Graffe in 1866, who described it as
“relapsing central leutic reintitis”.1 In 1965, Maumenee was the first to describe a leak at the level of
the RPE with utilization of fluorescein angiography in several patients.2 Subsequently, Gass drafted very
detailed descriptions of the fluorescein angiographic patterns and characteristics of CSCR. Gass coined
the term “central serous chorioretinopathy” in 1967.3
Although the condition is often referred to as “Central Serous Retinopathy”, it has been found that it is
not in fact a “retinopathy” rather a “choriorentinopathy”. Despite this misnomer, CSCR is the fourth
most common “retinopathy” after age related macular degeneration (ARMD), diabetic retinopathy, and
branch retinal vein occlusion.4
EPIDEMIOLOGY
Men are more likely to develop CSCR at a ratio of about 6:1. The mean age of onset of disease has been
found to be 41 years old. Although CSCR affects mainly middle aged males, several reports have
documented cases of disease in young and elderly patients of both sexes.5 CSCR occurs most
commonly in white and Asian populations, and appears to occur less frequently in African Americans.6
CSCR has the tendency to be more aggressive in African American patients. It has been postulated that
African-Americans have greater sympathetic reactivity to stressors which in turn causes disruption to
subfoveal choroidal blood flow, thus exacerbating the disease process.7
RISK FACTORS
Several risk factors have been identified that significantly increase risk of developing CSCR, however
many are very poorly understood. Over the past several years, infections, toxins, immunological
reactions, neuronal, circulatory, and hormonal regulatory factors have all been implicated in the
initiation of the damaging process that leads to CSCR.
One of the first and most recognized risk factors for developing CSCR is having a Type A personality.
Type A personality is defined as having quickness to anger, high levels of competitiveness, and having
the compulsion to always be in control. CSCR is associated with high levels of stress and anxiety
hormones, particularly cortisol and epinerpherine. Those with Type A personalities under stress have
higher levels of endogenous stress hormones, often up to 40x the normal level of cortisol and 4x that of
epinerpherine.8
On a similar note, a few specific systemic diseases related to having elevated endogenous
corticosteroids have been found to be predisposed to developing CSCR. Cushing’s syndrome can result
from either high levels of endogenous or exogenous administration of corticosteroids, resulting in
elevated levels of systemic cortisol.9 Women who are pregnant also may have elevated endogenous
cortisol. Several studies have linked this elevation of cortisol levels to CSCR.10 Along the same lines,
elevated levels of endogenous epinephrine, such as in patients with obstructive sleep apnea and
systemic hypertension, has been linked with higher risk of CSCR.11
There is also extensive literature that suggests that exposure to exogenous corticosteroids significantly
increases incidence of CSCR. Multiple systemic conditions are treated with corticosteroids (ex. asthma,
autoimmune disorders, joint inflammation, dermatological conditions, allergic rhinitis, degenerative disc
disease requiring epidural, organ transplantation, etc), with varying administration routes, all of which
have resulted in secondary CSCR.12Ocular conditions treated with systemic steroids and periorbital/
intraocular injections of Kenelog (optic neuritis, ischemic optic neuropathy, diabetic retinopathy, solar
retinopathy, scleritis, anterior uveitis, chorioretiniits, etc) have also been shown in literature to develop
subsequent CSCR.13
CLASSIFICATION
CSCR can broadly be divided into acute, recurrent, and chronic groups. The importance of distinguishing
between these specific categories refers to the long term visual prognosis of the patient, and whether or
not treatment should be necessitated. The term acute CSCR refers to a self limiting condition which
resolves within a few months of initial symptoms, without treatment and with minimal residual changes
to the retina. On the other hand, chronic CSCR is defined as “a serous macular elevation, visible
biomicroscopically or detected by OCT, that is associated with RPE atrophic areas and subtle leaks or ill
defined staining by FA.”14 Chronic cases of disease can further be categorized by chronic CSCR following
a single attack, recurrent resolving CSCR and recurrent non-resolving CSCR. Recent studies have shown
that 51% of untreated patients suffer a single acute resolving attack, while the remaining 49% have a
more complicated version of the disease.15 Polak et al noted that the major distinction between chronic
and acute disease is the fact that chronic disease has widespread pigment epithelial changes without
overt detachment in most cases, whereas in acute diseases there is focal pigment epithelial abnormality
and marked detachment.16
CLINICAL PRESENTATION
Patients will report with a multitude of symptoms upon developing CSCR, many of which can be verified
with classic ophthalmic examination techniques. Visual acuity may vary, affecting some patients
profoundly and others will not demonstrate a measureable decrease in vision. When shown an Amsler
Grid, patients often report an acute onset of central scotoma, metamorphopsia, and micropsia.
