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Background: Central serous chorioretinopathy (CSCR) is a disease in which aserous detachment of the neurosensory retina occurs over an area of leakagefrom the choriocapillaris through the retinal pigment epithelium (RPE). Othercauses for RPE leaks such as choroidal neovasculari!ation inflammation ortumors should "e ruled out to make the diagnosis.

CSCR may "e divided into # distinct clinical presentations. Classically CSCR iscaused "y one or more discrete isolated leaks at the level of the RPE as seen onfluorescein angiography ($%). &owever it is now recogni!ed that CSCR maypresent with diffuse retinal pigment epithelial dysfunction (eg diffuse retinalpigment epitheliopathy chronic CSCR decompensated RPE) characteri!ed "yneurosensory retinal detachment overlying areas of RPE atrophy and pigmentmottling. 'uring $% "road areas of granular hyperfluorescence that contain oneor many su"tle leaks are seen.

Pathophysiology: Previous hypotheses for the pathophysiology have included

a"normal ion transport across the RPE and focal choroidal vasculopathy. headvent of indocyanine green (C*) angiography has highlighted the importanceof the choroidal circulation to the pathogenesis of CSCR. C* angiography hasdemonstrated "oth multifocal choroidal hyperpermea"ility and hypofluorescentareas suggestive of focal choroidal vascular compromise. Some investigators"elieve that initial choroidal vascular compromise su"se+uently leads tosecondary dysfunction of the overlying RPE.

Recent studies employing multifocal electroretinography have demonstrated"ilateral diffuse retinal dysfunction even when CSCR was active only in one eye.hese studies support the "elief of diffuse systemic effect on the choroidal

vasculature.

ype % personalities and systemic hypertension may "e associated with CSCR.he pathogenesis here is thought to "e elevated circulating cortisol andepinephrine which affect the autoregulation of the choroidal circulation.

Mortality/Morbidity: Serous retinal detachments typically resolve spontaneouslyin most patients with the vast ma,ority of patients (-/01) returning to #2#3 or"etter vision. Even with return of good central visual acuity many of thesepatients still notice dyschromatopsia loss of contrast sensitivitymetamorphopsia or rarely nyctalopia.

Patients with classic CSCR (characteri!ed "y focal leaks) have a 4/31

risk of recurrence in the same eye.

Risk of choroidal neovasculari!ation from previous CSCR is considered

small (531) "ut has an increasing fre+uency in older patients diagnosedwith CSCR.

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% su"set of patients (3/61) may fail to recover #27 or "etter visual

acuity. hese patients often have recurrent or chronic serous retinaldetachments resulting in progressive RPE atrophy and permanent visualloss to #2# or worse. he final clinical picture represents diffuse retinalpigment epitheliopathy.

Race: CSCR appears uncommon among %frican %mericans "ut may "eparticularly severe among &ispanics and %sians.

Sex: Classically CSCR is most common in male patients aged #/33 years withtype % personality. his condition affects men 8/6 times more often than itaffects women.

Age: Recent reports have descri"ed patients with later age of onset (93 y). $orinstance Spaide et al reviewed 67 consecutive patients with CSCR and foundthe age range at first diagnosis to "e ##.#/-#.0 years with a mean age of 40.-

years.

Changes in the presentation and demographics of CSCR are o"served

with increasing age at first diagnosis. Classically patients tend to "e maleand present with focal isolated RPE leaks in one eye.

Patients diagnosed at 3 years or older are found to have "ilateraldisease demonstrate a decreased male predominance (#.8:6) and showmore diffuse RPE changes. $urthermore these patients are more likely tohave systemic hypertension or a history of corticosteroid use.

History:

Patients typically present with acute symptoms of visual loss and

metamorphopsia (especially micropsia). Other symptoms includedecreased central vision and a positive scotoma.

he decreased vision usually is improved "y a small hyperopic correction.

