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Choriocapillaris & Choroid

The deepest layers. Choroidal thickness mapping, Haller vs Sattler layer differentiation, and pachychoroid spectrum disorders.

Choroid Analysis on En Face OCT

The choroid is the most metabolically active tissue in the eye per unit volume. It supplies the outer retina and RPE, regulates ocular perfusion pressure, and is the origin of several visually devastating disease processes — yet it remained largely inaccessible until enhanced depth imaging (EDI) OCT and swept-source OCT (SS-OCT) brought its internal architecture into view.

Clinical Priority: Choroidal thickness and vascular morphology are directly relevant to AMD, central serous chorioretinopathy (CSC), polypoidal choroidal vasculopathy (PCV), and high myopia management. En face imaging at the choroidal level reveals structural signatures that cannot be appreciated on standard B-scan alone.

Choroidal Anatomy on OCT

Choroidal Layer Architecture on EDI-OCTBruch's MembraneCHORIOCAPILLARIS — fenestrated, 10-20 μm, supplies RPE + outer retinaSATTLER'S LAYER — medium vessels 20–50 μmHALLER'S LAYER — large vessels 50–300 μm; pachychoroid target layerSuprachoroidal / ScleraEDI-OCT or SS-OCT required for reliable Haller layer delineation • Normal SFCT: 287 ± 76 μm

Choroidal layer anatomy: choriocapillaris, Sattler's medium vessels, Haller's large vessels — Educational illustration, not a clinical scan

The choroid consists of three vascular layers, from innermost to outermost:

  • Choriocapillaris: A 10–20 μm layer of fenestrated capillaries immediately beneath Bruch's membrane. It supplies the outer retina and RPE. On OCTA en face, it appears as a uniform, fine lobular flow pattern — voids here are the earliest measurable sign of AMD and choriocapillaris ischemia.
  • Sattler's layer: Medium-caliber vessels (20–50 μm diameter). On B-scan, these appear as ovoid hypo-reflective structures. On en face, medium vessel lumens are visible as distinct dark ovals against a brighter inter-vessel stroma.
  • Haller's layer: Large choroidal vessels (50–300 μm diameter). The most posterior choroidal layer, best imaged with EDI-OCT or SS-OCT. Haller vessel diameters are the primary substrate of pachychoroid disease — dilated Haller vessels compress the overlying choriocapillaris.

Choroidal thickness is measured perpendicular from the outer border of Bruch's membrane to the inner scleral surface. Normal subfoveal choroidal thickness (SFCT) is approximately 287 ± 76 μm, with wide inter-individual variation (100–500+ μm). Age reduces SFCT by ~1.56 μm per year. Axial length is inversely correlated: each diopter of myopia reduces SFCT by approximately 15–20 μm.

Pachychoroid Spectrum

Pachychoroid Disease SpectrumIncreasing structural disruption →PPEPachychoroid PigmentEpitheliopathyRPE changesno fluidthick choroidNo treatmentCSCCentral SerousChorioretinopathySub-retinal fluidRPE leakvery thick choroidPDT / observationPachy-NVPachychoroidNeovasculopathyType 1 CNVno exudationthick choroidMonitor ± anti-VEGFPCVPolypoidal ChoroidalVasculopathyBVN + polypsserosanguineous PEDthick choroidAnti-VEGF ± PDTPeripapillary PachyPeripapillaryPachychoroid Syndromeperipapillary SRFdisc margin arcthick peripapillaryPDT if persistentAll entities share: thick choroid, dilated Haller vessels, RPE dysfunction — treatment differs by entity

Pachychoroid disease spectrum: PPE → CSC → Pachy-NV → PCV → Peripapillary syndrome — Educational illustration, not a clinical scan

Pachychoroid disease is defined by focal or diffuse choroidal thickening (>300 μm subfoveal), dilated outer choroidal vessels (pachyvessels), attenuation or loss of the inner choroidal layers, and outer retinal changes related to resultant RPE dysfunction. The spectrum includes a continuum of related entities:

