Clinical Research

Comparison of autofluorescence and optical coherence

tomography findings in acute and chronic central serous
chorioretinopathy
Ulucanlar Eye Research Hospital, Ankara 06240, Turkey
Correspondence to: Ufuk Elgin. Ulucanlar Caddesi, Kale
mah. No.59, Altindag, Ankara 06240, Turkey. ufukelgin@
superonline.com
Received: 2012-11-14 Acceped: 2013-08-27
Abstract

AIM: To discuss and compare the fundus

autofluorescence (FAF) and optical coherence
tomography (OCT) in acute or chronic central serous
chorioretinopathy (CSCR).

METHODS: Medical records of 100 cases of CSCR

were reviewed. Acute and chronic cases were evaluated
according to the duration of decreased visual acuity,
serous retinal detachment (RD) and focal leakage on
fluorescein angiography (FA). Chi-square test was used
for statistical analysis.

RESULTS: Forty cases had acute and 60 cases had

chronic CSCR. FAF showed focal hypo-autofluorescence
in 34 (85%) and iso-autofluorescence in 6 (15%) of acute
cases and hypo-autofluorescence in 51 (85%), hyper -
autofluorescence in 6 (10%) and iso-autofluorescence in
3 (5%) of chronic cases. OCT showed serous RD with
distinct borders correlated with FAF findings (hypo -
autofluorescence) in all acute CSCR cases. In chronic
CSCR group, OCT showed serous RD with indistinct
borders correlated with FAF findings. The differences
between the OCT and FAF findings of the two groups
were significant ( =0.000).

CONCLUSION: OCT and FAF findings can support the

clinical observations in differential diagnosis of acute
and chronic CSCR and help clinicians to evaluate retinal
pigment epithelium, outer segments of photoreceptors
and the components of serous RD.

