Wang.2008.Central Serous Chorioretinopathy

Introduction

Central serous chorioretinopathy(CSC) is one of several chorioretinaldisorders characterized by serousdetachment of the neurosensory retinaand ⁄or the retinal pigment epithelium(RPE). CSC is one of the 10 mostcommon diseases of the posterior seg-ment of the eye and a frequent causeof mild to moderate visual impair-ment. Spontaneous resolution is com-mon in acute CSC with monofocal orpaucifocal RPE changes. Lack of suchresolution can often be managed byphotocoagulation therapy directed atfoci of RPE leakage. Recurrent orpersistent detachment is often associ-ated with more diffuse RPE change,which is also seen in relation to secon-dary subretinal neovascularization. Inthis article, we review the literature onCSC with emphasis on diagnosis,management, and major unresolvedissues relating to this disease.

Methods

The purpose of this article is to reviewthe scientific literature, with emphasison publications made after the exten-sive review by Yannuzzi (1987). Thesurvey was closed on 18 September2006. Publications were retrieved usingPubMed (http://www.ncbi.nlm.nih.gov/entrez) using the search terms ‘centralserous’, ‘central serous retinopathy’and ‘central serous chorioretinopathy’.The review includes papers of rele-vance, omitting duplications of previ-ous findings, some small case reports

Review Article

Central serous chorioretinopathy

Maria Wang,1 Inger Christine Munch,1 Pascal W. Hasler,1

Christian Prunte2 and Michael Larsen1,3

1Department of Ophthalmology, Glostrup Hospital, University of Copenhagen,Copenhagen, Denmark2Department of Ophthalmology, Medical University of Vienna, Vienna, Austria3Kennedy Center, National Eye Clinic, Copenhagen, Denmark

ABSTRACT.

Central serous chorioretinopathy (CSC) is a disease of the retina characterized

by serous detachment of the neurosensory retina secondary to one or more focal

lesions of the retinal pigment epithelium (RPE). CSC occurs most frequently in

mid-life and more often in men than in women. Major symptoms are blurred

vision, usually in one eye only and perceived typically by the patient as a dark

spot in the centre of the visual field with associated micropsia and metamorp-

hopsia. Normal vision often recurs spontaneously within a few months. The

condition can be precipitated by psychosocial stress and hypercortisolism.

Ophthalmoscopic signs of CSC range from mono- or paucifocal RPE lesions

with prominent elevation of the neurosensory retina by clear fluid – typical of

cases of recent onset – to shallow detachments overlying large patches of irre-

gularly depigmented RPE. The spectrum of lesions includes RPE detachments.

Granular or fibrinous material may accumulate in the subretinal cavity. Serous

detachment often resolves spontaneously. From first contact, counselling about

the potential relation to stress and glucocorticoid medication is warranted.

After 3 months without resolution of acute CSC or in chronic CSC, treatment

should be considered. Resolution of detachment can usually be achieved in acute

CSC by focal photocoagulation of leaking RPE lesions or, in chronic CSC, by

photodynamic therapy. The effect of therapy on long-term visual outcome is

insufficiently documented. Reattachment within 4 months of onset is considered

a relevant therapeutic target because prolonged detachment is associated with

photoreceptor atrophy. This suggests that the value of treatment depends upon

proper selection of cases that will not resolve without therapy. Chronic CSC

may be difficult to differentiate from occult choroidal neovascularization secon-

dary to CSC. Patients with chronic CSC who receive glucocorticoid treatment

for systemic disease can often be managed without having to discontinue this

medication.

Key words: central serous chorioretinopathy – choroidal neovascularization – retinal degenera-

tion – retinal detachment – retinopathy – review

Acta Ophthalmol. 2008: 86: 126–145ª 2007 The Authors

Journal compilation ª 2007 Acta Ophthalmol Scand

doi: 10.1111/j.1600-0420.2007.00889.x

Acta Ophthalmologica 2008

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and minor reviews. Additional publi-cations that illustrate methodologicalprinciples or fundamental physiologywere included as deemed relevant.

Nosographic history

CSC was first described by Albrechtvon Graefe in 1866 (Yannuzzi 1987).The condition has been given variouslabels, including idiopathic central ser-ous choroidopathy (Gass 1967), cen-tral serous pigment epitheliopathy,central serous retinopathy (Yannuzzi1987) and the currently favouredterm, central serous chorioretinopa-thy. Chronic CSC is also known as dif-fuse retinal pigment epitheliopathy.

Epidemiology

The epidemiology of CSC has notbeen systematically surveyed. The lit-erature consistently reports a higherprevalence in men than in women inclinic-based patient populations, menaccounting for 88% (Spitznas & Huke1987), 83% (Castro-Correia et al.1992), 79% (Wang et al. 2005), 73%(Tittl et al. 1999) to 72% (Spaideet al. 1996) of study populations. CSCis found from early adulthood andthere is no apparent upper age limit(Schatz et al. 1992; Spaide et al.1996). The peak prevalence is around45 years. In women and in patientswith chronic CSC, the peak preval-ence tends to be higher (Gackle et al.1998; Wang et al. 2005). Bilateralinvolvement has been reported in 40%of cases (Gackle et al. 1998). Amongnon-surgical retinopathies, CSC mayrank fourth in incidence after age-rela-ted macular degeneration (AMD), dia-betic retinopathy and branch retinalvein occlusion; CSC may be secondonly to AMD as the presumed causeof subretinal neovascularization.

Diagnosis

Definition

Active CSC is characterized by detach-ment of the neurosensory retina causedby accumulation of serous fluidbetween the photoreceptor outersegments and the RPE in combinationwith monofocal or multifocal changesin the RPE. The detachment should

not be attributable to holes or tears inthe retina, neovascularization, inflam-mation, neoplasia or specific hereditarydisease. The retinal detachment usuallyinvolves the fovea but exceptions tothis rule can be found. Unlike heredit-ary chorioretinal degenerations, thepattern of RPE anomaly in CSC is geo-metrically irregular in that it generallylacks symmetry about the facial mid-line (as seen in retinitis pigmentosa)and rotational symmetry about thecentre of the fovea (as seen in bull’s eyedystrophies). The diagnosis of chronicCSC requires multifocal or diffuseRPE depigmentation combined with aserous detachment of the retina. Inac-tive CSC, defined by the retina beingfully attached, may be diagnosticallychallenging because the residualabnormalities of the RPE may resem-ble those of other conditions, but oftena history characteristic of acute CSCdating back years or decades can be eli-cited. Neovascular CSC is usually asequel of chronic CSC. Macularhaemorrhage in CSC should alwayslead to the suspicion of subretinalneovascularization (Schatz et al. 1977).

Past medical history

Patients are generally in good health.Some may have experienced previousepisodes of transient blurred vision.

Family history

Reports of two or more cases withina family suggest that a hereditarypredisposition to CSC may exist(Oosterhuis 1996; Park et al. 1998). Afluorescein angiography study of sib-lings, uncles and nieces of 27 patientswith chronic CSC demonstrated RPEatrophy in 35 of 80 relatives, of which22 were classified as unrecognizedcases of chronic CSC (Weenink et al.2001). The available studies arenot informative as to the mode ofinheritance.

Symptoms

CSC of recent onset is associated withblurred vision with a relative centralscotoma, metamorphopsia, dyschrom-atopsia, micropsia, hypermetropiza-tion and reduced contrast sensitivity.In some patients, CSC is preceded oraccompanied by migraine (Gass 1967).

Symptoms are usually confined tothe centre of the visual field andfrequently the primary complaint is

one of transiently seeing a dark spotin the centre of the visual field in oneeye (Fig. 1), with or without accom-panying metamorphopsia (Fig. 2).Best-corrected visual acuity rangesfrom 20 ⁄ 20 to 20 ⁄ 200; a hyperopicshift is a common finding, correspond-ing to the anterograde displacement ofthe neurosensory fovea (Klien 1956;Peyman & Bok 1972). Scanning laserophthalmoscopic microperimetry hasdemonstrated a 10–100 fold reductionof sensitivity within the affected partof the visual field (Toonen et al.1995). The dark spot, which is thesubjective representation of a relativescotoma in the centre of the visualfield (Faschinger & Brunner 1982), isusually most prominent in the morn-ing immediately after awakening.Patients often report seeing it mostclearly when opening their eyes andlooking at the ceiling of their bed-room, presumably because the typicalceiling is bright white and unstruc-tured. The spot can often be madevisible later in the day by blinking.These characteristics are typical of arelative scotoma, and like the relativescotoma produced by light (i.e. anafter-image) it fades within a fewseconds, presumably because of theTroxler effect, a retinal function thatsubtracts any stationary background

Fig. 1. Subjective impression of relative cen-

tral scotoma illustrated by a patient during

acute CSC. The image subtends 4 degrees vis-

ual angle vertically and 3 degrees horizontally.

The patient described a grey spot that was

most easily recognizable within the first

10 seconds of opening his eyes in the morn-

ing. The scotoma then disappeared, but could

be made to reappear briefly by blinking. The

appearance was variable from day to day, but

did not exceed the dimensions shown above.


