Central serous chorioretinopathy (CSC) is characterized by a collection of fluid at the posterior pole of the eye, causing a localized neurosensory retinal detachment. It typically affects young-to-middle aged males and presents with mild-to-moderate vision loss. The cause is believed to be a defect in the retinal pigment epithelium and choroidal vasculature that allows fluid to accumulate subretinally. Imaging such as fluorescein angiography and optical coherence tomography are useful for diagnosis and monitoring the condition. While often self-limiting, CSC can become chronic in some cases and lead to complications if not properly managed.

1. CSRCSR
Dr.Shah-Noor Hassan FCPS,FRCSDr.Shah-Noor Hassan FCPS,FRCS
Vitreo-Retina ConsultantVitreo-Retina Consultant
Bangladesh Eye Hospital & instituteBangladesh Eye Hospital & institute

2. History
 1866: von Graeffe: Relapsing Central Leutic
Retinitis
 1955: Bennet : Central Serous
Retinopathy (CSR)
 1965: Maumenee : Leak from RPE
 1967: Gass : Idiopathic Central Serous
Choroidopathy (ICSC)
 Current name : Central Serous
Chorioretionopathy (CSC)

3. Definition
 Idiopathic, sporadic, self-
limiting
 Collection of fluid at posterior
pole
 Acute, localised
neurosensory detachment
 Young male
 Mild to moderate visual loss
 Single or few leaks on FA

4.  Asymmetrical bilateral chronic disease with
 Acute exacerbation during periods of:
 Stress
 Steroid intake
 High BP spikes
 Unknown factors
Recent Concept

5. Demography
 Sex: ♂ > ♀ (9:1)
 Age: 25-45 yrs
 Increased incidence in females & elders
 Rarely familial
 Bilaterality:
 10-25% symptomatic
 45% on FA
 More in elders

7. Classification
 Klein (1953):
 Central retinopathy
 Central chorioretinopathy
 Central choriopathy (juvenile disciform macular
degeneration)
 Maumenee (1960) & Wessing (1977):
 Type I : Subsensory fld. : 94%
 Type II : Sub-RPE fluid : 3%
 Intermediate: Both areas : 3%

8. Classification
 Nadel (1979):
 Unilateral CSR
 Uniocular RPE changes
 Binocular RPE changes
 Bilateral CSR
 Lodato & Brancato (1988):
 Simple (55%)
 Multifocal (30%)
 Chronic (15%)

9. Classification
 Patnaik (1983):
 Type I : Unilateral, single leak, benign, idiopathic
 Type II: Bilateral, Multifocal PEDs, recurrent,
granulomatous choroiditis (TB/Toxo)
 Castro-Correia (1992) & Bujarborua (2001):
 Single episode ⇒ Resolves
 Recurrent episodes ⇒ Resolve
 Recurrent episodes ⇒ Chronicity
 Single episode ⇒ Chronicity

10. Classification
 Commonly accepted:
 Typical CSR
 Classic CSR
 Chronic CSR
 Atypical CSR
 Decompensated RPE
 Diffuse retinal pigment epitheliopathy
 Zweng & Little (1977)

11. Chronic CSR
 Atypical CSR, Decompensated RPE,
Diffuse retinal pigment epitheliopathy (≅ 10%)
 Widespread pigment alteration of RPE
 Long-standing SRF (>6mths)
 Chronic steroid intake after organ transplantation
 Asian descent
6mths
Apr Oct

12. Pathogenesis – Theories
 Gass’ hypothesis (1967)
 Piccolino’s hypothesis (1981)
 Spitznas’ hypothesis (1986)
 Yannuzzi’s hypothesis (1986)
 Marmor’s hypothesis (1988)
 Guyer’s hypothesis (1994)
 Ciardella’s hypothesis (2001)

13. Gass’ Hypothesis (1967)
 Hyperpermeability of choriocapillaris ⇒
serous exudation (sub-RPE or sub-sensory)
 Stress ⇒ Physiologic decompensation at
sites of congenital structural defects

14. Piccolino’s Hypothesis (1981)
 RPEpithelitis or choroidal perfusion defect ⇒
RPE cell junction damage
 Strong adhesion force ⇒ No detachment
 Strong choriocapillaris
hydrostatic pressure ⇒
Serous detachment

15. Spitznas’ Hypothesis (1986)
 RPE cells secrete ions around rods & cones
 Choroidal fluid gets dragged subretinally
 Adjacent RPE cells overwork to remove fluid
 Seen as scarring
after resolution

16. Behaviour
Yannuzzi’s Hypothesis (1986)
 Multifactorial concept ⇒ Host specificity
 Related to balance of:
 Genetic endowment
 Environment
 Behavioural pattern
 Adrenergic alteration ⇒
 Choriocapillaris damage
 RPE cell degeneration
 BRB breakdown
EnvironmentGenetics