KEYWORDS: central serous chorioretinopathy; fluorescein

angiography; fundus autofluorescence; optical coherence
tomography
DOI:10.3980/j.issn.2222-3959.2014.02.29
Teke MY, Elgin U, Nalcacioglu-Yuksekkaya P, Sen E, Ozdal P,
Ozturk F. Comparison of autofluorescence and optical coherence
tomography findings in acute and chronic central serous
chorioretinopathy. 2014;7(2):350-354
INTRODUCTION
C
entral serous chorioretinopathy (CSCR), which was
described by von Grafe in 1886, is a frequent retinal
disease and characterized by serous sensorial retinal
detachment (RD) due to the primary dysfunction at the level
of the choroid and one or more focal lesions of retinal
pigment epithelium (RPE)
[1-4]
. Although macula is frequently
affected and the disease can be recurrent, the visual prognosis
is generally good. The disease has several names like CSCR,
idiopathic central serous choroidopathy and central serous
epitheliopathy because of unclear etiopathogenesis
[3,4]
. It can
be classified as acute (symptoms and diagnostic findings
<6mo), chronic (symptoms and diagnostic findings 6mo)
and recurrent (more than 1 acute attack). The duration of the
disease is the most important factor for the discrimination of
acute and chronic terminology.
Fundus autofluorescence (FAF) has been widely used in the
diagnosis of retinal diseases for recent years. It is an
imaging method for metabolic mapping of naturally or
pathologically occurring fluorophore of the ocular fundus
[5,6]
.
Lipofuscin precipitate is the main source of autofluorescence.
The main component of lipofuscin is A2E and its formers are
A2PE-H2, A2PE and A2-rodopsine which are all
autofluorescent and found in outer segments of
photoreceptors before phagocytosis
[7]
. In normal conditions
FAF image of optic disc reveal no autofluorescence because
of the absence of RPE and FAF of macula reveals
hypo-autofluorescence because of the absorbance of blue
light by lutein and zeaxanthin. The increased metabolic
activity of RPE is generally associated with hyper-
autofluorescence and the opposite is also correct. Except
these conditions, the uniform appearance caused by
physiological level and distribution of lipofuscin in RPE is
known as isoautofluorescence
[5-7]
.
Although indocyanine green angiography (ICG) is the golden
standard, FAF and optical coherence tomography (OCT) are
also important for the diagnosis of the disease. The FAF of
CSCR cases was thought to arise not only from the RPE, but
FAF and OCT in central serous chorioretinopathy
350
Int J Ophthalmol, Vol. 7, No. 2, Apr.18, 2014 www. IJO. cn
Tel:8629-82245172 8629-82210956 Email:ijopress@163.com
also from the back surface of the retina with a diffuse and a
punctuate characteristic of autofluorescence
[8]
. OCT shows
hyper intense granules caused by the occurrence of brush
border appearance in the area which fits with the outer
segments of photoreceptors and outer segments which were
widely scattered in subretinal space and over RPE due to the
prolonged serous detachment especially after 6wk
[9-11]
.
In our study, our aim was to discuss and compare the fundus
FAF and OCT findings of acute or chronic CSCR cases.
SUBJECTS AND METHODS
Medical records of 40 acute and 60 chronic CSCR cases that
had been diagnosed between June 2010 and October 2011 in
Retina Department of Ulucanlar Eye Research Hospital, were
reviewed. CSCR had been diagnosed on the basis of clinical
findings, color fundus photography, fluorescein angiography
(FA) leakage pattern and OCT. All study procedures were
conducted in accordance with the Declaration of Helsinki,
and informed consent was obtained from all the participants.
Our presentation was approved by Ethics Committee of
Ankara University, school of medicine.
All of the cases had a complete ophthalmological
examination. Also their color fundus photography, FAF
(488 nm) with Heidelberg Retina Angiograph 2 (HRA 2 ,
Heidelberg engineering, Germany), FA (KOVA imaging
systems, Japan) and spectral-domain OCT (SD-OCT)
(Heidelberg Engineering, Heidelberg, Germany) findings in
