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A LONG-TERM FOLLOW-UP STUDY OFSEVERE VARIANT OF CENTRAL SEROUSCHORIORETINOPATHYSANAE OTSUKA, MD, NORIO OHBA, MD, PHD, KUMIKO NAKAO, MD, PHD

Purpose: To facilitate understanding of the long-term course and visual outcome of a

severe variant of central serous chorioretinopathy.

Design: Consecutive observational case series.

Patients and Methods: The authors reviewed 25 patients with multifocal posterior

pigment epitheliopathy and bullous retinal detachment, who had a mean follow-up time of

10.6 years (range, 622 years), with reference to the demographic feature, fundus

changes, recurrence, and final anatomic and visual outcome. Two patients underwent

optical coherence tomography.

Results: The patients were 21 men and 4 women, with a mean age at disease onset of

43.1 years (range, 3063 years). Twenty-one patients were otherwise healthy, and four

developed ocular disease during systemic corticosteroid therapy for metabolic or autoim-

mune diseases including systemic lupus erythematosus. The disease was bilateral in 21

patients (84%). Nine patients (36%) presented initially with classic central serous chori-

oretinopathy, followed by its severe variant 7 months to 9 years later. Active disease was

characterized by multifocal exudative lesions in the posterior pole and bullous retinal

detachment with shifting subretinal fluid in the inferior periphery. Optical coherence to-

mography of exudative lesions disclosed cloudy and fibrinous subretinal fluid. The exu-

dative lesions were self-limited or responded to photocoagulation. During the follow-upperiod, 13 patients (52%) showed 1 to 5 recurrent disease, but the disease eventually

became quiescent with multifocal atrophic scars in the posterior pole with or without

atrophic tracts in the inferior periphery. Final best-corrected visual acuity was 20/20 or

better in 24 of 46 affected eyes (52%) of 25 patients and 20/40 or better in 37 eyes (80.4%).

Conclusions: A severe variant of central serous chorioretinopathy characterized by

multifocal posterior exudations and bullous inferior retinal detachment with shifting sub-

retinal fluid may affect otherwise healthy, middle-aged males or individuals receiving

systemic corticosteroid therapy for metabolic or autoimmune diseases. Exudative chori-

oretinal lesions are self-limited or respond to photocoagulation. Recurrence is common,

but the disease eventually becomes quiescent with favorable visual acuity unless the

macula is damaged.

RETINA 22:2532, 2002

Central serous chorioretinopathy (CSC) is a well-defined condition that has a long history of clin-

ical investigations. In early 1970s to mid-1980s,

a number of cases presenting with multifocal exuda-

tive lesions in the posterior pole and nonrhegmatog-

enous retinal detachment with shifting subretinal fluid

were described with various diagnostic nomencla-

tures, including bullous retinal detachment, peculiar

type of secondary retinal detachment, multifocal se-

rous choroidopathy, multifocal posterior pigment epi-

theliopathy, and peripheral retinal detachment with

retinal pigment epithelial atrophic tract.112 Further

From the Department of Ophthalmology, Kagoshima UniversityFaculty of Medicine, Kagoshima-shi, Japan.

The authors have no proprietary interest in this study.Reprint requests: Norio Ohba, MD, Department of Ophthalmology,

Kagoshima University Faculty of Medicine, Sakuragaoka 8-35-1,Kagoshima-shi 890-8521, Japan; e-mail: [email protected]

25

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studies have defined the clinical characteristics of thedisease and led to a view that it is a severe variant or

atypical form of CSC, rather than a distinct clinicalentity.1316 However, little information is availableregarding the long-term course of the severe variant ofCSC. We review 25 such cases with a mean follow-uptime of 10.6 years and report the ultimate visual and

anatomic outcome of severe CSC.

