1. Central Serous Chorioretinopathy
여의도 성모병원
박 영 근

2. M/62 백○호 2008.5.30 P.I ) blurred vision (OD) for 1 yr Past Hx.)
DM/HBP(-/-)
Ocular op/trauma (-/-)
Eyedrop(-)
Medication (-)
VA OD 0.32(1.0 x +1.50Ds)
OS 0.5 (1.0 x +1.75Ds : -0.50Dc Ax 100)
MR OD +1.50Ds
OS +1.75Ds -0.50Dc Ax 99
IOP 17/16 mmHg
Amsler grid: OD metamorphopsia(+)
정부용

4. M-OCT

5. FAG

6. Differential diagnosis
Imp: R/O Chronic CSC(OD) -> P) FRP(OD)
Differential diagnosis
1. Age related macular degeneration 2. Polypoid choroidal vasculopathy 3. Infectious and inflammatory disorders : serous macular detach presumed ocular histoplasmosis syndrome(POHS), Harada’s disease, posterior scleritis, sympathetic ophthalmia, idiopathic uveal effusion syndrome 4. Tumor choroidal melanoma, choroidal hemangioma, choroidal metastasis, choroidal osteoma, leukemic choroidal infiltrates 5. Vascular disorders SLE, polyarteritis nodosa, scleroderma, dermatomyositis, relapsing polychondritis, malignant hypertension, toxemia of pregnancy, DIC
ARMD 50세 이상에서 꼭 구분이 필요. CSC 에서 more diffuse RPE damage, multifocal areas of leakage, subretinal deposits of fibrin and lipids , FA 에서 CSC 는 well-defined pinpoint leakage 관찰 , ARMD 는 well-defined CNV 관찰
PCV: 구분하는데 ICG 필요 a small-caliber vascular network terminating in multiple, polypoidal lesions.

7. F/U (2008.7.7) VA 0.25 IOP: 9 mmHg /OD Plan) 1m F/U POD #1mo.
SSRD – Dec.
FAG leaking(-)

8. F/U (2008.8.6) VA 0.32 IOP: 13 mmHg AC : deep & cell(-) Fd : SSRD (-)
Plan) 4m f/u
Fds SSRD(-)

9. F/U ( )
VA 0.08
IOP: 16mmHg

10. F/U M-OCT

11. FAG

12. F/U 3 months later (2010.9.14) VA 0.08 IOP: 13 mmHg
AC : deep & cell(-)
Fd : nl optic disc c SSRD(+)
/OD
Plan) Intravit. Avastin inj.(OD)

13. F/U 2 months later 2008.6 FRP(OD)
ST. Avastin inj.(OD)
VA 0.16
Plan) F/U 6mo. later

15. Central Serous Chorioretinopathy
Accumulation of transparent fluid at the posterior pole of the fundus
1. Typical CSC: young patients
acute localized detachment of the retina
mild to moderate loss of visual acuity
one or a few focal leaks (FAG)
2. Chronic CSC: diffuse retinal pigment epitheliopathy
chronic corticosteroid usage
3. Bullous RD: after organ transplantation using corticosteroids

16. Central Serous Chorioretinopathy
Pathogenesis
1. Choroidal hyperpermeability
2. Impaired RPE function
Choroidal hyperpermeability
RPE pump decompensation
RPE defect
Neurosensory retinal detach

17. Pathophysiology 1. choroid dysfunction theory
choroidal hyperpermeability  causes serous detachments of the RPE  induce a rip or decompensation of the RPE.  RPE leakage (diffusion of water, electrolytes, and proteins)  a neurosensory retinal detachment.
Alterations in choroidal circulation may also cause choroidal ischemia.