the initial and follow-up visits were also reviewed.
Cases were divided into acute and chronic-recurrent CSCR
according to the duration of decreased visual acuity (VA),
clinical findings of CSCR and focal leakage on FA. Acute
cases were defined as: duration of decreased VA, clinical
findings (ophthalmoscopically visible neurosensory
detachment) and FA findings (focal leakage) <6mo (group 1).
Chronic- recurrent cases were defined as: duration of
decreased VA, residual and recurrent symptoms, FA findings
(one or more sites of focal, diffuse or mottled leakage, RPE
alterations) 6mo (group 2). Chi-square test was used for
statistical analysis.
RESULTS
Group 1 consisted of 30 (75%) male and 10 (25%) female
cases with the mean age of 38.4!6.9 (27-59 years) and group
2 consisted of 52 (86.7%) male and 8 (13.3%) female cases
with the mean age of 46.7!8.1 (35-65 years) (Table 1).
The mean best-corrected visual acuity (BCVA) (logMAR) at
the time of the diagnosis was 0.1!1 in acute CSCR cases and
0.2 !1.3 in chronic cases. Acute CSCR cases had higher
initial VA levels than chronic cases and the difference was
statistically significant ( =0.01) (Table 1).
In initial examinations of all acute CSCR cases (Figure 1A),
FA showed hyper-fluorescence due to the leakage from the
site of the RPE defect in the serous detachment area in late
phases (Figure 1B, 1C). OCT of the same shows serous
detachment with distinct border but without any changes in
the outer segments of photoreceptors (Figure 1D). FAF
photography revealed hypo-autofluorescence in 34 (85%)
cases (Figure 1E) and iso-autofluorescence in 6 (15%) cases
in the areas which fitted with the focal leakage sites in FA. In
36 (90%) cases hypo-autofluorescence and in 4 (10%) cases
isoautofluorescence were seen in FAF photography in the
areas which fitted with the serous detachment. In group 1,
OCT showed pigment epithelial detachment (PED) and serous
RD with distinct borders in all cases (Table 2) (Figure 1D)
and the mean central macular thickness was 360 !140 "m.
After the resorbtion of serous detachment, 15 (37.5%) cases
in group 1 showed speckled hyper-autofluorescence in FAF
photography. Figure 1D shows horizontal section of macular
OCT and the leakage point can not be seen. If OCT section
crossed the point of leakage which was shown by FA, the
leakage site of RPE could be observed by OCT. Figure 1F
shows OCT section from the leakage point observed in FA.
After the resorption of acute attack (Figure 2A), FA shows
window defect due to RPE atrophy at the leakage site (Figure
2B). OCT shows probably resorbed serous detachment and
some irregularities associated with the outer segments of
photoreceptors (Figure 2C) and related mottled hyper-
Table 1 Comparison of the demographic characteristics and best-
corrected visual acuity values of the cases
Parameters Acute CSCR Chronic CSCR P
No. of cases (n) 40 60
Age(a) 38.46.9 46.78.1
1
0.000
Sex, n (%)
M 30 (75) 52 (86.7)
2
0.08
F 10 (25) 8 (13.3)
BCVA (logMAR) 0.11 0.21.3
1
0.01
BCVA: Best-corrected visual acuity; CSCR: Central serous
chorioretinopathy;
1
Statistically significant, t-test;
2
Statistically
insignificant, Chi-square test.
Table 2 Comparison of the FA, FAF and OCT findings of the cases n (%)
Parameters Acute CSCR Chronic CSCR P
FA findings,
Hypo-fluorescence 34 (85) 0 (0)
1
0.000
Hyper-fluorescence 0 (0) 60 (100)
Iso-fluorescence 6 (15)
FAF at the focal leakage site in FA
Hypo-autofluorescence 34(85) 51 (85) 0.48
Hyper-autofluorescence 0 (0) 6 (10)
Iso-autofluorescence 6 (15) 3 (5)
FAF of serous RD
Hypo-autofluorescence 36 (90) 0 (0)
1
0.000
Hyper-autofluorescence 0 (0) 54 (90)
Iso-autofluorescence 4 (10) 6(10)
PED
+
3 (7.5) 3 (5) 0.44
PED
-
37 (92.5) 57 (95)
OCT
Distinct borders 40 (100) 0 (0)
1
0.000
Indistinct borders 0 (0) 60 (100)
FA: Fluorescein angiography; CSCR: Central serous chorioretinopathy; FAF:
Fundus autofluorescence; RD: Retinal detachment; OCT: Optical coherence
tomography; PED: Pigment epithelial detachment;
1
Statistically significant.