Patients and Methods

We reviewed clinical records of patients with cen-tral serous chorioretinopathy (CSC) between 1978 and

2000 in the Kagoshima University Hospital, and se-lected cases of a severe form of CSC featured bymultifocal exudative lesions in the posterior pole andnonrhegmatogenous peripheral retinal detachmentwith shifting subretinal fluid. We studied 25 patients

with severe CSC who were followed up for more than6 years and reviewed the clinical records with refer-ence to sex, age at onset, medical history, clinicalfeature, treatment, and follow-up results. Routine ex-

aminations included visual acuity test, contact lensbiomicroscopy, indirect binocular ophthalmoscopy,

andfluorescein angiography. In addition, two patientswere examined by optical coherence tomography. Forreference, demographic data of 445 patients with clas-sic CSC who were seen during the same study periodwere also reviewed.

Results

Table 1 summarizes the clinical characteristics of25 patients with severe variant CSC. They were 21men and 4 women with an age at disease onset of 30

to 63 years (mean, 43.1 years). The male/female ratio(21/4) was comparable with that of 445 referentialpatients with classic CSC. The disease affected botheyes in 21 cases (84%); this bilateral involvement ofsevere variant CSC was significantly more frequent

than that of classic CSC33 of 445 patients (7.4%)with classic CSC having bilateral disease.

As the initial presentation, 16 cases (64%) showedmultifocal exudative lesions in the posterior pole with

Table 1. Clinical Information of 25 Patients With Severe Variant Idiopathic Central Serous Chorioretinopathy

Case

No. Sex

Age at

onset, yr

Eyes

affected

Classic

ICSC at

onset? Treatment Recurrence?

Follow-up,

yr

Findings at Final Examination

Best-Corrected VA Fundus Abnormalities

1 M 37 Bilateral Yes LPC (single) No 16 RE: 20/400; LE: 20/28

Macular atrophy, peripheral

mottling

2 M 54 Unilateral No LPC (single) No 9 RE: 20/20 (LE: normal) Inferior tract atrophy

3 M 31 Bilateral Yes LPC (repeat) Yes 22 RE: 20/25; LE: 20/12.5 Multiple atrophic scars

4 M 50 Bilateral No LPC (repeat) Yes 12 RE: 20/220; LE: 20/50

Macular atrophy, posterior

scars

5 F 51 Bilateral No LPC (single) No 14 RE: 20/220; LE: 20/220

Multifocal scars, inferior

tract atrophy

6 M 46 Bilateral Yes LPC (repeat) Yes 13 RE: 20/16; LE: 20/16 Multiple posterior scars

7 M 39 Unilateral No LPC (single) No 12 RE: 20/16 (LE: normal) Multiple posterior scars

8 M 38 Bilateral Yes No Yes 12 RE: 20/400; LE: 20/16 Inferior tract atrophy

9 M 43 Bilateral No No Yes 9 RE: 20/20; LE: 20/100 Multiple posterior scars

10 M 51 Bilateral No No No 9 RE: 20/20; LE: 20/25 Inferior tract atrophy

11 M 38 Bilateral No LPC (repeat) No 9 RE: 20/12.5; LE: 20/16 Inferior tract atrophy

12 M 38 Bilateral No LPC (repeat) Yes 8 RE: 20/400; LE: 20/100 Macular atrophy

13 M 39 Bilateral No LPC (single) No 8 RE: 20/16; LE: 20/12.5 Multiple posterior scars

14 M 45 Bilateral Yes LPC (single) No 17 RE: 20/28; LE: 20/16 Multiple posterior scars15 F 34 Bilateral Yes LPC (single) No 7 RE: 20/33; LE: 20/20 Multiple posterior scars

