RVO & CSC: Basic OCT Patterns

Retinal vein occlusion and central serous chorioretinopathy both cause macular fluid, but the pathophysiology, fluid compartment, and treatment approach are entirely different. OCT — especially en face — distinguishes them clearly and drives management.

The Key Distinction: RVO creates intraretinal fluid (cystoid spaces within layers). CSC creates subretinal fluid (between photoreceptors and RPE — a smooth dome). Getting this right is the foundation of correct management.

Retinal Vein Occlusion (RVO): OCT Findings

RVO: BRVO sectoral CME vs CRVO diffuse macular oedema — Educational illustration, not a clinical scan

🔭 Clinical Reference — CC BY 4.0

OCT B-scan showing massive cystoid macular edema in retinal vein occlusion

Retinal vein occlusion (RVO) on OCT (Fig.5). Massive cystoid macular oedema (CME) with large intraretinal cysts collapsing normal retinal architecture. Retinal thickness often >600 μm. Compare with normal contour on fellow eye scan. — Kulyabin M et al. Sci Data 11:365 (2024), CC BY 4.0

RVO causes venous outflow obstruction — blood backs up, retinal capillaries become hyperpermeable, and fluid accumulates within the retinal layers. The two major types have distinct OCT presentations:

Feature	BRVO (Branch)	CRVO (Central)
Fluid distribution	Sectoral — one or two quadrants	Pan-macular, symmetric
Cyst morphology	Smaller cysts, often paracentral	Large cysts, often involving fovea
Retinal thickening	Asymmetric — follows vein territory	Diffuse, often severe (>500 μm)
Outer retinal changes	EZ relatively preserved early	EZ frequently disrupted
HRF / Hard exudates	Common at area of stasis	Common throughout posterior pole

On en face imaging, BRVO produces a sectoral pattern of dark cysts that maps beautifully to the affected vein territory — the geographic boundary is typically sharp at the affected vein's drainage zone. CRVO shows diffuse, bilateral intraretinal cysts across the macula.

Prognostic Marker: In RVO, EZ disruption length at the foveal center strongly predicts final visual acuity. Chronic edema (months to years) leads to progressive EZ loss — the structural damage may be irreversible even if the edema eventually resolves. Treat early.

Central Serous Chorioretinopathy (CSC): OCT Findings

Acute CSC: dome-shaped SRF, RPE leak, pachychoroid — Educational illustration, not a clinical scan

CSC is fundamentally a choroidal disease — pachychoroid and abnormal choroidal permeability lead to RPE breakdown and subretinal fluid accumulation. The key OCT features:

Subretinal fluid (SRF): The hallmark. A smooth, dome-shaped clear space between the outer surface of the photoreceptors (EZ) and the RPE. The fluid itself is optically empty (hypo-reflective).
RPE detachment (PED): Often present — flat, serous PED adjacent to the SRF. In CSC, the PED is typically serous (clear fluid beneath RPE) rather than drusenoid.
Pachychoroid: Thickened choroid (>300–350 μm subfoveal), dilated Haller layer vessels. Best seen on EDI-OCT or SS-OCT.
RPE atrophy / pigment changes: In chronic CSC (>3–4 months), secondary RPE changes develop — irregular RPE signal, hyperreflective foci, RPE atrophy on en face
No intraretinal fluid (in acute CSC): The retinal layers above the SRF are typically normal. The absence of IRF helps distinguish CSC from wet AMD.

CSC vs. Wet AMD: The Critical Differential

CSC vs wet AMD: age, fluid type, OCTA, choroid — Educational illustration, not a clinical scan

Subretinal fluid in a middle-aged patient raises two differential diagnoses: CSC or occult CNV (type 1 MNV). The distinction has major treatment implications:

Feature	CSC	Type 1 CNV (occult wet AMD)
Patient age	30–55 years, male-predominant	Typically >55, equal sex
SRF characteristics	Smooth dome, clear	May be more irregular
RPE elevation	Serous PED, smooth	Fibrovascular PED, irregular
Choroidal thickness	Increased (pachychoroid)	Variable, often thinner in late AMD
Drusen	Absent (no AMD)	May be present
Hyperreflective material sub-RPE	Absent	Fibrovascular tissue present

Monitoring Protocols

RVO monthly to quarterly; CSC observe then PDT if persistent — Educational illustration, not a clinical scan

Acute RVO: Monthly OCT with anti-VEGF (per SCORE2/BRAVO/CRUISE protocols); assess for non-perfusion concurrently
Chronic RVO (stable): Every 2–3 months after stabilization; earlier if symptoms change
Acute CSC: OCT at 6–8 weeks — majority resolve spontaneously. If persists >3 months, refer for photodynamic therapy (PDT) evaluation
Chronic CSC: Every 3 months; monitor for secondary CNV (occurs in ~5–10% of chronic cases)

Key Takeaways

RVO = intraretinal fluid (cystoid) in the territory of the affected vein
CSC = subretinal fluid (smooth dome) + pachychoroid, no intraretinal cysts
EZ disruption in RVO predicts poor visual recovery — treat promptly
CSC vs. wet AMD differential is critical — pachychoroid and age help distinguish
Chronic CSC (>3 months) warrants PDT evaluation and monitoring for secondary CNV

Educational illustration — RVO cystoid IRF (blue) vs. CSC subretinal fluid dome (cyan) and RPE detachment (indigo). Real clinical scans in full course.

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In This Course

1. Retinal Layer Anatomy & Normal Findings 2. B-Scan Interpretation Fundamentals 3. Introduction to En Face Views 4. AMD: OCT Findings & En Face Correlation 5. Diabetic Retinopathy: OCT Assessment 6. RVO & CSC: Basic OCT Patterns 7. ERM & Macular Hole: Surgical Decision Points