351
Figure 1 Images of a case with acute CSCR A: Color fundus photography of an acute CSCR 37-year-old male case shows serous
detachment; B,C: FA of the same case shows hyper-fluorescence at the leakage site which begins at the 35
th
second and increases in late
phases; D: Horizontal section of OCT of the same case shows serous detachment with distinct border but without any changes in the outer
segments of photoreceptors and serous fluid; E: Fundus autofluorescence photography reveals hypo-autofluorescence in the serous
detachment area with distinct borders and also hypo-autofluorescence at the leakage site in FA surrounded by iso-autofluorescence area of
normal retina.
Figure 2 Images of a case with chronic CSCR A: Color fundus photography of a 45-year-old chronic CSCR case shows yellowish-white
precipitates in macular area and RPE atrophy; B: The late phases of FA of the same case shows patchy hyper-fluorescence due to diffuse
leakage just above fovea and a window defect due to RPE atrophy at the leakage site; C: Horizontal section of OCT shows resorbed serous
detachment and precipitations over RPE; D: FAF photography shows scattered hyper-autofluorescence in the area of resorbed serous
detachment.
autofluorescence in FAF (Figure 2D). Figure 2C shows
horizontal section of macular OCT and it is difficult to say
that it shows resorbed serous detachment definitely. But a
shallow serous detachment under fovea and some
irregularities of RPE and atrophic regions can be seen but not
so clearly. Shallow serous detachment associated with CSCR
FAF and OCT in central serous chorioretinopathy
352
Int J Ophthalmol, Vol. 7, No. 2, Apr.18, 2014 www. IJO. cn
Tel:8629-82245172 8629-82210956 Email:ijopress@163.com
may remain for a long time and cause changes and
irregularities of RPE and IS/OS band.
In chronic cases, FA showed hyper-fluorescence at the
original leakage sites in late phases in all cases (Figure 2B).
FAF revealed hypo-autofluorescence in 51 (85%) cases, hyper-
autofluorescence in 6 (10%) cases and iso-autofluorescence
in 3 (5%) cases at the original leakage sites which fitted with
the hyper-fluorescence in FA. In 54 (90% ) cases hyper-
autofluorescence and in 6 (10%) cases iso-autofluorescence
were seen in FAF photography in the areas which fitted with
the serous detachment (Table 2). OCT showed shallow
serous RD in all chronic CSCR cases and the mean central
macular thickness was 250 !101 "m. 45 (75% ) cases in
group 2 showed mottled hyper-autofluorescence in FAF
photography. In chronic cases with shallow or prominent
serous detachment, OCT showed hyper-intense granules
caused by scattered outer segments of photoreceptors and
brush border appearance. FAF photography of these sites
revealed hyper-autofluorescence and was accordant with
OCT findings. Color fundus photography of none of the
chronic CSCR cases show drusen, edema, exuda or choroidal
neovascular membrane related with age-related macular
degeneration (ARMD) and because of this ARMD was not
thought in the differential diagnosis.
DISCUSSION
The current study examines FA, FAF and OCT findings in
CSCR and compares these findings in acute and chronic
cases. In spite of its unclear etiology, the liquid is inversely
pumped into the subretinal space and cause neurosensory
detachment in CSCR by the dysfunctions of mainly RPE but
also choroid
[1-4]
. Guyer
[12]
investigated the indocyanine
green angiography (ICG) of CSCR cases and postulated that
serous RD was caused by defects in RPE structure and its
metabolic activity induced by the pressure on RPE due to the
increase in choroidal permeability. Recurrent epinephrine
injection was reported to cause similar clinical findings like
in CSCR in animal models and histopathological examination
showed focal RPE degeneration and the endothelial cell
defects in choriocapillaris
[13]
.
Emotional stress, corticosteroid use, some systemic diseases,
familial and racial factors and pregnancy have been reported
to be risk factors of the disease
[1-4,14-16]
. Although spontaneous
resorbtion generally occurs in 3-4mo, 4% of chronic cases
developed RPE insufficiency named as sick RPE syndrome
[1]
.
The disease is more frequent in young men and it reaches its
peak at the age of 45. Older and female cases are known to
have chronic CSCR more than male and younger cases
[1-4]
.
Also in our study, chronic cases were found to be
significantly older than acute CSCR cases but both of the
groups had male predominance.
FAF is one of the most important diagnostic methods of
retinal diseases for recent years. Macula is
hypo-autofluorescent in iso-autofluorescent retina in healthy
people because of lutein and zeaxanthin pigments which
protect it from oxidative stress. They can filter blue light and
reduce lipofuscin formation
[5-7]
. In spite of the different
pathogenesis of serous detachment in different retinal
disorders; the main source of autofluorescence of the macula
is the precipitates of lipofuscin granules in outer retinal layers
and subretinal space, due to the impaired phagocytosis of
outer segments of photoreceptors by RPE
[5-7]
. In our study, the
FAF images showed hypo-autofluorescence at the focal
leakage site in FA in the great majority of acute and chronic
CSCR cases. Except chronic recurrent cases the area of
serous RD was also hypo-autofluorescent but in recurrent
cases, hyper-autofluorescence was detected in the RD area.
In many other reports, the FAF images also showed
hypo-autofluorescence at the focal leakage site which was
thought to be caused by the destruction of RPE and/or
blockage by subretinal fluid accumulation
[17-18]
. Dinc
[17]
showed hypo-autofluorescence in 80% of acute CSCR and
88.2% of chronic recurrent CSCR in FAF photography. Also
in our study, 85% of acute cases and 85% of chronic cases
showed hypo-autofluorescence which was thought to be
related with reduced metabolic activity. But von R#ckmann
[18]
found an opposite result and postulated that increased
autofluorescence might occur at the site of the leakage and in
the area of RD in acute CSCR cases probably caused by