Contrast sensitivity and color saturation are often diminished. Patients will demonstrate an increase in
macular photostress test time. 17
Upon examination of the fundus with contact lens biomicroscopy, a serous macular neurosensory
detachment will be present without subretinal bleeding. There are often subretinal lipofuscin deposits
present in the area of detachment, referred to as “dots”. Other varying characteristics often found
when evaluating CSCR are RPE detachments, areas of retinal epithelial mottling and atrophy (often in a
gutter configuration) and subretinal fibrin (especially when the episode happens after pregnancy).
The actual cause of visual loss in CSCR results from the after effects of the neurosensory detachment of
the retina, including foveal attenuation, cystoid macular degeneration, and damage of the foveal
photoreceptor layer. 18 Unlike the profound visual loss that is associated with a rhegmatogenous retinal
detachment, the photoreceptors have an unexplained ability to function in the area above serous retinal
detachments seen in CSCR. 19
In most untreated cases of CSCR, visual acuity will recover quite well, however the quality of vision may
suffer. Wong et al concluded that optometrists’ too often “trivialize the situation as patients
sometimes suffer the consequences following presumed resolution of the disease”. Patients often
remain with symptoms, and may complain of metamorphopsia, decrease in brightness, and alterations
in color vision of the affected eye for up to several months following resolution of CSCR.20
PATHOPYSIOLOGY
One of the most least understood aspects about CSCR is whether the pathophysiology of this condition
is related to a disorder of primarily the choroid, the retinal pigment epithelium, or both; and whether
this disorder is a focal phenomenon or widespread. With the advent of new imaging technology and
techniques designed to further understand the structure and function of the retina, a better
understanding has been established regarding the pathophysiology of CSCR. Data currently supports
both theories; however a definitive conclusion has still yet to be determined.
Choroid Dysfunction Theory
Gass suggested that a focal increase in the permeability of the choriocapillaris was the primary cause of
damage to the overlying RPE in patients with CSCR. He suggested that this could create detachment of
the RPE, serous retinal detachment and, in 10–15% of patients, serofibrinous subretinal exudation.21
Following the work of Gass, a groundbreaking study suggested a potential model for the pathogenesis of
CSCR based on ICG-videoangiography (ICG-V). Patient with CSCR showed a common finding of diffuse
hyperpermeability around active leakage sites seen with ICG-V but not with FA.22 This finding suggested
that hyperpermeability was at the level of the choroid rather than the RPE. They proposed that
choroidal hyperpermeability causes serous detachments of the RPE, which can induce a small rip or
decompensation of the RPE, forming an area of leakage. This in turn leads to diffusion of water,
electrolytes, and proteins that causes a neurosensory retinal detachment.
More support of the choroidal dysfunction theory of CSCR involves the postulation that focal areas of
choroidal ischemia may be the cause of alterations within choroidal circulation. On study utilizing
Fluorescein angiography (FA) and indocyanine green angiography (ICG-A) with a scanning laser
ophthalmoscope and a digital imaging system were performed to evaluate choroidal circulation changes
in CSCR.23 They found that dilated capillaries and dilated draining venules in one or more choroidal
lobules, following a localized delay in arterial filling. They suggested that this might explain the
choroidal hyperpermeability in the area of the damaged RPE. These observations are suggestive of a
localized lobular inflammatory disease or ischemic choroiditis.