EntityKey FeaturesEn Face Signature
Pachychoroid pigment epitheliopathy (PPE)RPE changes without fluid, thick choroidDrusenoid deposits over pachyvessels
Central serous chorioretinopathy (CSC)Sub-retinal fluid, RPE dysfunctionSRF footprint on outer retinal slab
Pachychoroid neovasculopathyType 1 CNV without exudationFlat irregular PED over pachyvessel
Polypoidal choroidal vasculopathy (PCV)Polypoidal lesions, serosanguineous detachmentsBranching vascular network on OCTA
Peripapillary pachychoroid syndromePeripapillary SRF, thick peripapillary choroidSRF arc pattern around disc margin
Clinical Context: Not every thick choroid is pachychoroid disease. Conditions including VKH syndrome, posterior scleritis, and hypotony also produce choroidal thickening. Pachychoroid disease is typically unilateral, onset age 30–60, often linked to psychological stress or systemic corticosteroid use.

Choroidal Vascularity Index

Choroidal Vascularity Index (CVI): Formula and Clinical ValuesCVI = Luminal Area / Total Choroidal AreaLuminal area(vessel lumen)Stromal area(intervessel)Normal CVI ≈ 0.65 (65% vascular)Binarized from EDI-OCT using Niblack thresholdThickness-independent vascular health metricCVI Clinical Reference ValuesNormalCVI ≈ 0.65 (0.60–0.70)Early AMDCVI ↓ (stromal expansion)Advanced GACVI markedly ↓Diabetic choriod.CVI ↓ even pre-DRCSC / PachychoroidCVI ↑ (dilated lumens)Glaucoma (NTG)CVI ↓ (perfusion impairment)CVI separates vascular from stromal choroidal changes — complementary metric to thickness

CVI formula, calculation method, and reference values across disease states — Educational illustration, not a clinical scan

The choroidal vascularity index (CVI) is a quantitative measure of the luminal (vascular) area relative to the total choroidal area on a B-scan cross-section. It is calculated from binarized EDI-OCT using adaptive threshold methods:

CVI = Luminal area ÷ Total choroidal area

Normal CVI is approximately 0.65 (65% of choroidal cross-sectional area is vascular lumen). CVI provides a single metric that reflects choroidal vascular health independently of thickness — useful because thickness alone conflates vascular and stromal components.

  • AMD: CVI decreases with disease progression; early CVI reduction may precede drusen development in fellow eyes of wet AMD patients
  • Diabetic choroidopathy: CVI reduction occurs even in the absence of clinical diabetic retinopathy, suggesting early choroidal involvement in diabetic disease
  • Glaucoma: Reduced CVI has been reported in normal-tension glaucoma, consistent with vascular perfusion impairment as a contributing mechanism
  • Limitations: Requires EDI-OCT with good signal penetration through the choroid; automated choroidal vessel segmentation remains imperfect; inter-device variability limits cross-study comparison

Haller & Sattler on En Face

Haller and Sattler Layers on En Face — Normal vs PachychoroidNormal Haller slab en faceOrganized radial-lobular patternPachychoroid Haller en faceDilated irregular dark vascular lakesSattler layer (medium vessels)Fine dark dots / short segmentsHaller: dilated in pachychoroid (large dark lakes) • Sattler: fine dots • SS-OCT for best delineation

Haller en face: normal organized vessels vs dilated pachychoroid lakes; Sattler fine dot pattern — Educational illustration, not a clinical scan

En face imaging at the choroidal layer levels — separate Haller and Sattler slabs — reveals internal choroidal architecture that is invisible on standard B-scan. This capability requires SS-OCT (1050 nm wavelength) or high-quality EDI-SD-OCT with careful manual segmentation boundaries.