Other clinical signs include a delayed retinal recovery time following

photostress loss of color saturation and loss of contrast sensitivity.

Physical:

Clinical e;am shows a serous retinal detachment "ut no su"retinal "lood.he neurosensory retinal detachment may "e very su"tle re+uiringcontact lens e;am for detection.

Pigment epithelial detachments RPE mottling and atrophy su"retinal

fi"rin and rarely su"retinal lipid also may "e seen.

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Causes: Previous hypotheses for the pathophysiology have included a"normalion transport across the RPE and focal choroidal vasculopathy. he advent ofC* angiography has highlighted the importance of the choroidal circulation tothe pathogenesis of CSCR.

C* angiography has demonstrated "oth multifocal choroidalhyperpermea"ility and hypofluorescent areas suggestive of focal choroidalvascular compromise. Some investigators "elieve that initial choroidalvascular compromise su"se+uently leads to secondary dysfunction of theoverlying RPE.

Recent studies employing multifocal electroretinography have

demonstrated "ilateral diffuse retinal dysfunction even when CSCR wasactive only in one eye. his supports the "elief of diffuse systemic effecton the choroidal vasculature.

Systemic associations of CSCR include organ transplantation e;ogenoussteroid use endogenous hypercortisolism (Cushing syndrome) systemichypertension systemic lupus erythematosus pregnancy and use ofpsychopharmacologic medications.

$inally type % personalities and systemic hypertension may "e associated

with CSCR presuma"ly "ecause of elevated circulating cortisol andepinephrine which affect the autoregulation of the choroidal circulation

Lab Studies:

ultiple patches of

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hyperfluorescence presuma"ly are due to choroidal hyperpermea"ilitywhich in later phases results in silhouetting or negative staining of largerchoroidal vessels.

Medical Care: Efficacy of tran+uili!ers or "eta/"lockers is unknown.

$urthermore a recent evaluation of #7 consecutive patients with CSCR foundthat use of psychopharmacologic agents (eg an;iolytics antidepressants) was arisk factor for CSCR. ?se of corticosteroids in the treatment of CSCR should "eavoided "ecause it may result in e;acer"ation of serous detachments alreadypresent.

Surgical Care:

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>ost patients receive follow/up care for # months to determine whether

the fluid resolves spontaneously.

Co!plications:

% small minority of patients develops choroidal neovasculari!ation at thesite of leakage and laser treatments. % retrospective review of casesshows that one half of these patients may have had signs of occultchoroidal neovasculari!ation at the time of treatment. n the other patientsthe risk of choroidal neovasculari!ation may have "een increased "y thelaser treatment.

%cute "ullous retinal detachment may occur in otherwise healthy patientswith CSCR. his appearance may mimic @ogt/Boyanagi/&arada diseaserhegmatogenous retinal detachment or uveal effusion. % case report alsohas implicated the use of corticosteroids in CSCR as a factor increasing

the likelihood of su"retinal fi"rin formation. Reducing the corticosteroiddose fre+uently will lead to resolution of the serous retinal detachment.

Prognosis:

Serous retinal detachments typically resolve spontaneously in mostpatients with the vast ma,ority of patients (-/01) returning to #2#3 or"etter vision.

Patients with classic CSCR (characteri!ed "y focal leaks) have a 4/31

risk of recurrence in the same eye.

Even with return of good central visual acuity many of these patients still

notice dyschromatopsia loss of contrast sensitivity metamorphopsia ornyctalopia.

% su"set of patients (3/61) may fail to recover #27 or "etter visualacuity. hese patients often have recurrent or chronic serous retinaldetachments resulting in progressive RPE atrophy and permanent visualloss to #2# or worse. he final clinical picture represents diffuse retinalpigment epitheliopathy.

Risk of choroidal neovasculari!ation from previous CSCR is consideredsmall (531) "ut has an increasing fre+uency in older patients diagnosedwith CSCR.