However, the cause of the choroidal abnormality is still unknown. It has been suggested that the answer
may lie in changes of the autoregulation in the choroidal blood flow.24
RPE dysfunction theory
An alternative theory suggests that CSCR results from dysfunction of the RPE. This occurs following an
undefined insult to the RPE, resulting in either a few impaired RPE cells or even a single RPE cell which
causes a reverse in fluid movement in a chorioretinal direction. This subsequently leads to leakage of
fluid in the subretinal space and finally to the development of a neurosensory retinal detachment.
Spitznas suggested that focal damage to the RPE can reverse the direction of ion secretion and thus lead
to greater fluid movement towards the retina than to the choroid.25
IMAGING
Fluorescein angiography
Fluorescein angiography (FA) is one of the most widely used imaging techniques used to diagnose
disorders of retina, particularly those involving areas of subretinal leaking. The most important
angiographic feature is an expanding point of fluorescein leakage under a serous detachment of the
neurosensory retina without the presence of subretinal neovascularization. The leakage site is
hypopigmented due to movement of choroidal fluorescence. The hallmark of CSCR is the presence of a
“smokestack” leak, with a reported prevalence ranging from 7%26 to 25%27 . Other less common
patterns include “inkblot” and “mushroom” leaks.28
Fluorescein angiography reveals leaks in the RPE which is present in about 95% of all cases of CSCR.
Most of the leaks are located 0.5 – 1.5 mm away from the center of the fovea, and only 10% are found
closer to the fovea. The most common sites of leakage are the superior nasal quadrant of the posterior
pole. In cases of chronic CSCR multiple RPE leaks are often visualized.29
Optical coherence tomography (OCT)
Optical coherence tomography (OCT) is a very valuable tool in diagnosing CSCR. OCT holds many
advantages to FA, as it is a noninvasive test that is very easily performed, and provides a high resolution
three-dimensional image of anatomy of the retina. In patients with active and inactive CSCR, a serous
neurosensory retinal detachment is often imaged, many times with an associated pigment epithelial
detachment within or outside the area of retinal detachment. Studies also revealed areas of multiple
small PED’s within the area of the macula and along the vascular arcades.30 When focusing your
attention to the RPE layer of the retina, the image often shows a single or multiple small defects. One
particular study performed OCT on 21 eyes with CSCR and found RPE abnormalities in 95% of the eyes
with a tiny defect of the RPE within the pigment epithelial detachment. These defects corresponded to
leakage points found on fluorescence angiography, thus supporting the RPE dysfunction theory.31
Another important finding seen with OCT involves choroidal thickness. Using SD-OCT, the mean
thickness of the choroid in patient with CSCR was found to be thickened two-fold when compared to the
average population, with mean thickness was found to be 505 µm compared with 272 µm in normal
individuals.32 Researchers suggest the thickening of the choroid relates to increased hydrostatic
pressure, and this finding is supportive of the choroid dysfunction theory.
Indocyanine Green Angiography
Indocyanine green angiography (ICGA) is useful when studying and diagnosing CSCR because it is used
primarily to image abnormalities within the choroidal structure. This is particularly useful because
choroidal dysfunction is one theory of the pathology of CSCR. One study revealed that 63-100% of cases
of CSCR demonstrate significant choroidal filling delays, which supports the theory this phenomenon
would cause retinal ischemia, which in turn increase choroidal hyperpermeability and lead to serous
detachment of the retina. 33 Along the same lines, areas of choroidal hyperfluorescence indicate
choroiocapillary nonperfusion, which is commonly seen in patients with CSCR.34 Again, these choroidal
circulatory disturbances may be responsible for the subsequent vascular hyperpermeability.