defective degradation of phagosomal material which would
result in an increase of autofluorescence. They thought this
could be due to inadequate production of degradative
enzymes or acidification of the phagosomes. But increased
metabolic activity of the RPE was a confusing cause of hyper
autofluorescence in their cases because of the malnutrition of
photoreceptors and RPE-cells.
FAF shows different characteristics in acute and chronic
CSCR cases as in our study
[16-19]
. In acute cases hypo-
autofluorescence is predominant because of the blockage by
serous effusion. Autofluorescence increases in time in
chronic CSCR and cases with persistent serous RD
[18,20,21]
. The
reason of increased autofluorescence in these cases is the
accumulation of the outer segments of photoreceptors in
subretinal space and the dispersed chromophores in the field
of serous RD. So not only RPE atrophy but also serous RD
may cause hyper-autofluorescence
[5,8,16,20]
. Spaide and
Klancnik
[8]
demonstrated that the sources of these subretinal
precipitations were the outer segments themselves and
macrophage cells those phagosited these outer segments.
These precipitations cause mottled hyper-autofluorescence
which was observed in 75% of our chronic cases.
Hyper-autofluorescence may also be observed after the
resorbtion of serous detachment. Dinc
[17]
observed
353
mottled hyper-autofluorescence in 36% of their cases after
resorbtion of RD like in 37.5% of our cases (Figure 2D).
OCT is also a useful diagnostic tool in CSCR. Matsumoto
[22]
demonstrated the elongation of outer segments of
photoreceptors and narrowing of the outer nuclear layer in
OCT. In Kon
[10]
study, OCT showed, yellow hyper
reflective subretinal and intraretinal precipitations not only in
the posterior of RD but also within the RD. Dinc
[17]
demonstrated hyper reflective foci in OCT which were
associated with hyperautofluorescent regions in FAF
photography. In our study, we also observed hyper reflective
foci in acute and chronic CSCR both in serous detachment
area and posterior of RD in OCT which was in accordance
with hyperautofluorescent regions in FAF.
This report emphasizes the importance of OCT and FAF
findings in addition to clinical ophthalmic examination not
only in the diagnosis but also in discrimination of different
stages of CSCR. As some changes occur in the leakage point
of RPE and serous RD area in time, acute and chronic CSCR
cases show different clinical and imaging characteristics. At
that point, the results of FA, FAF and OCT support and
complement each other and they can help the clinicians not
only in diagnosis and follow-up but also in planning their
cases treatments perfectly.
ACKNOWLEDGEMENTS
Conflicts of Interest: Teke MY, None; Elgin U, None;
Nalcacioglu-Yuksekkaya P, None; Sen E, None; Ozdal P,
None; Ozturk F, None.
REFERENCES
1 Gemenetzi M, De Salvo G, Lotery AJ. Central serous chorioretinopathy:
an update on pathogenesis and treatment. 2010;24 (12):
1743-1756
2 Wang M, Munch IC, Hasler PW, Pr#nte C, Larsen M. Central serous
chorioretinopathy. 2008;86(2):126-145
3 Ross A, Ross AH, Mohamed Q. Review and update of central serous
chorioretinopathy. 2011;22(3):166-173
4 Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy
and glucocorticoids. 2002;47(5):431-448
5 Spaide RF. Autofluorescence from the outer retina and subretinal space.
Hypothesis and Review. 2008;28(1):5-35
6 Choudhry N, Giani A, Miller JW. Fundus autofluorescence in geographic
atrophy: a review. 2010;25(5-6):206-213
7 Liu J, Itagaki Y, Ben-Shabat S, Nakanishi K, Sparrow JR. The
biosynthesis of A2E, a fluorophore of aging retina, involves the formation of
the precursor, A2-PE, in the photoreceptor outer segment membrane.
2000;275(38):29354-29360
8 Spaide RF, Klancnik JM Jr. Fundus autofluorescence and central serous
chorioretinopathy. 2005;112(5):825-833
9 Ozmert E, Batiog F. Fundus autofluorescence before and after
photodynamic therapy for chronic central serous chorioretinopathy.
2009;223(4):263-268
10 Kon Y, Iida T, Maruko I, Saito M. The optical coherence tomography-
ophthalmoscope for examination of central serous chorioretinopathy with
precipitates. 2008;28(6):864-869
11 Gupta V, Gupta A, Dogra MR, Singh I. Reversible retinal changes in the
acute stage of sympathetic ophthalmia seen on spectral domain optical
coherence tomography. 2011;31(2):105-110
12 Guyer DR, Yannuzzi LA, Slakter JS, Sorenson JA, Ho A, Orlock D.
Digital indocyanine green videoangiography of central serous
chorioretinopathy. 1994;112(8):1057-1062
13 Yoshioka H, Katsume Y, Akune H. Experimental central serous
chorioretinopathy in monkey eyes: fluorescein angiographic findings.
1982;185(3):168-178
14 Spahn C, Wiek J, Burger T, Hansen L. Psychosomatic aspects in
patients with central serous chorioretinopathy. 2003;87
(6):704-708
15 Schultz KL, Birnbaum AD, Goldstein DA. Ocular disease in pregnancy.
2005;16(5):308-314
16 Eandi CM, Ober M, Iranmanesh R, Peiretti E, Yannuzzi LA. Acute
central serous chorioretinopathy and fundus autofluorescence.
2005;25(8):989-993
17 Dinc UA, Tatlipinar S, Yenerel M, G$rg#n E, Ciftci F. Fundus
autofluorescence in acute and chronic central serous chorioretinopathy.
2011;94(5):452-457
18 von R#ckmann A, Fitzke FW, Fan J, Halfyard A, Bird AC.
Abnormalities of fundus autofluorescence in central serous retinopathy.
2002;133(6):780-786
19 Framme C, Walter A, Gabler B, Roider J, Sachs HG, Gabel VP. Fundus
autofluorescence in acute and chronic-recurrent central serous
chorioretinopathy. 2005;83(2):161-167
20 Iida T, Spaide RF, Haas A, Yannuzzi LA, Jampol LM, Lesser RL.
Leopard-spot pattern of yellowish subretinal deposits in central serous
chorioretinopathy. 2002;120(1):37-42
21 Wang M, Sander B, la Cour M, Larsen M. Clinical characteristics of
subretinal deposits in central serous chorioretinopathy.
2005;83(6):691-696
22 Matsumoto H, Kishi S, Sato T, Mukai R. Fundus autofluorescence of
elongated photoreceptor outer segments in central serous chorioretinopathy.
2011;151(4):617-623
FAF and OCT in central serous chorioretinopathy
354