16 M 36 Bilateral No LPC (repeat) No 6 RE: 20/16; LE: 20/12.5 Multiple posterior scars

17 M 56 Bilateral No LPC (repeat) Yes 7 RE: 20/16; LE: 20/33 Multiple posterior scars

18 M 37 Unilateral No No Yes 8 RE: 20/16; LE: 20/16 Inferior tract atrophy

19 M 40 Bilateral Yes No Yes 9 (RE: normal) LE: 20/220 Multiple posterior scars

20 F 63 Bilateral No LPC (single) No 7 RE: 20/100; LE: 20/16 Peripapillary atrophy

21 M 56 Unilateral No No No 7 LE: 20/200 (RE: normal) Macular atrophy

22 F 49 Bilateral Yes LPC (repeat) Yes 7 RE: 20/28; LE: 20/20 Multiple posterior scars

23 M 30 Bilateral No LPC (repeat) Yes 11 RE: 20/16; LE: 20/16 Inferior tract atrophy

24 M 36 Bilateral Yes No Yes 6 RE: 20/12.5; LE: 20/25 Multiple posterior scars

25 M 41 Bilateral No No Yes 20 RE: 20/200; LE: 20/16 Macular atrophy

VA, visual acuity; LPC, laser photocoagulation; RE, right eye; LE, left eye.

26 RETINA, THE JOURNAL OF RETINAL AND VITREOUS DISEASES 2002 VOLUME 22 NUMBER 1

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peripheral retinal detachment. Nine cases (36%) pre-sented initially with features of classic CSC, followed

by development of severe CSC 7 months to 9 yearslater; 6 of these had severe CSC in association with

systemic corticosteroid therapy for the initial disease.With regard to medical history, 21 cases (84%)were otherwise healthy. The remaining 4 cases (16%)

developed severe variant CSC during systemic corti-costeroid therapy for systemic disorders, includingsystemic lupus erythematosus, renal insufficiency, andrheumatoid arthritis. There was no difference in theocular signs and symptoms between the idiopathic

cases and those with systemic disorder.Biomicroscopy and ophthalmoscopy during the ac-

tive phase revealed multiple focal lesions in the pos-terior pole, characterized by doughnut-shaped, 0.5- to

2-disk diameter, yellowwhite exudative retinalchanges. Bullous retinal detachment was invariable in

the inferior periphery, characterized by accumulationof subretinal fluid shifting towards the posterior pole

on a supine position. Fluorescein angiography of pos-terior exudative lesions disclosed early hyperfluores-cent foci due to marked dye leakage from the choroid,

followed by its extension and later staining of thesurrounding retina (Figures 1 through 3). Optical co-herence tomography through the exudative lesionsdemonstrated a domelike detachment of thickenedneurosensory retina and semitransparent subretinal

space due to light reflections from fibrinous contents(Figure 4).

Of 46 affected eyes of 25 cases, 14 eyes of 8 casesshowed spontaneous regression of exudative lesions

Fig. 1. Case 1 (in Table 1).A (right eye), Fundus photograph taken on

the initial presentation at age 37 years, illustrating a serous retinal de-tachment in the macula. B (right eye), Seven months after presentation,the patient presented with severe visual loss and superior field defectbecause of multifocal exudative lesions in the posterior pole and bullousretinal detachment in the inferior quadrants. This photograph was taken afew days after photocoagulation therapy. C (right eye) and D (left eye),

At age 53 years, 16 years after disease onset. Fundus photographs show focal chorioretinal atrophies with photocoagulation-induced pigmentproliferation in the posterior fundus.

27FOLLOW-UP STUDY OF CENTRAL SEROUS CHORIORETINOPATHY OTSUKA ET AL

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and reattachment of the inferior retina in a few

months. Thirty-two eyes of 17 cases underwent argon-laser photocoagulation to the exudative lesionssin-

gle procedure in 8 cases and repeat in 9 casesandthey showed resolution of choroidal exudations within1 to 2 months.

Recurrence of severe CSC was not uncommon.During a mean follow-up of 10.6 years (range, 6 22years), 13 cases (52%) had recurrence: one recurrencein 8 cases, 2 recurrences in 3 cases, and 3 to 5recurrences in 2 cases. The interval between recur-

rences ranged from 6 months to 11 years (mean of allrecurrences, 4.7 years).