Fundus Autofluorescence
Fundus autofluorescence (FAF) uses stimulated emission of light from certain fluorophores, mainly
lipofuscin in order to provide an image of the retina. Lipofuscin content is an indirect measurement of
metabolic activity of RPE cells and at the level of the RPE lipofuscin build-up is related to phagocytosis of
photoreceptor outer segments. As mentioned earlier, appearance of the fundus in patients with CSCR
often have small, subretinal “dots” in the area of detachment. Many have hypothesized that these
“dots” are accumulations of lipofuscin.35 One study indicated that 65% of patients with CSCR had
lipofuscin deposits that were imaged with both FAF and confirmed with OCT scans.36
FAF is very useful in diagnosing and classifying between acute and chronic cases of CSCR. In cases of
acute CSCR, areas of hyperautofluorescence indicate areas of serous retinal detachment. On the other
hand, chronic CSCR demonstrates both areas of hyper and hypoautofluorscence. The relevance to
hypoautofluorescence in cases of chronic CSCR relates to treatment strategies. Some suggest that areas
of hypoflurorescence near the central macula would not respond well to laser therapy. It has also been
noted that hypoflurorescence near the central macula in patients with increased age is a good predictor
of decreased visual acuity upon resolution of CSCR.37
TREATMENT
There are few randomized controlled trials with respect to the treatment of CSCR. In approximately
90% of patients, CSCR is self limiting and spontaneously resolves.
The first line of treatment for CSCR should involve a thorough systemic medical history, and
discontinuation of all steroid medications, if possible. Studies indicate that 90% of serous detachments
will resolve upon discontinuation of steroid.38 Lifestyle counseling and other psychological therapies
may be suggested as an attempt to reduce stress and anxiety levels. If the patient’s symptoms continue
for more than 3 months without resolution, introduction of other therapies should be considered.
Laser focal photocoagulation
Laser photocoagulation works by applying energy to the retina and changing the RPE’s ability to act as a
barrier to diffusion. The fluid within a serous retinal detachment in CSCR has a very high concentration
of protein and facilitates diffusion of fluid from the choroid underneath the retina. Photocoagulation
allows the both the fluid and protein to return in the correct direction back into the choroid due to the
permeability of the RPE.39 Current studies indicate that treatment with laser photocoagulation reduces
the length of detachment by up to one month, and decrease the rate of recurrence over an 18 month
span from 34% in the untreated group to 0% in the treated group.40 The benefit of quicker resolution of
CSCR however does not appear to be correlated with improved visual acuity.
Unfortunately laser is only an option for areas of extrafoveal leakage. In all cases, laser treatment
results in focal collateral retinal damage. Potential complications include thermal rupture of Bruch’s
membrane with or without hemorrhage, secondary choroidal neovascular membrane (CNVM), and
misplaced laser spots.41
Photodynamic Therapy
Photodynamic therapy (PDT) with vertiporfin (Visudyne) offers a more precisely directed alternative to
photocoagulation. PDT is directed towards the pathological hyperpermeable choroidal microcirculation
responsible for CSCR. Vascular remodeling results in decreased permeability and termination of focal
RPE leakage.42
PDT has been shown to cause a resolution of serous detachment and improvement in VA and symptoms
through interventional and retrospective studies. These studies were performed under “Treatment of
ARMD with PDT” (TAP) protocols, with undesirable reports of complications including changes of the
RPE, choriocapillary hypoperfusion, and development of CNVM.43
A series of studies with modifications of TAP protocols were performed in order to reduce potential
complications. One study introduced “safety enhanced PDT” with the use of half-dose vertiporfin
(3mg/m2). Findings demonstrated significant improvement of retinal function only in cases of CSCR
without PED, and showed no undesirable side effects. These findings have been shown effective at loses
as low as 30% of vertiporfin.44 One other protocol using decreased flux has also shown promise. Lowfluence PDT (25 J/cm2 @ 300mW) resulted in reduction of serous retinal detachment and increase in