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stimulus (Fig. 3). The entopic spot pro-duced by a serous retinal detachmentcan be made visible to the patient byusing the pinhole flicker test, as whenthe retinal vessels are visualized (Iwami1995). The patient looks at a brightlylit uniform surface through a pinholeheld 0.5–1.0 cm in front of the eye. Thepinhole plate is then moved sidewaysa few millimetres back and forth at afrequency of about 4 Hz. In contrastto acute CSC, patients with sequels ofCSC or chronic CSC may have blurredvision, but rarely (if ever) complain ofseeing a dark spot.

Visual function and psychophysical tests

Functional testing of eyes with serousretinal detachment has demonstratedthat a minimal relative afferent pupil-lary defect may be present, as mayreduced critical flicker-fusion thresh-olds, prolonged visual evoked poten-tial (VEP) latencies, dyschromatopsia– most often with a tritan axis(Williams 1976) – and depression ofcentral visual field sensitivity. Afterresolution, the afferent pupillarydefect and critical flicker-fusionthresholds are first to improve, fol-lowed by visual acuity, VEP latencyand colour discrimination. The thresh-old differential light sensitivity in thecentral visual field is slowest toimprove (Folk et al. 1984).

Biomicroscopy

The subretinal fluid in CSC is com-monly clear, but granular or fibrinousdeposits may be present in the subreti-nal space (Ie et al. 1993; Wang et al.2002). The accumulation of granularmaterial between the RPE and theneurosensory retina increases in rela-tion to the duration of symptoms

(Wang et al. 2005). Other characteris-tics include the absence of the normalfoveal light reflex and a distinct visi-bility of the yellow foveal xanthophyll,presumably caused by increased scat-ter in the thickened perifoveal tissueof the detached retina (Spaide et al.1996; Gass 1991; Ie et al. 1993).

Despite a marked propensity of theserous detachment to involve thefovea, to be centred in the fovea andto reach its maximum height in thefovea, the primary lesion in the RPEis rarely subfoveal. Indeed, it can belocated anywhere in the posterior polewithin or immediately outside the tem-poral vascular arcades (Gomez-Ullaet al. 1993). Large bullous detach-

ments often show the phenomenon ofsubretinal fluid shifting position withchanges in posture.

Abnormalities of the RPE are pre-sent, by definition, in CSC. Whenmost prominent, these abnormalitiesare seen as one or more yellow spotsor a small pigment epithelial detach-ment. The RPE detachment can occa-sionally be seen to be ruptured, therupture being the site of profuse angi-ographic leakage (Fig. 5). Recent opti-cal coherence tomography (OCT)studies suggest that retinal pigmentepithelial detachment may be presentin most cases of CSC (Saito et al.2005; van Velthoven et al. 2005; Mita-rai et al. 2006). It is unknown whether

Fig. 3. After-image effects similar to those seen by patients with a relative central scotoma in

central serous chorioretinopathy can be elicited by gazing at the black dot in the left side of the

image for half a minute and then shifting one’s gaze directly to the white dot in the right side

of the image. Four phenomena will be observed: (1) immediate appearance of a dark after-

image corresponding to the shape and diameter of the white area; (2) gradual fading of the

after-image within a few seconds; (3) appearance of a transient bright after-image seen for only

a fraction of a second immediately after closing the eyelids; and (4) transient reappearance of

the after-image after blinking, when the eyelids are opened. The fading of the after-image is

attributable to the Troxler effect, i.e. the subtraction of entoptic images that are stationary in

relation to the retinal photoreceptor matrix, in this case the entoptic image of the serous

detachment.

(A) (B) (C)

Fig. 2. Subjective impression of relative paracentral scotoma in active acute central serous chorioretinopathy, as illustrated by the patient (differ-

ent from the patient who produced Fig. 1). Features of abnormal vision include metamorphopsia (A), dyschromatopsia (all), reduced contrast

(B, C), subjective luminosity increase (B) and decrease in luminosity (C). The patient used blinking to elicit and ⁄ or enhance the symptoms.


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small sources of leakage are indeedsmall pigment epithelial detachmentbeyond the resolution of current ima-ging techniques. Less prominentabnormalities at the level of the RPEcan be made visible during biomicros-copy using choroidal retroillumina-tion. These appear as minute refractilegranules deep in the retina. Unlikedegenerative conditions such as retini-tis pigmentosa or photocoagulationscarring, geographic RPE atrophydoes not occur in CSC, whereas hypo-pigmented RPE is a frequent finding,characterized biomicroscopically bytranslucency without transparency. Itis not often that true hyperpigmenta-tion occurs, but dense subretinaldeposits can look like hyperpigmenta-tion when seen in choroidal retroillu-mination. Hypopigmentation of theRPE is more prominent on fluoresceinangiography than on biomicroscopy.The diagnosis of CSC is supported byCSC-compatible RPE changes in thefellow eye.

Less frequent manifestations ofCSC include retinal capillary dilation,choriocapillaris atrophy, atrophictracts of the RPE and inferior periph-eral dependent serous retinal detach-ment (Yannuzzi et al. 1984). Whentelangiectasia, leakage, retinal lipiddeposition and ⁄or cystoid macularoedema are seen (Yannuzzi et al.1984), these features likely attest tothe presence of choroidal neovascular-ization (CNV).

The subretinal fluid in CSC is usu-ally clear, but the subretinal cavitymay contain granular or cloudy mater-ial of a pale yellowish hue (Spaideet al. 1996). Non-granular subretinalmaterial is often called fibrin. Thesubretinal material may disappear butit often leaves an imprint of permanentRPE hypopigmentation (Fig. 8) withassociated fluorescein angiographictransmission hyperfluorescence. Smallgranular subretinal deposits are associ-ated with a favourable prognosis (Per-kins et al. 2002), probably becausethey signify a short duration of detach-ment (Wang et al. 2005). Notably,chronic detachments with subretinaldeposits leave highly visible imprints(Gismero et al. 2003). Long-standingserous detachment of any type may befollowed by attenuation of the RPEcorresponding to the detachment, andit may persist after resolution (Wanget al. 2002). Subretinal fibrosis can

arise as a consequence of CNV(Fig. 11) or independently of neovascu-larization, as a result of severe fibrin-ous deposition (Fig. 12). The fibrinousmaterial may play a role in anchoringa partly detached retina to an under-lying pigment epithelial detachment(Hussain et al. 2006) (Fig. 5).

Fluorescein angiography

The diagnosis of classic CSC can oftenbe made without fluorescein angiogra-phy, but angiography is a critical ele-ment in the differential diagnosis,notably of subretinal neovasculariza-tion, and in the planning of treatment.The diagnosis of CSC should not bemade in the absence of fluoresceinangiographic RPE abnormalities. Thesecan range from a single clearly demar-cated focus of RPE translucency andleakage to extensive areas of irregularhypopigmentation and fluorescence-blocking elements with or withouttrue pigmentation. Non-pigmentedelements that block choroidal fluores-cence often display marked auto-fluorescence (Framme et al. 2005).

A prominent angiographic charac-teristic of CSC is that of an expandingpoint of fluorescein leakage under aserous detachment of the sensoryretina, without signs of subretinal neo-vascularization (Fig. 4) (Robertson1986). Usually, one or two leakagepoints are seen. The site of leakage isoften hypopigmented, showing trans-mission of choroidal fluorescence. Thehypopigmentation of the RPE is notassociated with choriocapillaris atro-phy or geographic atrophy of theRPE. Most leakage points are locatedwithin 0.5–1.5 mm of the centre of thefovea (Spitznas & Huke 1987). Less

than 10% of cases demonstrate leak-age in the foveal area. The most com-mon location of leakage points is thesuperonasal quadrant of the posteriorpole. The serous detachment mayinvolve the site of leakage in CSC butoften the two are not visibly connec-ted. In a minor fraction of cases – 7%in one study (Spitznas & Huke 1987)and 25% in a study of acute casesonly (Yamada et al. 1992) – the leak-ing dye is seen to stream upwardsfrom the site of hypopigmentation ina ‘smokestack’ pattern (Fig. 5). It risesvertically to expand laterally at thetop of the subretinal cavity in a mush-room- or umbrella-like fashion. It isunknown whether the flow is causedby a temperature gradient, by a den-sity gradient existing between thenewly secreted fluid and surroundingfluid that has been in the subretinalcavity long enough to have cooled orto have come hyperdense because ofpreferential resorption of water andsmall solutes. In other cases of CSC,multiple distinct foci of hyperfluores-cence are present, yet none of themdemonstrate expanding fluorescence(minimally enlarging spot configur-ation) whence it is difficult or imposs-ible to attribute the serous detachmentto a specific subset of leakage points.Finally, some cases show partial con-fluence of multiple irregularly distri-buted patches of hypopigmentation(multifocal ink-blot-like leakage)(Fig. 6). This order of listing isbelieved to reflect the development offundus changes over time in non-resolving CSC. The number of RPElesions and the configuration of lesionclusters are highly variable, rangingfrom a single focal lesion in one eyeonly to multiple clusters of lesions in

(A) (B)

Fig. 4. Acute central serous chorioretinopathy with multifocal RPE hyperfluorescence during

early phase fluorescein angiography (A). A cluster of point sources of leakage 1.5 disk

diameters temporal of the optic are visible in the late phase angiogram (B). Optical coherence

tomography demonstrated detachment of the entire macula.