18. Pathophysiology 2. RPE dysfunction theory
either a few impaired RPE cells or even a single RPE cell
 a reverse in fluid movement in a chorioretinal direction.
 leakage of fluid in the subretinal space
 development of a neurosensory retinal detachment.
focal damage to the RPE can reverse the direction of ion secretion and thus lead to greater fluid movement towards the retina than to the choroid

19. Pathophysiology 3. Combined choroid and RPE dysfunction theory
Alternatively there could be a combination of increased fluid leakage from the choriocapillaris and impaired RPE function.
A persistent choriocapillaris abnormality could lead to prolonged stress of the RPE cells, which would not be able to pump in a retinochoroidal direction and therefore fluid would accumulate and cause a neurosensory detachment.

20. Risk factors and associations
Type A personality
higher levels of cortisol and epinephrine compared with those with type B personalities.
Exogenous glucocorticoid administration
Elevate endogenous glucocorticoid levels
- Cushing’s disease
- organ transplantation and corticosteroid usage
- pregnancy
antihistamine (3.9) , antibiotic use (6.3)
alcohol (8.2) tobacco use (1.9)
Hypertension (2.28) psychopharmacological medication (2.6)
Stress also has a relationship with increased tobacco and alcohol use which can inhibit nitric oxide dilatation of vessels that feed the
choroid whilst causing norepinephrine vasoconstriction
[7]. Patients with CSCR have been shown to be more
stressed due to inadequate coping strategies

21. CSCR Treatment
First-line treatment for CSCR should involve a discontinuation of any steroid treatments.
Lifestyle counselling and other psychosocial therapies should be used as an attempt to reduce stress levels.
1. Focal photocoagulation
changes the ability of the RPE to act as a barrier to diffusion.
the subretinal fluid has high protein content and thus
photocoagulation allows the fluid and protein to move
back into the choroid.

22. CSCR Treatment 2. Photodynamic dynamic therapy
PDT is directed towards the pathological hyperpermeable choroidal microcirculation responsible for CSCR.
Vascular remodelling results in decreased choroidal permeability and termination of focal RPE leakage.
Photodynamic dynamic therapy is not a standard treatment for chronic CSCR due to reported complications of RPE changes, choriocapillary ischemia and choroidal neovascular membrane development.

23. CSCR Treatment 3. Other laser therapies
Micropulse diode (MPD) laser photocoagulation
Selective retina therapy (SRT)

24. CSCR Treatment
4. Anti-vascular endothelial growth factor intravitreal injections
In CSCR, vascular endothelial growth factor (VEGF) has a role in vascular permeability by changing tight junctions and inducing vascular fenestration.  Improvements in VA, neurosensory retina detachment resolutions, and in RPE leaks after anti-VEGF therapy.
In chronic CSCR found similar results without any negative effects.
Lim et al : VEGF levels in aqueous humor and plasma were increased in a portion of chronic CSC.

25. CSCR Treatment
4. Anti-vascular endothelial growth factor intravitreal injections
Anti-VEGF therapies may be more closely related to the effect on reduction of choriocapillaris fenestrations rather than the effect on restoration of retinal pigmentary epithelium tight junctions.
--- recurrence… reinjection…. (21%  12.5±5.5 months)
More research is required with regard to the mechanism of intravitreal anti-VEGF treatment.

26. CSCR Treatment 5. Corticosteroid antagonist
- mifepristone, ketoconazole ….  no significant improvement
6. Adrenergic receptor inhibitors
- due to the relationship between stress and high levels of adrenergic activity
7. Acetazolamide
- To accelerate resolution of acute CSCR.
- but no effect on recurrence rate or final VA.

27. Conclusion
Greater understanding of CSCR has changed initial beliefs that CSCR is a benign condition affecting young men with almost complete resolution. CSCR has a spectrum of presentations with more diffuse retinal dysfunction and variations between races.
CSCR can affect older individuals and in a subset of patients may lead to significant ocular morbidity. Treatments for CSCR are still evolving, in particular PDT using lower doses and reduced fluence showing promising results.
More research is required on ideal dosage and the role of alternative agents such as anti-VEGF.