visual acuity without damage to the choriocapillaris in 79-91% of patients.45
Intravitreal Bevacuzumab
Bevacuzumab (Avastin) is an anti-vascular endothelial growth factor that is primarily used for the
treatment of exudative age-related macular degeneration (ARMD) and has been highly studied for the
use of retinal conditions. In CSCR, VEGF has a role in vascular permeability by changing tight junctions
and inducing vascular fenestration. It has been suggested that use of bevacuzumab may not affect the
underlying cause of CSCR directly, but rather act on tight junctions only. Studies report resolution of
neurosensory detachment, with improvements in visual acuity and RPE leaks after anti-VEGF therapy,
with mixed results.46 In cases of chronic CSCR with accumulations of subretinal granular deposits from
the phagocytosis of photoreceptor segments (“dots”), it has been postulated that these “dots” could
prevent the anti-VEGF treatment in chronic CSCR.47
Acetazolamide
Acetazolamide (Diamox) is a carbonic anhydrase inhibitor which has many ophthalmic uses, including
reduce subretinal fluid in various disorders. It has been suggested that oral administration of
acetazolamide may accelerate resolution of acute cases of CSCR. Clinical trials have found that
acetazolamide has been found successful in shortening the length of time serous detachment.
However, the treatment has shown no effect on recurrence rate or any increase in final visual acuity.48
Clinicians suggest that this treatment option has potential to be used for patients in need of accelerated
resolution of an episode of acute CSCR, such as those that are monocular. In view of potential side
effects of acetazolamide such as aplastic anemia, parathesias, nervousness and gastric upset, along with
its contraindication for patients with sulfa allergy, its use is limited in the face of other more effective
interventions.
Ketoconazole
Ketoconazole (Nizoral) is oral antifungal medication that is an adrenocorticoid antagonist. Those with
CSCR have been found to have elevated endogenous levels of cortisol. In a small study of 15 patients,
200mg of ketoconazole was administered for four weeks. The patients demonstrated significantly
reduced levels of urinary cortisol, there were no improvements found in resolution of disease or visual
acuity when compared to the control group.49 Although reducing endogenous corticosteroids seems to
offer a rational approach in resolution of disease, clinical studies offered no benefit.
Mifepristone
Mifepristone (RU-486) is a high affinity progesterone and glucocorticoid antagonist. Mifepristone is
used clinically in voluntary early pregnancy termination. A recent small prospective study displayed
great promise, where patients were orally given a 200mg dose of mifepristone for 90 days, showed
dramatic improvement in symptoms and disease resolution. 50 Due to the moral debate of this
medication, and its high cost of treatment ($200 for a 200mg dose), ophthalmic use of mifepristone may
be severely delayed in the United States, however further investigation is warranted.
Sleep apnea
A recent series of observational case reports has demonstrated a relationship with CSCR and obstructive
sleep apnea syndrome. One study revealed that 22% of 56 consectutive patients with acute CSCR
suffered from obstructive sleep apnea syndrome, whereas only 2% of the general population suffers
from obstructive sleep apnea.51 Observational case reports have demonstrated resolution of CSCR and
treatment of obstructive sleep apnea syndrome, with rapid resolution of bilateral CSCR with treatment
of newly diagnosed obstructive sleep apnea.52 Clinicians should consider this diagnosis with CSCR and
refer for a sleep study when deemed appropriate.
DISCUSSION
Central serous chorioretinopathy (CSCR) is a chorioretinopathy characterized by an exudative
neurosenosory retinal detachment with or without an associated detachment of the retinal pigment
epithelium. CSCR has several recognized risk factors, and can manifest in several different categories of
disease. Patients’’ symptoms vary greatly from mild disturbance to severe visual significance. CSCR
usually is self limiting and resolves spontaneously in 4 to 8 weeks. If the patient’s symptoms continue
for more than 3 months without resolution, introduction of other therapies should be considered.