Recurrence was common, but the disease eventu-ally became quiescent with multifocal atrophic scars.

Five patients had atrophic tracts in the inferior periph-ery. Thefinal best-corrected visual acuity in a total of46 affected eyes of 25 patients was 20/20 or better in24 eyes (52%) and 20/40 or better in 37 (80.4%) eyes.Four of the 46 affected eyes (8.7%) had poor visual

acuity results of 20/200 or less because of macular

atrophies. Figure 5 compares the best-corrected visualacuity between the active and convalescent phase ofthe disease, illustrating that the ultimate visual out-

come is similar between cases with and without pho-tocoagulation therapy.

Selected Case Reports

Case 1

A previously healthy 37-year-old man presented with mild

blurred vision in the right eye (Table 1). Best-corrected visual

acuity was 20/25 in the right eye and 20/12.5 in the left eye.Anterior segments and media were unremarkable. Ophthalmo-

scopic examination of the right eye revealed a round area of serous

retinal detachment in the macula that was compatible with classic

CSC (Figure 1A). Seven months later, he reported severe visual

loss in the right eye and upper visual field loss in both eyes, with

best-corrected visual acuity of 20/1000 in the right eye and 20/12.5

in the left. Ophthalmoscopic examination disclosed in both eyes

yellowish, discrete, exudative lesions of approximately 1 disk

diameter in the posterior pole and bullous retinal detachment in the

inferior peripheral fundus; the subretinal fluid shifted towards the

posterior pole on a supine position. Fluorescein angiography re-

vealed early hyperfluorescent leakage foci from the choroid, which

increased in intensity and size in the late phase of angiography.

Argon-laser photocoagulation was given to the exudative lesions

(Figure 1B), which resolved the posterior exudations in 1 month.The patient was observed for the subsequent 16 years with no

further recurrence. On the last examination at age 53 years, oph-

thalmoscopy of the right eye demonstrated several atrophic scars in

the posterior fundus and mottled appearance in the inferior periph-

eral fundus (Figure 1C), with best-visual acuity of 20/400 because

of macular atrophy. Ophthalmoscopy of the left eye disclosed a

3-disk diameter atrophic scar in the posterior pole that spared the

fovea, with best-corrected visual acuity of 20/28 (Figure 1D).

Case 3

A 31-year-old manfirst noted central visual loss of the right eye

and was diagnosed with classic CSC, which resolved in response to

argon-laser photocoagulation (Table 1). Five years later at age 36years, he had a recurrent episode in the same eye that resolved

spontaneously. At age 39 years, he again felt an acute blurring in

the right eye, with best-corrected visual acuity of 20/28 in the right

eye and 20/16 in the left. Visual field test revealed superior field

defect in the right eye. Ophthalmoscopy of the right eye revealed

multiple, yellowish, doughnut-shaped exudative lesions of a vari-

able size in the posterior pole and shallow inferior peripheral

retinal detachment accompanied by numerous yellow subretinal

deposits (Figure 2A). Fluorescein angiography of the right eye

disclosed intense subretinal leakage in areas corresponding to

exudative lesions. The asymptomatic left eye showed mild oph-

thalmoscopic and fluorescein angiographic abnormalities. Laser

photocoagulations to the exudative lesions resolved the posterior

Fig. 2. Case 3.A,Fundus photograph of recurrent disease 8 years afterdisease onset, illustrating multifocal exudative lesions of variable sizein the posterior pole and shallow retinal detachment with numeroussubretinal yellow deposits in the inferior periphery. B, Fundus photo-graph taken 22 years after disease onset, illustrating chorioretinal

atrophic scars in the posterior pole.