17. Pathogenesis – Theories
 Chronic choriocapillaris disturbance
 Failure of RPE cell pump
 Pooling in sub-RPE space
 Sub-retinal fluid accumulation

18. Pathogenesis – Theories
 Raised choroidal hydrostatic pressure
 ICGA:
 Choroidal vascular hyperpermeability
 Delayed filling
 Also in non-leaky areas & in fellow eyes
 Infectious Theory:
 Tuberculosis
 Toxoplasmosis
 Viral theory

19. Pathogenesis
 Increased stress
 Type-A personality
 Hypochondriacs & hysterics
 Increased cortisol levels
 Cushing’s disease
 Pregnancy
 Steroid intake
 Increased catecholamine levels
 Hypertension

20. Pathogenesis – Theories
 Role of catecholamines
 Vasoconstriction
 Altered choroidal blow flow
 Role of corticosteroids
 ↓se nitric oxide (vasodilator)
 ↑se capillary fragility
 Delayed RPE healing
 Reversed RPE polarity
 ↑se catecholamine response

21. Stages
 I = RPE inflammation
 II = Increase in inter-RPE cell spaces
 III = Crenation of RPE
 IV = Degeneration & atrophy
 V = Recurrance
 VI = Neovascularisation

22. Symptoms
 Minor blurring of vision (6/6 to 6/60)
 Metamorphopsia, Micropsia
 Dyschromatopsia (67%)
 Blue-yellow defect, red-shift
 Poor contrast sensitivity
 Hypermetropisation
 Central scotoma
 Photopsia

23. Signs – Sensory Retina
 Well-defined transparent blister
 Halo of light reflex
 Yellowish foveal
discolouration
 Increased
xanthophyll visibility

24. Signs – Sensory Retina
 Yellowish-white sub-retinal deposits (≅10%)
 Proteinaceous deposits
 s/o inactive disease
 “Bath-tub” effect
 SR & sub-RPE fibrin
 Intra or SR lipid
(leopard-spot pattern)
 Cloudy & grayish SRF
 Punctate hemorrhage

25. Signs – RPE
 Serous PED:
 Single or multiple (<1/4DD)
 Bilateral
 Pigment migration
 RPE atrophy

26. Signs – RD
 Peripheral dependent bullous RD with
connecting atrophic RPE tracts
 Flask, teardrop, dumbbell, hourglass pattern
 Telangiectasia & CNP
 Pigment migration & deposits
 Gass: “Pseudo-RP-like CSR”

29. Signs – CNVM
 Incidence: 4% in chronic RPEpitheliopathy
 CNVM in CSR are Type II membranes
 Types of CNVM:
 Diffuse & irregular leaks
 Typical membrane
 Post laser therapy
 Cause:
 Damage to RPE-Bruch’s membrane complex
 Ischemia of choriocapillaris
1 mth

30. Signs – Other Complications
 Cystoid macular edema
 Intracytoplasmic edema of Müller cells ⇒ Cell
death & degeneration ⇒ Cystoid spaces
 Detachment, SRF & fibrin ⇒ Toxic to retina ⇒
Ischemia ⇒ Retinal vascular leakage
 Ring-like “bull’s eye” RPE window defect
 Long-standing CSR
 Choriocapillaris atrophy

31. CSR in Women
 More common than previously thought
 Age: 40-60 yrs
 Unilateral in 90%
 Pregnancy (3rd
trimester), SLE
 Role of catecholamines, corticosteroids,
estrogen, prostacyclin

32. Systemic Associations
 Pregnancy
 End-stage renal disease
 Organ transplantation
 Systemic steroid intake
 Choroidal ischemia
 SLE, PAN, Wegener’s granulomatosis
 DIC, TTP, Toxemia of pregnancy

33. Natural Course
 Spontaneous resolution (80%)
within 3 mths with VA > 6/9
 Recurrences:
 30-50% cases
 50% within 1 year
 10% have > 2 episodes
 Severe & permanent visual loss (10%):
 Persistent detachment
 CNVM, CME, RPE atrophy
Day 0
1 mth
3 mths

34. Imaging Techniques
 Fundus Fluorescein Angiography (FFA)
 Indocyanin green Angiography (ICGA)
 Optical Coherence Tomography (OCT)

35. FFA
 ≥ 1 hyperfluorescent leaks
from RPE
 Pattern:
 Ink-blot
 Smoke-stack
 Point (< 1/5 DD)
 Combinations
 No definite leak

36. FFA – Pattern
 Ink-blot (85%):
 Even spread in all directions
 Smoke-stack (10%):
 Shimizu & Tobari (1971)
 Rises superiorly ⇒ Expands laterally
 Mushroom-like
 Umbrella-like
 No definite leak (5%):
 Hyperfluorescent patches