Much is still no known regarding the pathophysiology of the disease, however with the advent of new
imaging technology and techniques designed to further understand the structure and function of the
retina, a better understanding has been established regarding the pathophysiology of CSCR. A wide
variety of treatment strategies have been postulated targeted towards pathophysiological defects
within the retina causing CSCR.
In the previously described case, the patient was diagnosed with chronic nonresolving CSCR OD, and
chronic resolving CSCR OS. The patient had several risk factors, including being a middle aged white
male with an admitted Type A personality who was under great deals of stress due to going back to
school, and received multiple steroid treatments with cortisone injections in his shoulders and knees for
an arthritic condition and use of a steroid based inhaler for asthma. The patient has been visually
symptomatic for several years, with noticeable Amsler Grid defects and mild changes in visual acuity.
With use of OCT and FA, along with regular fundus examinations, the patient has had multiple accounts
of serous retinal detachments without PED’s OU, permanent macular thickening, and macular RPE
mottling. Subretinal “dots” were not present upon examination.
Previous treatment strategies included observation, discontinuation of steroids, and implementing
coping strategies to relieve physiological stress and anxiety levels. The patient is currently still
symptomatic, and exhibits signs of chronic CSCR. If additional treatment strategy were to be
introduced, “safety enhanced” and low-fluence PDT would be a very logical choice. This treatment is
rather safe, results in minimal side effects, and has been shown in literature to reduce serous
detachments and improve visual acuity in even chronic cases of CSCR without PED.53 Upon further
investigation of efficacy in use of CSCR, use of intravitreal injection of Bevacuzumab and/or oral use of
mifepristone may be useful in the future if this patient fails with PDT treatment.
REFERENCES
1
Von Graefe A. Kurzere Abhandlungen. Notizen und casaistische Mitheilungen vermischten Inhalts: VI. Ueber
zentrale recidivirende Retinitis. Albrecht Von Graefes Arch Klin Exp Ophthalmol 1866; 12: 211–215.
2
Maumenee AE. Symposium on macular diseases: clinical manifestations. Trans Am Acad Ophthalmol Otolaryngol
1965; 69: 605–613.
3
Gass JDM. Pathogenesis of disciform detachment of the neuroepithelium: II. Idiopathic central serous
choroidopathy. Am J Ophthalmol 1967; 63: 587–615. 4, 47 Wang M, Munch IC, Hasler PW, et al. Central serous
chorioretinopathy. Acta Ophthalmologica 2008; 86:126–145.
4
Wang M, Much IC, Hasler PW, et al. Central Serous chorioretinopathy. Acta Ophthalmologica 2008;86:126-145
5
Haimovici R, Koh S, Gagnon DR, et al. Risk factors for central serous chorioretinopathy: a case–control study.
Ophthalmology 2004; 111:244–249.
6
Chan W-M, Lai TYY, Tano Y, et al. Photodynamic therapy in macular diseases of Asian populations: when East
meets West. Japanese J Ophthalmol 2006; 50:161–169.
7
Balo KP, Mihluedo H. Idiopathic central serous chorioretinopathy: two case reports observed in Togo. Medecine
tropicale 1996; 56:381–383.
8
Yannuzzi LA. Type A behavior and central serous chorioretinopathy. Trans Am Ophthalmol Soc 1986; 84:799–845.
9
Bouzas EA, Scott MH, Mastorakos G, et al. Central serous chorioretinopathy in endogenous hypercortisolism.
Arch Ophthalmol 1993; 111:1229-1233.
10
Mayo GL, Tolentino MJ. Central serous chorioretinopathy in pregnancy. N Engl J Med 2005; 353, e6.
11
Leveque TK, Yu L, Musch DC, et al. Central serous chorioretinopathy and risk for obstructive sleep apnea. Sleep
Breath. 2007;11:253-257.
12
Carvalho-Recchia CA, Yannuzzi LA, Negrao S, et al. Corticosteroids and central serous chorioretinopathy.
Ophthalmology. 2002;109:1834-1837.