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both eyes. Pigment epithelial detach-ments are occasionally seen in CSC,as isolated lesions or adjacent to areasof mottled RPE, suggesting the pres-ence of occult CNV (Fig. 7).

Hyperpigmentation is seen morerarely in CSC; it should be distin-guished from subretinal deposits asso-ciated with angiographic choroidalshadowing (Figs. 6 and 8) (Iida et al.

2002). Such deposits appear to beprominent in CSC arising during preg-nancy (Sunness et al. 1993).

The area of detachment in relationto the area of leakage is higher insmokestack cases than in pin-pointleak cases without the smokestackphenomenon (Friberg & Campagna1989). Assuming that the extent of thedetachment is proportional to the rateof leakage, this is evidence that smo-kestack cases leak faster than otherlesions. Particularly high rates of leak-age appear to be associated with RPEdetachments with a tear at the edge,the fluid leaking through this openinginto the subretinal cavity. In one thirdof the cases, the point of leakage isin the papillomacular bundle, mostcommonly above the horizontal raphe(Wessing & Meyer-Schwickerath 1971).

Autofluorescence fundus photography

The autofluorescence characteristics ofthe fundus in CSC are clearly differentfrom healthy eyes. In acute CSC, hypo-flourescence has been demonstrated atthe very point of leakage (Eandi et al.2005). Acute CSC that has persistedfor some time often shows granular orsemi-confluent hyperfluorescence thro-ughout the area of detachment (Fig. 9).In chronic CSC, irregular patterns ofmixed hyper- and hypofluorescence canbe seen (Framme et al. 2005; vonRuckmann et al. 2002). After reattach-ment, the autofluorescent subretinaldeposits disappear slowly over a periodof several months (Fig. 9).

OCT

OCT can demonstrate shallow serousdetachments that are difficult to diag-nose using slit-lamp biomicroscopy(Wang et al. 1999). OCT is also usefulin determining whether reattachmenthas occurred after treatment. Especi-ally in chronic cases, OCT is usefulbecause morphological and functionalrestitution may be incomplete, thusproviding little clinical guidance (Heeet al. 1995). Recent use of three-dimensional OCT has revealed smallpigment epithelium detachments(PEDs) in 13 out of 29 patients withactive CSC; two of the 29 patientshaving RPE detachments larger than0.5 disc diameter (van Velthoven et al.2005). Multiple PEDs can be found insome cases, usually located superiorto the neurosensory detachment.

(A)

(B)

Fig. 5. Smokestack fluorescein angiographic type of central serous chorioretinopathy recorded

15 min after intravenous fluorescein injection (A). From the site of leakage, approximately

50 lm in diameter, located 700 lm inferior of the foveola, fluorescein-stained fluid is flowing

upward within a 3000 lm diameter cavity filled by colourless serous fluid, the hyperfluorescent

outline of which is faintly visible. Optical coherence tomography (B), approximately to scale, is

showing focal attachment of the neurosensory retina to the apex of a pigment epithelial detach-

ment.

(A) (B)

Fig. 6. Fundus photography (A) and fluorescein angiography (B) in the right eye of a 27-year-

old woman with systemic lupus erythematosus, lupus nephropathy, iatrogenic hypercortisolism

and well-controlled arterial hypertension. The patient had suffered, to variable degrees, from

painless blurred vision, dyschromatopsia and micropsia for more than 2½ years. Best-corrected

visual acuity in the right eye was 0.3. Fundus abnormalities included an irregular pattern of

hypopigmentation of the retinal pigment epithelium, amorphous subretinal deposits and a shal-

low serous detachment involving large parts of the posterior pole. These findings are highly sug-

gestive of chronic central serous chorioretinopathy.


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Electrophysiology

Focal electroretinography (ERG) hasdemonstrated reduced photoreceptorfunction of the detached retina in CSC(decreased amplitude and increasedlatencies of the b-wave, decreased oscil-latory potentials) (Papakostopouloset al. 1984; Miyake et al. 1988; Shiroy-ama & Miyake 1990). Multifocal ERG(mfERG) has demonstrated variabledegrees of dysfunction outside the areaof detachment (Marmor & Tan 1999)but normal function outside the area ofvisible fundus involvement (Vajaranantet al. 2002). Obviously, the delineationof past detachment is often uncertain.Subclinical fellow-eye involvement issuggested by the finding of abnormallylow mfERG amplitudes (Dohrmannet al. 2001), but the patient havinghad subclinical transient detachmentin the fellow eye cannot be excluded.Electro-oculography and ERG have

not shown signs of RPE dysfunctionin CSC (Gupta & Marmor 1995).

Course andcomplications, staging

Prospective studies of the natural his-tory of CSC are incomplete. The clas-sification in Table 1 is based onprevalent expert opinion about thestages of progression of the diseaseand fragments of evidence from alarge number of reports.

Acute CSC

Typical acute CSC is characterized bya duration of symptoms and ⁄or ret-inal detachment of less than 6 monthsand monofocal or paucifocal fluoresc-ein angiographic RPE leakage (Eandiet al. 2005). Large pigment epithelialdetachments can be seen in a small

fraction of patients with CSC – prob-ably less than 5% (Castro-Correiaet al. 1992; van Velthoven et al. 2005).Occasionally, the PED may rupture(Shanmugam & Bhende 2000), inwhich case pronounced angiographic‘blow-out’ leakage through the rip canbe observed.

Chronic CSC

Chronic CSC, which is also known asdiffuse retinal pigment epitheliopathy,is generally characterized by multifo-cal, irregularly distributed and oftenwidespread RPE changes associatedwith varying degrees of low-grade leak-age (Cohen et al. 1983; Beuchat et al.1988; Yannuzzi et al. 1992; Otsukaet al. 2002). The relation to acute CSCis documented by published cases oflong-term follow-up (Castro-Correiaet al. 1992; Bujarborua 2001; Katsim-pris et al. 2006). Chronic CSC ismore often bilateral and may occasion-ally present with gravitationaltracts (Brancato & Bandello 1991;Bujarborua 2001; Gismero et al. 2003),a term used for oblong, vertical pat-ches of RPE hypopigmentation thatextend inferiorly from the macula. Pre-sumably, gravitational tracts are pro-duced by subretinal fluid of highspecific gravity sinking toward theinferior fundus and dissecting its waythrough the subretinal space. CSC withinferior retinal detachment and ⁄ortracts of attenuated RPE pigmentationis also called atypical CSC. In a studythat recalled 50 out of 150 patients3 years after their first visit, diffuse epi-theliopathy had developed in eightpatients (Castro-Correia et al. 1992).The extent of RPE attenuation on fluo-rescein angiography has been found tobe predictive of subsequent visual out-come (Bandello et al. 2000, 2001). Ret-inal abnormalities also described inCSC include pigment migration, capil-lary teleangiectasia and capillary non-perfusion in the detached retina.

Sequels of CSC, inactive CSC and CNV

In the absence of retinal detachment,the diagnosis of CSC – or rathersequels of CSC – relies upon the his-tory (which may or may not beinformative) and on finding RPElesions characteristic of CSC. Thediagnosis should not be made in theabsence of fluorescein angiographicRPE changes. Lesions are often found

(A)

(B)

(C)

(D)

Fig. 7. Fundus photographs (A, B) and fluorescein angiograms (C, D) from a 54-year-old

woman who presented with pigment epitheliopathy between the fovea and the optic disk in

both eyes. In the right eye (A, red-free fundus photograph; C, fluorescein angiogram), the cir-

cumscribed area of mottled pigment epitheliopathy was associated with a pigment epithelium

detachment (PED) that extended under the fovea as well as a shallow serous detachment of the

fovea. Best-corrected visual acuity in the right eye was 0.7. The angiographic characteristics did

not enable a clear distinction between chronic central serous chorioretinopathy and occult su-

bretinal neovascularization. Following confluent photocoagulation treatment of the area of

mottled pigment epitheliopathy nasal of the fovea, all subretinal fluid resolved, as did the

patient’s symptoms. Best-corrected visual acuity achieved 1.0 within 1.5 months and the condi-

tion has remained stable for 8 years. Equally favourable outcomes have been reported following

photodynamic therapy of the primary RPE lesion. The left eye presented a PED between the

optic disk and the fovea and subretinal deposits, notably under the inferonasal rim of the fovea.

Confluent photocoagulation treatment of moderate intensity over the PED resulted in flattening

of the retina. The left eye has remained stable during 8 years of follow-up.


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in both eyes, but their distribution isnot usually the same. A shallowrelative scotoma may remain afterresolution of CSC, occasionally withmetamorphopsia (Natsikos & Hart1980), mild dyschromatopsia, andreduced contrast sensitivity.