Patient %ducation:

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f possi"le patients should avoid stressful situations. Patient participation

in stress/reducing activities (eg e;ercise meditation yoga) isrecommended.

Recent evidence associates systemic hypertension with CSCR "ut it is

unknown as to whether careful control of systemic hypertension willreduce the incidence of CSCR.

Caption:Picture 6. $luorescein angiography in the early recirculation phase of apatient with a locali!ed neurosensory detachment in the macula from central serouschorioretinopathy. ote the focal hyperfluorescence.

@iew $ull Si!e mage

e>edicine Doom @iew(nteractive)

Picture &ype:Photo

Caption:Picture #. $luorescein angiography in the late recirculation phase of thesame patient. ote the distri"ution of leakage of fluorescein dye within theneurosensory detachment.

pertengahan dan mungkin berkaitan dengan kejadian-kejadian stres kehidupan. Sebagian besar pasiendatang dengan penglihatan kabur, mikropsia, metamorfosia, dan skotoma sentralis yang timbulmendadak. Ketajaman penglihatan sering hanya berkurang secara sedang dan dapat diperbaikimendekati normal dengan koreksi hi-peropik kecil.Diagnosis ditegakkan dengan pemeriksaan fundus denganslitlamp\ adanya pelepasan serosa retinasensorik tanpa peradangan mata, neovaskularisasi retina, suatu lubang kecil optik, atau tumor koroid

bersifat diagnostik. Lesi epitel pigmen retina tampak sebagai bercak abu-abu kekuningan, bundar atauoval, kecil yang ukurannya bervariasi dan mungkin sulit dideteksi tanpa bantuan angiografifluoresens. Zat arna fluoresens yang bocor dari koriokapilaris dapat tertimbun di baah epitel pig-

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men atau retina sensorik, sehingga menimbulkan berma-cam-macam pola termasuk konfigurasicerobong asap yang terkenal itu.Sekitar !"# mata dengan korioretinopati serosa sentralis mengalami resorpsi spontan cairan subretinadan pemulihan ketajaman penglihatan normal dalam $ bulan setelah aitan gejala. %amun, alaupunketajaman penglihatan normal, banyak pasien mengalami defek penglihatan permanen, misalnya

penurunan ketajaman kepekaan terhadap arna, mikropsia, atau skotoma rela-tif. Duapuluh sampai &"

persen akan mengalami sekali atau lebih kekambuhan penyakit, dan pepiah dilaporkan adanyapenyulit'termasuk neovaskularisasi subretina dan edema makula sistoid kronik'pada pasien yangsering dan berkepanjangan mengalami pelepasan serosa.'a!bar ()*+,%ngiogram fluoresens korioretinopati sentralis memperlihatkan penyakit aktif dengan epitel pigmenretina (tanda panah kecil) dan pelepasan i sensorik (tanda panah "esar). Fuga terdapat dua fokus penyaG.H kitinaktif (tanda panah ter"uka).

(enyebab korioretinopati serosa sentralis tidak i ketahui) tidak terdapat bukti yang meyakinkan bahv*

penyakit bersifat infeksiosa atau disebabkan oleh distrg+ j epitel pigmen retina. otokoagulasi laser

argon yal diarahkan ke bagian yang bocor akan secara bermakn& mempersingkat durasi pelepasan

retina sensorik da+ mempercepat pemulihan penglihatan sentral, tetapi tidak terdapat bukti baha

fotokoagulasi yang segeja dilakukan akan menurunkan kemungkinan gangguan penglihatan

permanen. /alaupun penyulit fotokoagulasi laser retina sedikit, terapi fotokoagulasi laser segera

sebaiknya tidak dianjurkan untuk semua pasien kon0 retinopati serosa sentralis. Lama dan letak

penyakit* keadaan mata yang lain, dan kebutuhan visual oku-pasional merupakan faktor-faktor yang

perlu dipertim-bangkan dalam memutuskan pengobatan.