37. FFA – Ink-blot

38. FFA – Smoke-stackSmoke-stack

39. FFA – Smoke-stack
 Larger CSR
 Theories
 Jet-like projection of fluid from RPE defect
 Diffusion & convection rather than net fluid influx
 Increased concentration of proteins in SRF
 Low density fluorescein rises by convection
 Not all smoke-stacks form umbrellas
 Direction changes with head position
 Even downward spread has been seen

40. FFA – No Definite Leak
 Leaking point has healed
 Lies outside macular area
 In presence of choroidal
tumour
 Associated with ONH pit
07:19

41. FFA
 Location of leak:
 1mm-wide ring-like zone adjacent to fovea
 No rods in fovea ⇒ Weaker adhesions
 10% lie in the foveal area
 30% lie within papillomacular bundle
 SNQ > INQ > STQ > ITQ
 Window defects in uninvolved areas
 Choroidal hyper-permeability
 Mottled hyperfluorescence of RPE tracts

42. Parafoveal CSRParafoveal CSR

43. Atrophic Tract

44. FFA
 PED:
 Detected on FFA if missed clinically
 Early or delayed filling
 Puncture or blow-out at margin of PED

45. PED

46. ICGA
 ICGA & FFA leaks correspond
in 80% cases
 Choroidal vascular hyper-
permeability
 Unifying feature of all CSR types
 Best seen in mid-phase
 Localised in inner choroid

47. ICGA

48. ICGA
 Late phase:
 Centrifugally enlarging hyperfluor. patches
 Silhouetting of the larger choroidal vessels
 RPE atrophic areas:
 Hypofluor. areas with surrounding hyperfluor.
 PEDs:
 Early diffuse hyperfluor.
 Late hypofluor. with hyperfluor. ring
 PEDs in ARMD do not stain with ICG

49. FA + ICGA

50. OCT
 Role:
 Confirms diagnosis
 Quantifies detachment
 Observes progress or resolution
 Reduces need for FFA
 Other Findings:
 Intra-retinal edema
 Cystic changes
 No co-relation with colour vision abnormalities

51. Role of OCT
1 month later
6/18
6/9

52. New OCTs
 3-D view
 Deeper view

54. OCT
 B-Scan
 C-Scan

55. mf-ERG & f-ERG
 Standard ERG is normal
 mf-ERG & f-ERG:
 Deterioration of oscillatory potential & b-waves
more than a-waves
 Functional disturbance seen in all retinal layers
 Depressed signals from entire posterior pole in
both eyes

56. Contrast Sensitivity
 Acute stage:
 Deficient at mid & high spatial frequencies
 No co-relation with:
 Visual acuity
 Duration of disease
 Final picture of macula
 Similar findings in normal fellow eye also
 ? Role in early diagnosis

57. Photostress Recovery (PSRT)
 Types:
 Conventional PSRT (acuity chart) ⇒ Macular
 Pattern PSRT (pattern-VEP) ⇒ Macular
 Pupil PSRT (pupillometer) ⇒ Central 300
 Increased recovery time even upto 1 hour
 Microperimeter used with SLO:
 Reduced initial sensitivity change
 Unaffected areas show normal recovery

58. Others
 Rod dysfunction test:
 Dark adaptation
 Static perimetry
 Choroidal pulsation measurement:
 Laser interferometry
 With fundus camera

59. Differental Diagnosis
 Infectious & inflammatory diseases
 Tumours
 Vascular disorders
 Optic nerve pit
 ARMD
 IPCV
 CME
 Inferior RRD

60. Infectious & Inflammatory D.
 POHS:
 Peripheral “histo-spots”
 Peripapillary atrophy
 Arcuate striae in mid-periphery
 Idiopathic CNV in young:
 CNVM on FA
 Sub-retinal hemorrhage
 Unilateral
 No spontaneous resolution

61. Infectious & Inflammatory D.
 Harada’s disease:
 Vitritis
 Optic disc hyperemia
 Systemic associations
 Response to anti-
inflammatory Rx
 Toxoplasmosis:
 Focal retinitis involving
outer half
 Serology & skin test

62. Infectious & Inflammatory D.
 Sympathetic Ophthalmia:
 Intraocular inflammation
 Dalen-Fuchs nodules
(cellular RPE detachments)
 h/o trauma to fellow eye
 Posterior Scleritis:
 Scleral thickening
 Vitreous cells
 Pain on ocular movements
 “T-sign” on USG

63. Choroidal Tumours
 Melanoma, Hemangioma, Metastasis,
Osteoma, Leukemic infiltrates
 May rarely be confused clinically with large PEDs
 USG & FFA will diagnose