As with other lesions of the RPEand ⁄or Bruch’s membrane, subretinalneovascularization of choroidal originmay appear as a complication of CSC(Figs 10 and 11) (Faurschou et al.1977). CNV can arise at any timeafter CSC (Gomolin 1989) and usuallydoes so long after the resolution ofthe acute disease. In older patients,CNV following CSC is often assumedfalsely to be a manifestation of age-related macular degeneration (AMD),

but it is worth recalling that the diag-nosis of AMD cannot be made if theother eye is healthy and does notdemonstrate drusen. If photocoagu-lation treatment has been used to treatactive CSC, it will be difficult orimpossible to determine whether theCNV arose as a complication of CSCor as a complication of photocoagula-tion (Schatz et al. 1977). However, therisk of CNV in CSC is low: one studyreported a single case in 39 patientsfollowed for an average 9.6 years(0.3% per patient per year) (Dickhoffet al. 1989); another study found thatCNV developed in four eyes in threeout of 51 patients followed over amean of 34.7 months (2% per patientper year) (Bandello et al. 2001).

In severe CSC with subretinalfibrinous deposits, it appears thatinstead of resorption of the subretinalmaterial a subretinal fibrotic scar mayform directly without the involvementof subretinal new vessels (Fig. 12)(Schatz et al. 1995; Hooymans 1998).

Subretinal deposits in CSC

Subretinal material is frequently pre-sent in CSC, mostly as fine granules(Figs 8C and 11A) (Wang 2005), morerarely as confluent patches (Fig. 8B)with a more or less fibrinous appear-ance (Gass 1991). The amount ofsubretinal debris increases with theduration of symptoms (Wang 2005).The isolation of photoreceptor outersegment fragments (Matsuo et al.1986) from the aqueous humor ofpatients with the Schwartz syndromesuggests that such fragments may beresponsible for the granular subretinaldeposits in CSC (Larsen et al. 2004;Wang 2005; Schwartz 1973). Schwartzsyndrome is an open-angle intraocularhypertension syndrome with aqueouscorpuscles that is unresponsive toglucocorticoid therapy occurring inpatients with anterior retinal tears orora serrata dialysis. Aqueous cellsand ocular hypertension resolveshortly after repair of the retinaldetachment.

Visual prognosis

Acute CSC that resolves spontaneouslyor following treatment has a goodlong-term prognosis for visual function(Wong et al. 2004). Chronic CSC fre-quently results in considerable irrevers-ible visual acuity loss, despite somefunctional improvement early afterreapposition of the retina and a sub-sequent phase of slow visual recovery(Dohrmann et al. 2001). Among 47 USAir Force aviators with CSC, 51% hadrecurrent episodes, 17% had bilateraldisease and 13% underwent laser pho-tocoagulation (Green et al. 1988).Eighty-six per cent attained a final vis-ual acuity of 20 ⁄ 20 or better.

Recurrences develop in one third tohalf of cases after the first acute epi-sode, 10% having three or morerecurrences. About half of the patientsexperience recurrence within 1 year ofthe primary episode (Gass 1967;Ficker et al. 1988). Eyes with recur-rent disease tend to have reduced finalvisual acuity, stereopsis, colour vision

(A)

(B)

(C)

(D)

Fig. 8. Fundus photographic montage (red-free, greyscale) demonstrating evolution of subreti-

nal deposits over time in an otherwise healthy male, who presented at age 47 years with unila-

teral complaints of seeing a dark spot overlaid his central visual field in the left eye. The spot

was described as having the shape of the footprint of Donald Duck (A). Best-corrected visual

acuity in the left eye was 0.9. A yellowish patch of confluent subretinal material having said

shape was seen to extend from the superonasal macula to the temporal aspect of the fovea.

Photocoagulation treatment applied 0.5 disk diameter above and temporal of the optic disk was

followed by gradual resolution of the subretinal fluid, the residual substance presenting a mixed

diffuse and granular appearance 1.5 months after treatment (B), the appearance having changed

to a granular one at 6 months (C) and to multifocal patches of RPE hypopigmentation after

6 years (D). At this time, automated perimetry of the left eye (Humphrey 24–2, full threshold)

was entirely normal. Nevertheless, the patient described a distinct grey pattern overlaid his

central visual field, the drawing of which closely matched the pattern of hypopigmentation.


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and central visual field function.Examples of persistent loss of acuityand attenuation of the retina havemainly been reported in chronicallyrecurrent cases (Newman 2002; Wanget al. 2002).

Extraocular conditionsassociated with CSC

Early reports on CSC described thefrequent association of CSC withpsychosocial stress, particularly during

transient life crises (Yannuzzi 1987).Conflicts typically relate to depen-dency versus autonomy, submissionversus control, providing versus autar-chy and self-esteem (Spahn et al.2004) or, in lay terms, personally chal-lenging events such as impendingdivorce, bankruptcy, or critical illnessof close relatives. The patients aregenerally in good health and perfectlysane, but frequently have copingstrategies in critical life events thatbring them to accept great burdenswhile obtaining little relief of tension

(Conrad et al. 2000). These characteris-tics are typical of the Type A person-ality. A comparison of behaviour inpatients with CSC versus patients withother ocular disorders demonstratedthat Type A behaviour was signifi-cantly more frequent in CSC patients(Yannuzzi 1986, 1987). Increasedlevels of circulating catecholaminesmay be an important link between thetense, aggression-suppressing beha-viour displayed by the Type A person-ality when subjected to environmentalstress and the lesion of the RPE in

Table 1. Summary characteristics of central serous chorioretinopathy.*

Duration

Biomicroscopy,

IVFA, OCT Detachment Stress, hypercortisolism Treatment

Acute CSC Fine granular subretinal

deposits if duration more

than a few weeks;

monofocal leakage

High, bullous;

OCT > 100 lmsubretinal fluid

Common, recent Conservative, counselling;

if no resolution within

3 months of onset of

symptoms consider focal

photocoagulation or, in

cases where photocoagulation

is considered unsafe, PDT

Recurrent Paucifocal (1–5) Moderate,

51–100 lmCommon Photocoagulation if

deemed safe, PDT

otherwise

Chronic Multiple, semi-confluent

hypopigmented RPE lesions;

confluent subretinal

material

Shallow, often

< 50 lmPast, current, inconclusive

or none

consider PDT

Sequelae RPE depigmentation

without RPE atrophy

None Past, inconclusive

or none

None

Neovascular CNV plus CSC

sequelae; subretinal

fibrosis

Variable, mainly

around CNV

History of CSC and

associated RPE changes

PDT and ⁄ or intravitrealVEGF-inhibitor for active CNV

(blood, lipid, serous, detachment,

recent visual loss)

IVFA, intravenous fluorescein angiography; OCT, optical coherence tomography; CSC, central serous chorioretinopathy; PDT, photodynamic

therapy; RPE, retinal pigment epithelium; CNV, choroidal neovascularization.

*The table summarizes a large number of publications, of varying evidence levels. For a full discussion of each item, consult the text.

(A) (B) (C)

Fig. 9. Fundus autofluorescence photographs taken using fluorescein angiographic filters and a greyscale charge-coupled device fundus camera in

the left eye of the same patient as in Fig. 5. After resolution of the serous retinal detachment following photocoagulation treatment 1.5 months

earlier (A), moderately hyperfluorescent subretinal deposits were found throughout the area where the detachment had previously been located; a

more prominently hyperfluorescent area was seen where treatment had been applied near the rim of the optic disk. The hyperfluorescence of the

subretinal material faded with its gradual resorption and it was of granular appearance 6 months after treatment (B). A weak pattern of hyperflu-

orescence remained 6 years after treatment (C), except for a the dark area corresponding to the photocoagulation scar.


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CSC. Abnormally increased sympa-thetic nervous activity is supported bycardiac studies (Bernasconi et al.1998). Elevated circulating epineph-rine and norepinephrine levels havebeen measured in patients with CSC(Sun et al. 2003). Catecholamine levelshave been shown to return to normalduring the convalescent stage of thedisease. Endogenous serum cortisollevels are on average more than 50%elevated in patients with CSC, alsosupporting that a stress response isinvolved (Garg et al. 1997).

Systemic glucocorticoid treatment isassociated with increased risk ofdeveloping CSC (Carvalho-Recchiaet al. 2002), possibly with a particularrisk of developing chronic CSC (Polaket al. 1995). The disease can be seenin patients who use intranasal or inha-lation glucocorticoids (Haimoviciet al. 1997) but because CSC is a com-mon disease, it remains uncertainwhether the association is incidentalor causal. The same is true for the fre-quent elevation of urinary cortisolexcretion (Haimovici et al. 2003). Acase–control study of 312 patientsidentified the following risk factors:systemic glucocorticoid use [odds ratio(OR) 37.1], pregnancy (OR 7.1), anti-biotic use (OR 6.2), alcohol use (OR4.9), untreated hypertension (OR 3.3)and allergic respiratory disease (OR2.5) (Haimovici et al. 2004). The lattermay be related to the therapeuticuse of inhalation glucocorticoids.Subretinal fibrin may be more likely

to form in CSC associated withsystemic glucocorticoid treatment(Quillen et al. 1996).