On the Haller slab en face, large-caliber vessels appear as dark elongated ovals and branching structures against the brighter inter-vessel choroidal stroma. The normally thinner vessels of Sattler's layer appear as finer dark dots and short segments. Pathological dilation in pachychoroid disease converts the normal Haller vessel pattern into large, prominent, dark vascular lacunae that dominate the en face image.

  • Choriocapillaris flow voids (OCTA): Appear as dark spots on the choriocapillaris OCTA en face — not the same as Haller vessel imaging. Flow voids signal local ischemia and are strongly associated with AMD progression risk.
  • Pachyvessel recognition: Normal Haller vessels form an organized radial-lobular pattern. Dilated pachyvessels lose this regularity and appear as large, irregular lakes — often concentrated in one macular sector.
  • Layer selection: On SS-OCT systems, manufacturer presets for the "choroid" en face slab may not optimally separate Haller vs. Sattler layers; manual boundary adjustment improves specificity for disease characterization.

CSC vs PCV Differentiation

CSC vs PCV: Key Differentiating FeaturesCentral Serous Chorioretinopathy (CSC)Fluid:Clear serous SRF; no bloodPED:Flat, shallow serousOCTA:RPE window defects; Type 1 CNV in chronicChoroid:Very thick (>400 μm typical)Treatment:PDT or observe; anti-VEGF limited rolePrognosis:Good (acute); guarded (chronic >3 mo)No BVN on OCTAPolypoidal Choroidal Vasculopathy (PCV)Fluid:Serosanguineous; orange SRF / bloodPED:Hemorrhagic or serosanguineousOCTA:Branching vascular network (BVN) + polypsChoroid:Thick (>300 μm); dilated Haller vesselsTreatment:Anti-VEGF + PDT; monotherapy less effectivePrognosis:Risk large hemorrhage; guardedBVN on OCTA = hallmark of PCV; ICGA gold standardOCTA BVN is the key differentiator — when unavailable, indocyanine green angiography required for PCV diagnosis

CSC vs PCV differentiation: fluid character, OCTA findings, treatment, and prognosis — Educational illustration, not a clinical scan

CSC and PCV are both pachychoroid spectrum diseases with sub-retinal fluid, but they have different natural histories, treatment responses, and prognoses. Accurate differentiation directly guides management — and OCT alone is often insufficient.

FeatureCSCPCV
Sub-retinal fluidClear, serousOften serosanguineous (orange-red fundus hue)
PED typeFlat or shallow serous PEDHemorrhagic or serosanguineous PED common
OCTA en faceRPE window defects; Type 1 CNV in chronic CSCBranching vascular network (BVN) + polypoidal lesions
Choroidal thicknessMarkedly thick (>400 μm typical)Thick (>300 μm), but often less extreme
Treatment priorityPDT or watchful waiting for acute; half-dose PDT for chronicAnti-VEGF ± PDT; anti-VEGF monotherapy less effective
PrognosisGood for acute (<3 months); guarded for chronicRisk of large sub-retinal hemorrhage; guarded
Key Differentiator: The branching vascular network (BVN) on OCTA is the hallmark of PCV. On structural en face at the choroidal level, the BVN appears as a network of interconnected vessels terminating in polypoidal dilatations. When OCTA is unavailable, indocyanine green angiography (ICGA) remains the gold standard for PCV diagnosis — standard FA is often non-diagnostic.
Dilated Haller Serous PED Vitreous ILM/RNFL GCL+IPL INL OPL ONL ELM EZ / IZ RPE / BM Choroid

Educational illustration — Pachychoroid: dilated Haller layer vessels with serous RPE detachment. Real clinical scans in full course.

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In This Course

1. ILM Surface Analysis2. Superficial & Deep Capillary Plexus3. Outer Retina & RPE/Bruch's Complex4. Choriocapillaris & Choroid5. 10 Management-Changing Clinical Scenarios6. Artifacts, Segmentation Errors & Documentation