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Fig. 3. Case 16.A (right eye),Fundus photograph taken at an aggravatedcondition following systemic corticosteroid therapy, illustrating multipleexudative lesions in the posterior pole and extensive bullous retinaldetachment accompanied with choroidal detachment in the periphery. B(right eye),Fluorescein angiogram, showing several leakage points in the

posterior pole. C (left eye), Fundus photograph taken on the same day asphotograph A, demonstrating multiple exudative lesions sparing the mac-

ula.D (right eye) and E (left eye), Fundus photographs taken 6 years after disease onset, illustrating a complete resolution of exudative lesions withretention of multiple chorioretinal atrophic scars.


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lesions and the inferior retinal detachment in 2 months, with return

to nearly normal visual acuity. Four years later, the patient reported

acute blurred vision in the right eye, with best-corrected visual

acuity of 20/40 in the right eye and 20/12.5 in the left. The right eye

had serous retinal detachment in the posterior pole associated with

de novo focal exudative lesions that subsided spontaneously in 3

months, with visual acuity improvement to 20/25. At age 48 years,the patient had recurrence that resolved spontaneously in 2 months.

A subsequent follow-up showed no further recurrence disease. At

age 54 years, best-corrected visual acuity was 20/25 for the right

eye and 20/12.5 for the left. The fundus of both eyes had multiple

chorioretinal atrophic scars in the posterior pole and diffuse mot-

tled appearance in the inferior periphery (Figure 2B).

Case 16

A 40-year-old man with a short history of blurred vision at age

36 years presented with acute mild visual loss in the right eye.

Best-corrected visual acuity was 20/33 in the right eye and 20/16 in

the left (Table 1). Contact lens biomicroscopy and ophthalmoscopy

of the right eye disclosed multifocal exudative lesions in the

posterior pole and nonrhegmatogenous retinal detachment with

shifting subretinal fluid in the inferior periphery. The patient was

treated with a large dose of oral prednisolone tapered over 2

months, which aggravated the condition so that peripheral retinal

detachment became more bullous and accompanied with choroidal

detachment (Figure 3A). Fluorescein angiography was compatiblewith multifocal posterior pigment epitheliopathy (Figure 3B). The

left eye had several focal exudative lesions in the posterior pole,

but not inferior retinal or choroidal detachment, with normal visual

acuity because the macula was spared (Figure 3C). Repeated ses-

sions of argon-laser photocoagulation on the posterior exudative

lesions led to a slow resolution of the retinal and choroidal detach-

ment. The patient was observed for the next 6 years, during which

no recurrence occurred. At the last examination, best-corrected

visual acuity was 20/16 in the right eye and 20/12.5 in the left. Both

eyes had multiple atrophic scars in the posterior pole and mottled

appearance of the periphery due to atrophy of the retinal pigment

epithelium (Figure 3, D and E).

Fig. 4. Case 22. A, Ophthalmoscopic features of a doughnut-shapedfocal lesion with yellow-appearing exudation with central dark red re-gion. The straight line indicates 5-mm length area scanned by opticalcoherence tomography. B, Early phase of fluorescein angiogram, illus-

trating a leakage point of a major lesion from the choroid (arrow) and twoother minor lesions. C, Late phase offluorescein angiogram, illustrating

multifocal areas of intensefluorescein dye staining.D,Cross-sectional scan through the exudative lesion by optical coherence tomography, illustratingdetachment of thickened retina with cloudy subretinal space underneath an ophthalmoscopically yellow area and an optically clear subretinal spacecorresponding to a dark brown leakage area.


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Discussion

These results elucidate the clinical picture, demo-graphic feature, and long-term course of the severe

variant of CSC. During the active stage of the disease,ophthalmoscopic findings are characterized by multi-focal exudative lesions in the posterior pole and infe-rior retinal detachment with shifting subretinal fluid,and the fluorescein angiographic findings by intense

focal dye leakage from the choroid. The typical le-sions appear doughnut shaped with a dark browncentral area surrounded by yellowish turbid exu-dates.116 The optical coherence tomograms in our twopatients showed that the yellow-appearing focal exu-dates are optically cloudy. This new observation is

distinct from optical coherence tomograms of classic

CSC, in which the posterior retinal detachment areacontains optically clear, serous subretinal fluid.17,18

Thus, intense subretinal fluid accumulation of morefibrinous, weighty contents is likely to cause bullous

inferior retinal detachment with moveable subretinalfluid.