CSC has been described in relationto a large number of other systemicconditions, the majority of which areassociated with glucocorticoid treat-ment of conditions such as systemiclupus erythematosus and in relation toendogenous hypercortisolism (Ecksteinet al. 1993; Bouzas et al. 2002). Fifteenout of 16 patients with CSC amongorgan transplant recipients also suf-fered from systemic hypertension(Fawzi & Cunningham 2001; Fawziet al. 2006). The latency betweenonset of glucocorticoid treatment anddisease is generally in the range ofmonths, and there may be no lowerdose limit (Song et al. 1997). CSChas also been described in relationto the intake of methylenedioxy-methamfetamine (ecstasy) (Hassanet al. 2001).

Pregnancy has been reported to beassociated with CSC, perhaps becauseof the increase in circulating glucocor-ticoids (Chumbley & Frank 1974).The condition is most often present inthe third trimester and resolves within1–2 months of delivery (Quillen et al.1996).

Three reports from France havedescribed elevated prevalence ofHelicobacter pylori infection inpatients with CSC compared to thebackground population (Mauget-Faysse et al. 2002; Ahnoux-Zabsonreet al. 2004; Cotticelli et al. 2006). One

quarter of the population of Francehas a positive response to the C13-urea breath test for H. pylori, which ismuch higher than the prevalence ofCSC, indicating that the vast majorityof patients with H. pylori do notdevelop CSC.

A racial and hence genetic predispo-sition to CSC is suggested by the pre-valence of the disease being high inCaucasians and Hispanics and higherin Asians but extremely low in Afri-can Americans (Spaide et al. 1996;Fukunaga 1969; Desai et al. 2003).Patients with CSC achieved higherthan normal scores for hypochondriaand hysteria in a personality test andwere more likely to use psychomimeticmedication (Werry & Arends 1978;Tittl et al. 1999).

Pathogenesis of RPEdysfunction and serousdetachment

In acute cases, there is visible leakageof fluorescein-stained fluid from oneor more small lesions in the RPE. Themechanism whereby subretinal fluid isproduced in CSC is poorly under-stood. The constant inflow of fluid ina non-expanding subretinal cavity,which is seen to advantage in smoke-stack cases, is a vivid demonstrationthat the detachment is maintained bya balance between constant inflow andoutflow, the latter presumably taking

(A) (B) (C)

Fig. 10. Fundus photograph (A) and fluorescein angiograms (B, C) from the left eye of a 62-year-old man with a history of recurrent central serous

chorioretinopathy who presented with 2 months’ duration of blurred vision, best-corrected visual acuity 0.5, a serous foveal detachment and a cir-

cumscribed area of mottled RPE at the inferonasal rim of the fovea. Confluent moderately bleaching photocoagulation treatment of a small area of

pigment epitheliopathy was followed within 2 weeks by complete resolution of the serous detachment as well as disappearance of the symptoms. The

patient presented four months later, with a subfoveal choroidal neovascular membrane. Retrospectively, it may be argued that the patient had occult

choroidal neovascularization at presentation, although the late-phase hyperfluorescence was too weak to fulfil the conventional criteria for such a

diagnosis. When overt neovascularization was eventually diagnosed, it could have been a consequence either of photocoagulation unmasking the

existence of a membrane that was already present or of photocoagulation actually eliciting the development of a subretinal neovascular membrane.


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place across intact RPE and the retinalvessels.

The detachment is associated withleakage or secretion of fluid throughdysfunctional RPE or RPE defects.The possibility that simple focal lossof RPE cells could be responsible forthe leakage is excluded by the obser-vation that a defect of the RPE pro-motes resorption, rather than leakageof subretinal fluid (Negi & Marmor1984). Indeed, the rate of leakage in

CSC is so high that active pumping offluid across the RPE in the inwarddirection has been postulated. Alter-natively, the leakage may emanatefrom a localized injury of the chorio-capillaris with associated abnormallyelevated leakage from these vessels(Prunte 1995). This model is difficultto accept unless rupture of the RPE ispostulated; indeed, severe cases offocal leakage are often associated withruptured RPE detachments.

In CSC, serous detachment of theretina is almost invariably foveal,despite the source of leakage mostcommonly being extrafoveal. Theore-tically, this could be a consequence ofthe strength of the attachment of theretina being weaker in the fovea thanelsewhere in the retina because thesuction of the RPE exerts a weakerattraction on the thin foveal retinathan on the thicker extrafoveal retina,the latter presumably having the lowerhydraulic conductivity.

Experimental injection of epineph-rine in monkeys can produce posteriorpole serous retinal detachment (Yos-hioka et al. 1982). Fluorescein angiog-raphy demonstrates choroidal vascularleakage associated with histologicallyirregular, narrow choroidal arteriolesand choriocapillaries, hypertrophy ofBruch’s membrane and loss or degen-eration of the overlying RPE (Yos-hioka & Katsume 1982). This responseto adrenalin injection was abolishedby ganglionic blockade and by sys-temic pretreatment using an alpha-adrenergic blocker (Yoshioka 1991).These observations suggest that adre-nergic stimulation from the circulationand ⁄or the sympathetic nerves maylead to CSC by inducing choroidalvasoconstriction and alteration ofblood flow.

Indocyanine green angiography(ICGA) in patients with CSC has dem-onstrated evidence of choroidal lobu-lar ischaemia and choroidal venouscongestion (Hayashi et al. 1986;Prunte 1995; Prunte & Flammer 1996)(Fig. 13). Segments with late choroidalhyperpermeability also show a delay infilling. Focal areas of ICG hyperfluo-rescence can also be seen in clinicallyunaffected fellow eyes. The cause ofthe venous dilation has not been deter-mined. Theoretically, it may be aresponse to ischaemia and delayedarterial filling or a consequence of out-flow obstruction. ICGA hypofluores-cence induced by the shadowing effectof a detached retina or subretinaldeposits should not be mistaken fordelayed lobular filling.

ICG angiography is of value indiagnosing occult CNV in CSC,especially if performed using a con-focal scanning laser camera. In theabsence of CNV, ICGA is of nocertain value in the management ofCSC (Stanga et al. 2003). Choroidalvascular hyperpermeability at foci of

(A)

(B)

Fig. 11. Fundus photography (red-free, A) and mid-phase fluorescein angiography (B) from

the left eye of a 61-year-old man with a 20 year history of chronic recurrent central serous

chorioretinopathy. A lesion near the upper temporal vascular arcade shows expanding leakage

from a subretinal point source and a surrounding serous detachment that did not reach the

fovea. The subfoveal lesions demonstrated staining without leakage. Best-corrected visual acuity

in the left eye was 0.3. Punctate subretinal deposits were seen in the upper macula, and fibrin-

ous deposits without haemorrhage or hard exudate were found under the fovea. Three months

later, the patient presented with visual acuity 0.1 in the left eye and subretinal haemorrhage,

hard exudate and late angiographic leakage from a subfoveal occult-only choroidal neovascu-

larization (CNV). The history suggests that conversion from inactive occult subfoveal CNV to

active neovascularization occurred between the two visits.


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subretinal fluorescein leakage is afrequent finding (Piccolino & Borgia1994; Menchini et al. 1997; Uyamaet al. 1999; Constantinides 2000;Yannuzzi et al. 2003); however,

choroidal hyperpermeability can alsobe found without associated fluo-rescein leakage, as can subclinicalRPE detachment (Guyer et al. 1994;Iida et al. 1996).

Laser interferometry has demon-strated increased choroidal pulsationin CSC, supporting the presence ofa perfusion anomaly (Tittl et al.2003).

Pathogenesis of visualdysfunction

Reduced colour and contrast sensitiv-ity are present when the retina isdetached, regardless of the cause. Insome patients with CSC these sensorymodalities are also affected after reso-lution of the detachment (Bartos et al.1998). Several mechanisms may con-tribute to this functional defect: thelack of apposition of photoreceptorsand RPE cells; moderate oedema ofthe detached retina; the absence of thestray light-absorbing RPE right nextto the photoreceptors; photoreceptordisorientation interfering with theStiles–Crawford effect (Bek & Kandi2000); and impaired regeneration ofvisual pigment.

When the retina is detached inCSC, a relative central scotoma canbe documented by psychophysicalmeasurements (Burns et al. 1987). Intheory, this scotoma should be deeperunder scotopic conditions because theRPE visual cycle subserves exclusivelyor predominantly the rods, whereas aseparate visual cycle in the neurosen-sory retina supports cone function(Mata et al. 2005). Indeed, rod dys-function is more pronounced thancone dysfunction in CSC (Chuanget al. 1987). Patients often relate thattheir scotoma is most distinct whenthey leave their bed at night withoutturning the light on. Nevertheless,substantial photopigment regenerationappears to take place in the rod pho-toreceptors of the detached retina(Mori et al. 1990). Physiologically, theincreased length of diffusion betweenthe RPE and the photoreceptors maycontribute to the reduced sensitivityand ⁄or delayed adaptation of thedetached retina. Photostress testing inareas of serous detachment shows alower sensitivity change immediatelyafter bleaching than in healthy sub-jects and a slower recovery (Verma &Sahai 1990; Horiguchi et al. 1998).Delayed adaptation of the detachedretina is also supported by the demon-stration of elevated fatigability of the

(A) (B)

(C) (D)

Fig. 12. Development of subretinal fibrosis in direct transition from acute subfoveal accumula-

tion of fibrinous material at presentation (red-free fundus photography, A; early phase fluorescein

angiography, B; late phase, C) and follow-up 2.5 years later (D). Shortly after presentation, the

right eye underwent extrafoveal photocoagulation treatment to the hyperfluorescent area above

the subfoveal serous detachment (C). This was followed by resolution of the serous subretinal

fluid within 2 weeks and precipitation of subretinal material that was resorbed slowly over about

1 year, leaving a small area of subretinal fibrosis under the fovea at follow-up 2.5 years after

treatment. No evidence of subretinal neovascularization was seen at any time.