64. Vascular disorders
 Collagen vascular disorders (SLE, PAN)
 Fibrinoid necrosis of choroidal vessels
 Chronic intake of systemic steroids
 Malignant HT, Toxemia of pregnancy, DIC
 Acute multifocal occlusion of choroidal vessels
 Necrosis of overlying RPE (Elschnig’s spots)

65. Optic nerve pit
 Schisis-like separation
of macular layers
 Outer-layer detachment:
 No obvious connection with optic nerve pit
 Relatively opaque
 Inner-layer detachment:
 Communicates with optic nerve pit
 Transparent

66. Optic nerve pit
 FFA: no leak, no filling
 OCT: identifies schisis

67. ARMD
 CSR may be seen > 50 yrs
 CSR may show secondary CNV
 FFA: diffuse hyperfluorescence
 Ill-defined CNV or
 Diffuse ‘ooze’ of CSR
 ICGA:
 CSR: multifocal early hyperfluorescence that
fades in late phase
 ARMD: shows late hyperfluorescence

68. IPCV
 Isolated macular variant
 Polypoidal lesions resemble
PEDs
 ICG Angiography:
 Small-caliber vascular network
 Multiple polypoidal lesions

69. Others
 Inferior Rhegmatogenous RD
 Presence of break
 Dome shaped configuration
 Non-shifting fluid
 Photo-toxicity
 CME
 Role of steroids

70. Treatment
 Aim:
 To speed up recovery
 Improve vision quality
 Prevent recurrences
 Methods:
 Conservative approach
 Medical management
 Laser treatment

71. Conservative approach
 Reduce stress
 Avoid caffeine
 Less alcohol
 Avoid steroids

72. Medical management
 St John's Wort
 Acycloguanosine
 Procaine HCl (AntiCort)
 Picogenol
 Beta blockers
 Diazepam based tranquillizers
 Imipramine
 Indomethacin
 Alpha helical CRF
 Acetyl-L-carnitine
 RU-486
 Bilberry
 Eyebright
 Bayberry bark
 Capsicum leaves
 Anti-VEGFs
 Long list of
medications tried
 Finally, response is
to: “TIME”!

73. Medical management
 Ketoconazole & mifepristone
 Role of AKT
 IV Anti-VEGFs

74. 1 month: 6/9 (P)
Pre-Injection: 6/18
?PEDs!

75. Laser Treatment
 Advantages:
 Shortens the course of disease
 Reduces morbidity
 May reduce the recurrence rate
 Disadvantages:
 No effect on final visual acuity
 Possible complications

76. Gass Recomendations
 Wait 4 mths : Primary episode
 Wait 6 mths : Leak <1/4th
DD from fovea
 Wait 1 mth : Recurrence, with good prior
recovery
 Prompt Rx:
 Primary episode > 4 mths old
 Recurrence, with poor prior visual recovery
 Occupational demands
 Gass JDM. Stereoscopic Atlas of Macular Diseases: Diagnosis and Treatment. 3rd ed.
St. Louis: CV Mosby; 1987. p 46-59.

77. Early Treatment
 Affects people in prime of life
 Anxiety & Depression
 Reduced BCVA if resolution takes > 4 mths
 Impending foveal involvement
 Monocular patients
 Severe & Complicated CSR

78. Laser Treatment – Types
 Direct: Over the RPE leak
 Locally debrides RPE cells
 Replaced by healthy cells
 Indirect: Rim of detachment
 RPE breakdown allows fluid to pass into choroid
 Inflammatory material blocks leakage point
 Was advised in past for leaks within the FAZ or
on papillomacular bundle
 May be still used when no leak is seen
 “Sham” or “Photofomentation”

79. Laser Treatment – Method
 Generally avoided within FAZ
 Diode laser may be used within FAZ
 Spot size = 100-200μ
 Duration = 0.1-0.2 sec
 Power = 100-400 mW (diode > argon)
 Light grey burn achieved
 Re-treatment >1mth if leak persists

80. Laser Treatment – Prognosis
 Anatomic resolution:
 2 wks in typical CSR
 6 wks if turbid SRF
 Visual Recovery:
 4-12 weeks
 Recurrence:
 Generally adjacent to the original site of leakage
 Reactivation (inadequate laser)
 New leak

81. Laser Treatment
 Complications
 Secondary CNV (2-5%)
 Inadvertent damage to fovea
 Scotoma
 Slow enlargement of area of RPE atrophy
 Long-term outcome:
 > 85% show extremely good prognosis
 <12% show marked visual impairment

82. ICGA-guided PDT
 Has shown anatomic & functional
improvement
 Mechanism:
 Damage to choriocapillaris endothelium
 Causes reduction in hyper-permeability of
choriocapillaris
 Reperfusion within 2-3 weeks
 Indication:
 Diffuse decompensation of RPE