The severe variant or atypical presentation isthought to belong to the exaggerated end of the spec-trum of CSC.7,13 The condition affects predominantly

middle-aged males.116 In our case series, the meanage at onset was 43.5 years, and the male-to-femaleratio was 5.3, similar to our referential data of 445

patients with classic CSC. The ratio of bilateral/uni-lateral involvement 21/4 in our series is in agreementwith 17/1 and 28/9 in previous reports of severe vari-ant CSC.10,13 Thus, severe CSC is predominantly bi-lateral, in contrast to classic CSC, as our referential

data showed that 33 of 445 patients (7.4%) with

classic CSC were bilateral.Limited information is available about the long-

term course of the severe variant CSC. The severecondition may occur from the beginning or may fol-

low classic CSC. In our case series, 9 of 25 cases(36%) presented initially with features of classic CSC,followed by manifestation of multifocal posterior pig-ment epitheliopathy and inferior bullous retinal de-tachment 7 months to 9 years later. The multifocal,

exudative lesions are apparently self-limited or rapidlyresolve in response to photocoagulation, but recur-rence is not uncommon.13 In this long-term follow-up

study (mean, 10.6 years; range, 6 22 years), 13 of 25cases (52%) showed recurrences months to years after

complete regression. The number of recurrences wasvariable up to five times, and the longest intervalbetween recurrences was 11 years.

Recurrence of the severe variant CSC is common,but the disease eventually becomes quiescent, with

multifocal atrophic scars with or without peripheralretinal atrophic tract. The ultimate visual outcome isfavorable unless the macula is involved. Argon-laserphotocoagulation to active focal lesions has been rec-ommended for its rapid resolution.10,13 We performed

argon-laser photocoagulation in 17 of 25 cases andconfirmed its efficacy. It is, however, remarkable thatthe ultimate visual results were comparable betweenthe eyes with and without photocoagulation therapy.Similar results have been reported previously.14 A

randomized control study with long-term follow-up isneeded to determine if photocoagulation treatmentconfers any advantage.

The severe variant of CSC is composed of twoetiologically distinct types. One type affects otherwise

healthy adults with a yet-undefined underlying causethat is probably similar to classic CSC. The other type

is involved by systemic corticosteroid therapy formetabolic or autoimmune disorders such as systemiclupus erythematosus, sarcoidosis, multiple myositis,

and by corticosteroid therapy following renal trans-plantation.2,13,1921 A number of cases of corticoste-roid-induced severe variant CSC have been reportedin recent years, in which classic CSC is aggravated tosevere CSC after inappropriate systemic corticosteroid

therapy.3,4,13,18,19 This was also seen in our case series.Lastly, although the severe variant of CSC is prob-

ably rare as compared with classic CSC, reports fromAsian countries, particularly Japan,1,3,4,7,10,1216,18 out-

Fig. 5. Best-corrected visual acuity in 46 eyes of 25 cases of severe

variant of central serous chorioretinopathy, measured at the exudativephase (abscissa) and at the final examination (ordinate). White circlesrepresent 32 eyes of 17 cases undergoing argon-laser photocoagulation,and closed circles 14 eyes of 8 cases without photocoagulation.


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number those from the Western world. Whether thesevere variant of CSC has ethnic predilection remainsto be elucidated.

Acknowledgement

The authors thank Dr. Takashi Mizushima for technicalassistance in optical coherence tomography.

Key words: central serous chorioretinopathy, se-vere variant, long-term outcome, optical coherencetomography.

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