(A) (B)

Fig. 13. Indocyanine green angiography recorded using a scanning laser ophthalmoscope, from

the left eye of a patient with acute central serous chorioretinopathy. The early frame (A) shows

choroidal hypofluorescence corresponding to a two-disk-diameter-wide area of serous detach-

ment (inferior margin indicated by grey arrows). Smaller areas of selective choroidal hypofluo-

rescence near its upper border are marked using white arrows. During the angiographic mid-

phase (B), these hypofluorescent areas demonstrate choroidal venous dilation and leakage at

the locations in (B) that correspond to the white arrows in (A). An animated overlay of the

two images can be found at http://www.oculus.suite.dk/CSC_ICGA_Animation1.gif.


136

double-flash ERG (Elenius 1968). Inagreement with this, deeper scotomataare found with a flickering stimulusthan with a steady-state stimulus(Vingrys & Pesudovs 1999). It isunknown whether this is because conefunction is not entirely independent ofthe RPE or whether it demonstratesthe loss of a contribution of rods tophotopic vision.

Persistent visual loss despite reat-tachment of the retina has beenshown to be associated with atrophyof the outer retina (Wang et al. 2002;Piccolino et al. 2005). This may betaken as evidence that direct contactbetween the (rod) photoreceptor outersegment and the RPE is essential forthe survival of the photoreceptor and,possibly, for the cells of the RPE.

Differential diagnosis

The differential diagnosis of CSCrequires exclusion of other causes ofretinal detachment or RPE detach-ment, including rhegmatogenousdetachment (which is very rarely con-fined to the macula) and serous detach-ment of other causes (includingchoroidal tumour, choroiditis, hyper-tensive choroidopathy, diabetic macu-lar oedema, retinal vein occlusion,optic pit or other malformation andspecific retinal degeneration or dystro-phy). Additionally, the presence ofCNV, independent of CSC or as acomplication of CSC, must always besuspected.

Choroidal neovascularization

The presence of CNV is suggested bythe presence of subretinal haemor-rhage, hard exudate and visible newvessels on biomicroscopy or fluoresc-ein angiography (Schatz et al. 1977).Some cases of CNV, especially occult-only CNV, may lack such signs ofactivity. A classic fluorescein angio-graphic criterion for defining occultCNV is circumscribed late-phasefluorescence that is more prominentthan that of the optic disk. Cases ofchronic CSC with RPE hypopigmen-tation and, possibly, choroidal vascu-lar congestion come close to fulfillingthis criterion and may be difficult orimpossible to distinguish from occultCNV, although ICG angiographymay be of some value.

AMD

The diagnosis of AMD requires thepresence of drusen or the assumptionthat drusen were present but disap-peared with the development of CNVor geographic atrophy. UnilateralCNV and a healthy fellow eye withoutdrusen exclude the diagnosis of AMD(Schatz et al. 1992). Confluent drusenwith RPE detachment, pseudovitelli-form degeneration and pattern dystro-phy are rarely associated withsignificant serous detachment of theneurosensory retina.

Hypertensive choroidopathy

Arterial hypertension can be accom-panied not only by intraretinal vascularchanges and optic disk oedema but alsoby serous retinal detachment and RPElesions known as Elschnig spots. Theseare focal RPE hyperpigmentations 50–200 lm in diameter with a hypopig-mented halo. The lesions are believedto be caused by choroidal ischaemiasecondary to extreme vasoconstrictionduring arterial hypertension. The pur-ported mechanism is very similar tothat proposed for CSC. In this context,it is remarkable that CSC is associatedonly weakly with arterial hypertension(Haimovici et al. 2004) and that inCSC secondary to systemic glucocorti-coid therapy, arterial hypertension isconspicuously absent (Chaine et al.2001). Elschnig spots only develop in afraction of patients with arterial hyper-tension and in a highly variable pat-tern, but with a propensity for beinglocated above major choroidal vessels.These observations suggest that anidiosyncratic reaction in susceptiblesubjects is involved in producing focalchoroidal ischaemia in both condi-tions.

Pigment epitheliitis

Acute retinal pigment epitheliitis is anentity that has been observed inhealthy young adults who present withreduced visual acuity and a centralscotoma. The characteristic macularlesions, discrete pigment clumps withsurrounding hypopigmented halosthat show hyperfluorescence withoutleakage on fluorescein angiography(Chittum & Kalina 1987), are indistin-guishable from Elschnig spots. Acuteretinal pigment epitheliitis wasdescribed before the advent of OCT.

Idiopathic polypoidal choroidal

vasculopathy

Idiopathic polypoidal choroidal vascu-lopathy is characterized by polypoidaldilations of choroidal vessels, notablyin the peripapillary area, with asso-ciated serosanguinous detachment ofthe RPE and the neurosensory retina.If fluorescein angiography is not diag-nostic, indocyanine green angiographymay be helpful in displaying the vas-cular polyps (Schneider et al. 2001;Stanga et al. 2003; Yannuzzi et al.2000).

Isolated RPE detachment

Although not a common ophthal-moscopically visible component ofCSC, RPE detachment may occur inCSC in the absence of CNV. This sug-gests that isolated RPE detachment,in the absence of serous neurosensoryretinal detachment or other RPElesions typical of CSC, could be amanifestation of CSC. Indeed, caseshave been reported where such solit-ary RPE detachment converted spon-taneously to monofocal classic CSC(Bandello et al. 2000; Gomez-Ullaet al. 2000). Additionally, ICG angio-graphic findings have been interpretedas suggesting that a pattern of choroi-dal venous dilation and leakageunderlies both CSC and idiopathicRPE detachment (Giovannini et al.1997; Gomez-Ulla et al. 2000). A fewpatients with idiopathic, multiple ser-ous RPE detachments have been des-cribed in a clinicopathological study(Gass et al. 2005). Sporadic reports ofsuccessful elimination of RPE detach-ments following photocoagulationtreatment may represent cases of CSC(Fig. 7).

Vascular disorders

Systemic inflammatory disease may beassociated with CSC, which has beendescribed in patients with systemiclupus erythematosus, polyarteritisnodosa, sclerodermia, dermatomyositisand relapsing polychondritis (Ecksteinet al. 1993; Taga et al. 2001). Usually,it is impossible to determine whetherthe serous detachment is caused byinflammatory disease of the choroidalvessels or by systemic glucocorticoidtreatment. Of particular interest is thatsevere arterial hypertension (Venkateshet al. 2006), toxemia of pregnancy(Somfai et al. 2006) and disseminated


137

intravascular coagulation (DIC) canpresent with a neurosensory retinaldetachment. Endothelin-1 is a candi-date mediator for the vasoconstrictionthat is an essential feature of these con-ditions (Asakura et al. 1992). Theseobservations fit the concept that idio-pathic CSC is caused by choroidalvasoconstriction, as described earlier,suggesting that serous retinal detach-ment in arterial hypertension, toxemia,etc. is a type of secondary CSC, asopposed to idiopathic or primary CSC.

Vogt–Koyanagi–Harada’s disease

This posterior uveitis or panuveitiswith exudative retinal detachment anddisc hyperemia may have only poster-ior pole manifestations at presentationand the patient may fail to report pro-dromal central nervous system (CNS)symptoms. Vogt–Koyanagi–Harada’sdisease (VKH) is characterized byacute multifocal exudative posteriorpole pigment epitheliopathy with ser-ous detachment of the neurosensoryretina (Read et al. 2000), often moreextensive than in CSC. The multifocalRPE lesions are typically more numer-ous and more leaky than in CSC, theleakage coalescing over time to fill thesubretinal space. Because early, aggres-sive systemic glucocorticoid therapy isbelieved to reduce the risk of complica-tions and visual loss, early diagnosis ismandatory. The diagnosis is based onthe ocular characteristics and theassociation with Asian, Middle Easternor Native American ethnicity, concom-itant or closely associated aseptic men-ingitis, inner ear symptoms, anterioruveitis, alopecia, poliosis, and vitiligo.A favourable response to systemicglucocorticoid therapy will support thetheory that the condition is not CSC,whereas lack of response shouldprompt renewed diagnostic efforts. Ifserous retinal detachment develops ina patient with VKH during glucocor-ticoid treatment, the possibility ofglucocorticoid-induced CSC shouldbe considered (Schalenbourg et al.2002).