13
Harada T, Harada K. Six cases of central serous choroidopathy induced by systemic corticosteroid therapy. Doc
Ophthalmol 1985; 60: 37–44.
14
Spaide RF, Campeas L, Haas A, Yannuzzi LA, Fisher YL, Guyer DR et al. Central serous chorioretinopathy in
younger and older adults. Ophthalmology 1996; 103: 2070–2080.
15
Gilbert CM, Owens SL, Smith PD, Fine SL. Long-term follow-up of central serous chorioretinopathy. Br J
Ophthalmol 1984; 68:815–820.
16
Polak BCP, Baarsma GS, Snyers B. Diffuse retinal pigment epitheliopathy complicating systemic corticosteroid
treatment. Br J Ophthalomol 1995; 79: 922–925.
17
Colucciello M. Central serous retinopathy. Retinal Physician. 2008;5(7):26-34.
18
Iida T, Yannuzzi LA, Spaide RF, Borodoker N, Carvalho CA, Negrao S. Cystoid macular degeneration in chronic
central serous chorioretinopathy. Retina 2003; 23: 1–7.
19
Cardillo Piccolino F, De La Longrais RR, Ravera G, Eandi CM, Ventre L, Abdollahi A et al. The foveal photoreceptor
layer and visual acuity loss in central serous chorioretinopathy. AmJ Ophthalmol 2005; 139: 87–99.
20
Wong R, Chopdar A, Brown M. Five to 15 year follow-up of resolved idiopathic central serous chorioretinopathy.
Eye 2004; 18: 262–268.
21
Gass JD. Specific diseases causing disciform macular detachment. Stereoscopic Atlas of Macular Diseases 1997;
1: 52–70.
22
Guyer DR, Yannuzzi LA, Slakter JA, Sorenson JA, Allen H, Orlock D. Dinital indocyanine-green videoangriography
central serous chorioretinopathy. Arch Ophthalmol 1994:122:1057-1062.
23
Hayashi K, Hasegawa Y, Tokoro T. Indocyanine green angiography of central serous chorioretinopathy. Int
Ophthalmol 1986; 9: 37–41.
24
Ryan SJ. Central serous chorioretinopathy. Retina 3rd edn. 2001; 2: 1153–1181.
25
Spitznas M. Pathogenesis of central serous retinopathy: a new working hypothesis. Graefe's Arch Clin Exp
Ophthalmol 1986; 224: 321–324.
26
Spitznas M, Huke J. Number, shape, and topography of leakage points in acute type I central serous retinopathy.
Graefe's Arch Clin Exp Ophthalmol 1987; 225:437–440.
27
Yamada K, Hayasaka S, Setogawa T. Fluorescein-angiographic patterns in patients with central serous
chorioretinopathy at the initial visit. Ophthalmologica 1992; 205:69–76.
28
Bujarborua D, Nagpal P, Deka M. Smokestack leak in central serous chorioretinopathy. Graefes Arch Clin Exp
Ophthalmol 2009; 248:339–351.
29
Spitznas M, Huke J. Number, shape, and topography of leakage points in acute type I central serous retinopathy.
Graefe's Arch Clin Exp Ophthalmol 1987; 225:437–440.
30
van Velthoven MEJ, Verbraak FD, Garcia PM, et al. Evaluation of central serous retinopathy with en face optical
coherence tomography. Br J Ophthalmol 2005; 89:1483–1488.
31
van Velthoven MEJ, Verbraak FD, Garcia PM, et al. Evaluation of central serous retinopathy with en face optical
coherence tomography. Br J Ophthalmol 2005; 89:1483–1488.
32
Imamura Y, Fujiwara T, Margolis RON, Spaide RF. Enhanced depth imaging optical coherence tomography of the
choroid in central serous chorioretinopathy. Retina 2009; 29:1469–1473.
33
Prunte C, Flammer J. Choroidal capillary and venous congestion in central serous chorioretinopathy. Am J
Ophthalmol 1996; 121:26–34.