Optic nerve pit with serous macular

detachment

All patients who present with a serousdetachment of the macula or maculo-schisis should be examined for thepresence of an optic nerve pit. Thisabnormality of the optic nerve is not

associated with fluorescein angio-graphic leakage and may be more orless conspicuous, with or without avisible communication between the pitand the subretinal fluid.

Optic neuritis

Optic neuritis can result in complaintscomparable to those of patients withCSC, but in optic neuritis there is oftenmore prominent loss of colour satura-tion, brightness and contrast, includinga sensation of greyness without theTroxler effect seen in CSC. Meta-morphopsia is absent in optic neuritis.An afferent pupillary defect is promin-ent in optic neuritis and often demon-strable with the Pulfrich test, whereasit is minimal or absent in CSC (Sadun1990). During the acute phase, opticneuritis is associated with pain and ten-derness, which are never seen in CSC.After the resolution of optic neuritis,visual dysfunction comparable to thatseen in CSC may be found, withuncharacteristic dyschromatopsia andreduction of acuity and contrast. Incontrast to CSC, there is often a resid-ual relative afferent pupillary defectafter optic neuritis, a visual evokedpotential delay, and a reduced criticalflicker frequency (Han et al. 1985).

Posterior scleritis

This painful condition may be associ-ated with serous retinal detachment.Ultrasonography reveals posteriorscleral thickening and fluid in the sub-tenonal space.

Inflammatory choroiditis

Multifocal choroiditis (Gass & Little1995), uveal effusion syndrome, sym-pathetic ophthalmia (Gomez-Valcarcelet al. 2004) and other posterior poleinflammatory or infectious processesmay be associated with serous retinaldetachment. This is a characteristic ofthe active inflammatory stages ofsuch diseases. Serous detachment ishighly unlikely over a postinflamma-tory chorioretinal scar, unlessCNV has developed. It is importantto distinguish fluffy, elevated lesionsand granulomatous choroidal lesionsthat leak fluorescein from the non-expanding hyperfluorescent lesions ofchronic CSC, which are flat, exceptfor the occasional PED. Systemic dis-eases associated with choroiditisinclude systemic lupus erythematosus

and sarcoidosis (Eckstein et al. 1993;Cunningham et al. 1996). When con-sidering the diagnosis of choroiditis,it should be remembered that recur-rent or chronic CSC often leavesmultifocal irregular changes in funduspigmentation that may resemblesequels of inflammatory choroidopa-thy (Cunningham et al. 1996). Whensystemic glucocorticoid treatment hasbeen used in the treatment of sys-temic inflammatory disease, it is ourexperience that the treatment is morelikely than the disease to be respon-sible for the retinopathy (Fig. 6)(Bouzas & Mastorakos 1994; Gass &Little 1995). Discontinuation of glu-cocorticoid treatment may be fol-lowed by resolution of the retinaldetachment in CSC, but this responseis less certain if chronic CSC hasdeveloped. Although the associationbetween hypercortisolism and CSC isclearly accepted, a survey of patientswith Cushing’s syndrome found evi-dence of past or present CSC in only5% of cases (Bouzas et al. 1993).

When related to the use of exogen-ous glucocorticoids, CSC has a lessprominent male predilection, presentsmore often a chronic or atypical formand is more frequently bilateral (Quil-len et al. 1996; Bouzas et al. 2002).Glucocorticoids should not be used inthe treatment of CSC.

Choroidal tumours

Inferior detachments of the neurosen-sory retina are a common feature ineyes with choroidal haemangioma,melanoma, or metastatic tumour(Haut et al. 1984). Serous detachmentof the macula can also be seen in cho-roidal osteoma and leukaemic choroi-dal infiltration.

Treatment

The treatment of CSC is based largelyon uncontrolled observations. Thehigh spontaneous remission ratefavours conservative management,lifestyle counselling and discontinu-ation of glucocorticoid medication asfirst-line therapeutic options. Such astrategy can be expected to be fol-lowed by a resolution of detachmentin nearly 90% of cases within1.5 months (Sharma et al. 2004). Inmost cases, visual acuity returns to20 ⁄25 or better (Klein et al. 1974;


138

Watzke et al. 1974). Only 5% experi-ence severe vision loss (Gass 1967). Ifdetachment persists for more than3 months, photocoagulation or photo-dynamic therapy should be consid-ered.

Counselling

Counselling should suit the conditionand attitude of the individual patient.The interview should use neutralterms to prompt a general account ofthe patients well-being, rather thanleading questions that incorporateterms such as ‘stress’. Sufficient coun-selling to reassure the patient andenable relevant action may followfrom a simple explanation of theassociation between CSC and stress.Controlled trials or case observationson the effect of psychosocial therapyhave not been published.

Adrenergic receptor inhibition

The relation to stress and adrenergichyperactivity has prompted attemptsat systemic treatment of CSC by anti-adrenergic medication. An uncon-trolled case series of patients treatedusing the betaadrenergic inhibitormetoprolol described a promisingcourse in some patients (Avci & Deut-man 2005), but the treatment has notbeen adopted widely. In an uncon-trolled case series of 13 eyes with sub-type-unspecified CSC treated with thebeta-blocker metipranolol, two eyeshad persistent detachment after4 months of treatment (Chrapek et al.2002). Another uncontrolled trialfound no difference in the outcomebetween the non-selective beta-blockermetipranolol and the beta 1-selectiveblocker metoprolol; all patients (21and 30, respectively) experiencedremission within 3 months (Fabianovaet al. 1998). In experimental adren-alin-induced CSC in animals, alpha-adrenergic blockade is more effectivethan beta-blockade (Yoshioka 1991),but sporadic therapeutic tests inhumans have not led to any signifi-cant clinical use of this principle(Heinrich 1974).

Acetazolamide

Systemic acetazolamide treatment pro-motes the resorption of subretinalfluid and case reports suggest that itmay reduce subretinal fluid in CSC(Gonzalez 1992). However, there is no

evidence that treatment promoteshealing of the RPE lesion, long-termpreservation of visual function, or areduced rate of recurrence.

Photocoagulation

Retinal photocoagulation treatmenthas been used for decades in the treat-ment of CSC (Kanagawa & Matsu-bara 1970; Watzke et al. 1974).Photocoagulation accelerates resolu-tion of the detachment (Burumceket al. 1997). A prospective study com-pared eyes with leaks smaller than250 lm in diameter treated by argonlaser photocoagulation, with shamphotocoagulation or photocoagulationaway from the site of leakage(Robertson & Ilstrup 1983). Treat-ment appeared to shorten the dura-tion of detachment by approximately2 months and to reduce recurrenceswithin a follow-up period of18 months from 34% to none. Otherstudies have found no evidence ofeffect on long-term visual acuity orthe prevalence of chronic disease(Ficker et al. 1988; Gilbert et al.1984). The most benefit of treatmentappears to be earlier resolution of dis-ease. A retrospective comparison oftreated versus untreated cases over 11or more years of follow-up found thatsix out of six patients who were trea-ted had no recurrences whereas32 untreated patients had 17 recur-rences (Yap & Robertson 1996).Photocoagulation treatment is oftensuccessful in achieving retinal reat-tachment, but visual acuity failsto recover in about 10% of eyes(Yannuzzi et al. 1992).

A potential benefit of early resolu-tion may be mediated by a lower rateof RPE degeneration in treated eyes(Fuhrmeister 1983). The demonstra-tion that long-standing serous detach-ment is associated with retinalatrophy supports the theory that pho-tocoagulation may benefit visual out-come, given that a low rate ofcomplications can be achieved (Wanget al. 2002). The available data do notenable assessment of the long-termrisk of CNV.

The photocoagulation treatmentstrategy is to apply laser energy so asto obtain a confluent coagulation ofmoderate intensity covering the site ofleakage responsible for the fovealdetachment. Argon laser photocoagu-lation or photocoagulation using

another source of green light shouldbe directed to the site of leakage,using spot sizes of 200 lm diameter,exposure times of 0.2 seconds and alight intensity that enables bleachingwithout whitening of the outer retina(Robertson 1986; Greite & Birngruber1975). When multiple candidatelesions are present, the leakiest oneshould be treated first, provided thatit is not under or very nearly under thefovea. Subfoveal lesions should prob-ably not be photocoagulated becauseit entails a risk of damaging fovealphotoreceptors and of inducing secon-dary subretinal neovascularization.

Unlike treatment of CNV, it doesnot appear that CSC treatment that istoo mild to induce resolution cannot becorrected by a second treatment. Eyesthat have undergone photocoagulationtreatment demonstrate a risk of laterdevelopment of subretinal neovascular-ization, an event that can also occurwithout photocoagulation (Kanyange& De Laey 2002). The more intense thephotocoagulation, the higher is the riskof secondary CNV. The strategydescribed above is easily applicable inacute CSC, whereas identification ofthe site or sites of leakage responsiblefor detachment may be problematic inchronic CSC.

The available evidence suggests thatretinal atrophy can be avoided if reso-lution of detachment can be obtainedwithin 4 months of the onset of symp-toms (Wang et al. 2002). In long-standing serous detachments, theretina may demonstrate pigmentmigration, capillary dilation and capil-lary non-perfusion, to the extent thatatypical CSC has been described aspseudo-retinitis pigmentosa (Gass1977). Because the relation betweenthe onset of detachment and the onsetof symptoms is often uncertain, earliertreatment may be warranted – especi-ally if the presence of subretinal gran-ular deposits suggests that thedetachment has lasted longer than theduration of symptoms (Wang 2005).Further support for early treatmentincludes best-corrected visual acuity20 ⁄ 40 or less and multiple recurrences(Robertson 1986). Complications ofphotocoagulation treatment are rare(Robertson & Ilstrup 1983), but thetreatment should be used with cau-tion. Early photocoagulation may bewarranted by special occupationaldemands for binocular visual function.


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The RPE lesion responsible for sub-retinal fluid accumulation may belocated at a considerable distancefrom the fovea and even along thetemporal vascular arcades (Fig. 8)(Bonamour et al. 1977). A subfoveallocation is seen in 4% of cases (Bon-amour et al. 1977). This is usuallyconsidered a contraindication for pho-tocoagulation, although an anecdotalreport suggests that subfoveal photo-coagulation can be made withoutadverse effects if the fovea is detachedwhen treatment is applied (Gartner1987).

Lack of fluid resorption after pho-tocoagulation should lead to suspicionthat the serous detachment is causedby CNV rather than by CSC. Photo-coagulation in itself may cause dam-age to Bruch’s membrane and lead tothe induction of subretinal neovascu-larization or the development of aclassic CNV component by extensionfrom occult CNV.

A single paper has reported bettervisual outcome in 15 patients treatedby infrared 810 nm photocoagulationthan in 15 patients treated by argon514 nm laser photocoagulation (Ver-ma et al. 2004). However, conclusiveresults have not been produced.

Transpupillary thermotherapy

A small non-randomized study oftranspupillary thermotherapy (TTT)suggests that this treatment may accel-erate the resolution of CSC, but long-term safety and efficacy are notknown (Shukla et al. 2006).

Photodynamic therapy

Verteporfin photodynamic treatment(PDT) of chronic CSC has been des-cribed in uncontrolled case series.Resolution of serous detachment fol-lowed treatment in the majority ofpatients, as did visual improvement.No complications have been reported(Canakis et al. 2003, 2004; Cardilloet al. 2003; Valmaggia & Niederberger2006; Chan et al. 2003a; Yannuzziet al. 2003). PDT being a more recenttherapeutic option, it has been usedmainly in cases where it was thoughtwise to avoid photocoagulationbecause of a juxtafoveal or subfoveallocation of the RPE lesion, lack of aclearly defined leakage hotspot, con-cern about the potential induction ofCNV or suspicion that CNV was

already present. Under these circum-stances, PDT has also been followedby a favourable course in nine casesof acute CSC (Ober et al. 2005). In 18patients with chronic CSC, use ofhalf-dose PDT also appeared to beeffective (Lai et al. 2006); similar find-ings have been reported for themechanistically comparable ICG pho-tothrombosis technique (Costa et al.2002). The use of half-dose verteporfinor 50% reduced light fluence PDT issuggested as a precaution againstpermanent RPE or choriocapillarisdamage.

The treatment of subfoveal CNVsecondary to CSC has never been theobjective of a controlled clinical trial.PDT is widely favoured, by extensionof the experience with AMD-relatedCNV and numerous case reports of afavourable outcome with lasting reso-lution of fluid and visual improvementoften following only a single treatment(Canakis et al. 2003; Chan et al.2003b; Ergun et al. 2004).

A controlled trial of PDT in chro-nic CSC would involve the problemof differentiating chronic CSC alonefrom chronic CSC with occult CNV.ICG angiography may demonstrateCNV in some otherwise questionablecases, but the false-negative diagnosticrate is unknown. The issue is compli-cated because all major studies ofoccult CNV have applied treatmentonly to occult CNV with activity inthe form of subretinal haemorrhage,hard exudate or recent visual loss, therationale being that occult CNV oflesser activity grades cannot reliablybe distinguished from other causes ofsub-RPE hyperfluorescence on fluo-rescein angiography. Resolution ofintraretinal and subretinal fluid afterPDT may be attributable, theoretic-ally, to one or more of the knownconsequences of PDT: choriocapillarisphotothrombosis, RPE damage orCNV closure.

Comments

CSC is the prototype cause of serousretinal detachment involving thefovea. The symptoms of CSC reflectthe loss of contact between the pho-toreceptors and the RPE (a relativescotoma) and the bullous distensionof the foveal retina (metamorphopsiaand micropsia). The serous detach-

ment is secondary to focal lesions andpathological leakage through theRPE. The consequent impairment ofbinocular vision is often the predom-inant symptom.

The observation of foveal photore-ceptor atrophy despite successful reat-tachment after a duration ofsymptoms of approximately 4 monthssuggests that active treatment shouldcommence when the duration exceeds3 months, given that it will take sometime to bring about reattachment.Although the level of evidence for arole of stress is modest, it seems rea-sonable to counsel the patient aboutthe possible association with stressfrom the first visit. The history mustinclude current and past use of gluco-corticoid medication.

If the patient presents evidence ofchronic CSC, despite a short reportedduration of symptoms, it suggests thatasymptomatic detachment may havebeen present for longer than thepatient has been aware. Patients fre-quently overlook symptoms if onlyone eye is involved.

In CSC of recent onset, retinal pho-tocoagulation is usually successful inreducing or eliminating RPE leakageand hence in inducing resolution ofthe serous detachment. The immediatebenefit of treatment is early resolutionof subretinal fluid and, in the longterm, possibly a reduction of recur-rences and RPE degeneration. Photo-coagulation should be used withcaution because it can induce subreti-nal neovascularization, often manyyears after the primary incident.

Chronic CSC, also called diffuseretinal pigment epitheliopathy, pre-sents a more complex pattern of RPEabnormalities. Although severe wide-spread affection of the RPE may beseen early in the course of the disease,it appears to be associated primarilywith unresolving or chronically recur-ring serous retinal detachment.Indeed, irregular RPE hypo- andhyperpigmentation may be the corol-lary of photoreceptor atrophy in chro-nic detachment.

The effect of photocoagulation onchronic CSC is less convincing than inacute CSC. The risk of inducing CNVor, if already present, of inducing con-version to classic CNV of occult CNVmerits consideration of photodynamictherapy. PDT can be repeated inCNV, but repeated PDT is rarely if


140

ever needed in chronic CSC withoutCNV. The long-term efficacy andsafety of PDT in CSC have not beendescribed. Systemic medications haveno clear role in the treatment ofCSC.

Although improved visual acuityand reduction of symptoms, spontane-ously or following treatment, supportsthe theory that subretinal fluid hasbeen resorbed, functional recoverymay be incomplete even in the best ofcases if the detachment was long-standing. Therefore, OCT is an indis-pensable tool for the diagnosis andmanagement of all but the simplestcases of CSC.

The mechanism behind the prefer-ential detachment of the fovea bysubretinal fluid is unknown. Becausethe fovea is thinner than the rest ofthe macula (Fig. 14), higher hydraulicconductivity could render the fovealretina less susceptible to the suctionforce of the RPE and hence moreloosely attached than the surroundingretina.

When detached by CSC, the fovealdepression is often abolished and gen-eral thickening of the detached retinamay be seen (Iida et al. 2000). Thisindicates that the healthy retina ismaintained in a physiologically under-hydrated state by the suction force

generated with RPE pumping of fluidaway from the subretinal space. Theeffect is likely to increase the transpar-ency of the retina, in the same mannerthat the corneal endothelium keepsthe cornea clear (Fig. 14). The loss ofRPE suction in the presence of subfo-veal RPE or CNV may explain whythese conditions can be accompaniedby cystoid foveal oedema, in theabsence of intraretinal vascular leak-age (Iida et al. 2003). Loss of fovealunderhydration has optical effects, asshown by the increased brightness ofthe oedematous retina, presumably aconsequence of increased light scatter(Figs 7, 8 and 10). This phenomenonmust be considered when evaluatingpsychophysical studies of retinal func-tion in CSC because it will reduce per-formance for purely optical reasons,even in the absence of any compro-mise of neuronal function (Springeret al. 2006).

Acknowledgements

This study was supported by the Værnom Synet, Copenhagen, Denmarkand by a Patient-Oriented DiabetesResearch Career Award from theJuvenile Diabetes Research Founda-tion (grant number 8-2002-130).

Financial ⁄proprietaryinterest

The authors or the authors’ institu-tions have been reimbursed for con-sultancy work for manufacturers ofphotocoagulation and photodynamictherapy equipment and medications.

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Received on December 15th, 2006.

Accepted on December 30th, 2006.

Correspondence:

Michael Larsen

Department of Ophthalmology

Glostrup Hospital

DK-2600 Glostrup

Denmark

Tel: +45 4323 4835

Fax: +45 4323 4669

Email: [email protected]


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