34
Iida T, Kishi S, Hagimura N, Shimizu K. Persistent and bilateral choroidal vascular abnormalities in central serous
chorioretinopathy. Retina 1999; 19:508–512.
35
Spaide RF, Klancnik JJM. Fundus autofluorescence and central serous chorioretinopathy. Ophthalmology 2005;
112:825–833.
36
Maruko I, Iida T, Ojima A, Sekiryu T. Subretinal dot-like precipitates and yellow material in central serous
chorioretinopathy. Retina 2010.
37
von Rückmann A, Fitzke FW, Fan J, et al. Abnormalities of fundus autofluorescence in central serous retinopathy.
Am J Ophthalmol 2002; 133:780–786.
38
Sharma T, Shah N, Rao M, et al. Visual outcome after discontinuation of corticosteroids in atypical severe central
serous chorioretinopathy. Ophthalmology 2004; 111:1708–1714.
39
Leaver P, Williams C. Argon laser photocoagulation in the treatment of central serous retinopathy. Br J
Ophthalmol 1979; 63:674–677.
40
Robertson D, Listrup D. Direct, indirect, and sham laser photocoagulation in the management of central serous
chorioretinopathy. Am J Ophthalmol 1983; 95:457–466.
41
Ryan MT, Janice CL, Franco MR, et al. Photodynamic therapy as treatment of chronic idiopathic central serous
chorioretinopathy. Lasers Surg Med 2008; 40:671–675.
42
Ryan MT, Janice CL, Franco MR, et al. Photodynamic therapy as treatment of chronic idiopathic central serous
chorioretinopathy. Lasers Surg Med 2008; 40:671–675.
43
Treatment of age related macular degeneration with Photodynamic Therapy (TAP) Study group. Photodynamic
therapy of subfoveal choroidal neovascularization in age related macular degeneration with verteporfin. Arch
Ophthalmol 1999; 117: 1329–1345.
44
Zhao M-W, Zhou P, Xiao H-X, et al. Photodynamic therapy for acute central serous chorioretinopathy: the safe
effective lowest dose of verteporfin. Retina 2009; 29:1155–1161.
45
Shin JY, Woo SJ, Yu HG, Park KH. Comparison of efficacy and safety between half-fluence and full-fluence
photodynamic therapy for chronic central serous chorioretinopathy. Retina 2011; 31:119–126.
46
Kim H-S, Lee JH. The short-term effect of intravitreal bevacizumab for treatment of central serous
chorioretinopathy. J Korean Ophthalmol Soc 2010; 51:860–864.
47
Wang M, Much IC, Hasler PW, et al. Central Serous chorioretinopathy. Acta Ophthalmologica 2008;86:126-145
48
Gonzalez C. Serous retinal detachment. Value of acetazolamide. J Fr Ophtalmol 1992; 15:529–536.
49
Meyerle CB, Freund KB, Bhatnagar P, et al. Ketoconazole in the treatment of chronic idiopathic central serous
chorioretinopathy. Retina 2007; 27:943–946.
50
Nielsen JS, Bachhawat A, Jampol LM. A case of chronic severe central serous chorioretinopathy responding to
oral mifepristone: update. Retina. 2008; 28:1363.
51
Kloos P, Laube I, Thoelen A. Obstructive sleep apnea in patients with central serous chorioretinopathy. Graefes
Arch Clin Exp Ophthalmol. 2008;246:1225-1228.
52
Jain AK, Kaines A, Schwartz S. Bilateral central serous chorioretinopathy resolving rapidly with treatment for
obstructive sleep apnea. Graefes Arch Clin Exp Ophthalmol. 2010 Jan 5.
53
Shin JY, Woo SJ, Yu HG, Park KH. Comparison of efficacy and safety between half-fluence and full-fluence
photodynamic therapy for chronic central serous chorioretinopathy. Retina 2011; 31:119–126.