Vascular Layer Analysis on OCTA

Vascular Layer Analysis on OCTA

The retina is nourished by two distinct vascular systems: the retinal vasculature (from the central retinal artery, supplying the inner two-thirds) and the choroidal vasculature (supplying the outer third, including the photoreceptors). OCTA separates these systems into discrete depth-resolved layers, each of which tells a different clinical story.

In Tier 2, you learned to read en face OCT projections of each retinal layer — the structural appearance of the NFL, GCL, outer nuclear layer, RPE, and choroid as seen from above. OCTA builds directly on that knowledge: the same layer boundaries that define your structural en face slabs define your vascular slabs. Where your structural en face showed tissue density, your OCTA en face shows blood flow. The anatomy is the same; the variable being imaged is different.

Superficial Capillary Plexus (SCP)

The superficial capillary plexus occupies the inner retina from the inner limiting membrane to the inner plexiform layer. It contains the large arterioles and venules of the central retinal artery circulation alongside the superficial capillary network. On en face OCTA, the SCP is the most visually recognizable layer — you see the arcade pattern of the superior and inferior vessels converging toward the optic disc, with the FAZ as a well-defined avascular circle at the foveal center.

Normal SCP appearance: The major arcades are bright and well-defined. The FAZ is clearly delineated, roughly circular, and typically 0.2–0.4mm² in area. The capillary network between the arcades is reasonably dense, with the density tapering toward the foveal edge. The temporal quadrant superior and inferior to the FAZ shows slightly higher capillary density than the nasal quadrant.

Pathological SCP findings:

• Capillary non-perfusion areas (NPA): Dark zones within the capillary network where flow signal is absent. In early NPDR, these appear as small focal NPA between the arcades. In severe NPDR and PDR, they coalesce into large zones of complete non-perfusion.
• FAZ enlargement: Progressive NPA from the foveal edge outward enlarges the FAZ. When capillaries at the foveal perimeter are lost, the photoreceptors they supplied lose metabolic support — and vision loss follows. FAZ area on the SCP slab is the standard measurement for ischemia quantification.
• Neovascularization (NVE/NVD): In proliferative DR, new vessels appear as irregular, high-flow tufts on or within the SCP slab. They lack the organized arcade pattern of normal vessels and often extend anteriorly into the vitreous. NVD (disc neovascularization) appears as a disorganized tangle of new vessels overlying the optic nerve head.
• Vascular tortuosity: Irregular, corkscrew vessel patterns in the SCP indicate arteriolar or venular pathology. Vein occlusion produces marked tortuosity of the affected quadrant veins.

SCP in RVO: In BRVO, the SCP shows sectoral NPA in the affected quadrant — the superior or inferior arcade depending on which vein is occluded. In CRVO, the NPA is diffuse across all quadrants, and the FAZ may be severely enlarged. Collateral vessels develop at the optic disc over weeks to months, appearing as irregular anastomotic channels crossing the horizontal raphe on the SCP slab.

Deep Capillary Plexus (DCP)

The deep capillary plexus occupies the inner nuclear and outer plexiform layers — situated deeper in the retina than the SCP, sandwiched between the structural layers that are metabolically most demanding for photoreceptor function. On en face OCTA, the DCP appears as a denser, finer capillary mesh than the SCP, with a slightly larger FAZ (because the avascular zone at the foveal center extends to a slightly wider diameter at this deeper plane).

The DCP is clinically important for two reasons: it is more sensitive to early diabetic capillary loss than the SCP, and it supplies the metabolically active inner nuclear layer, whose dysfunction precedes outer retinal damage in ischemic disease.

DCP in early diabetic retinopathy: The first histopathological change in diabetic retinopathy is selective loss of pericytes from the retinal capillaries. These pericyte-deficient capillaries are concentrated in the perivenular capillary network of the deep plexus. OCTA studies consistently show that perivenular capillary dropout in the DCP precedes visible changes on the SCP slab in early NPDR. When you are looking for the earliest OCTA evidence of diabetic microvascular disease, examine the DCP.

Practical DCP imaging: Because DCP capillaries are finer and denser than the SCP, spatial resolution matters more for the DCP. A 3×3mm OCTA protocol provides enough scan density to visualize DCP capillary loss clearly. On 6×6mm scans, the DCP can be visualized but fine capillary detail is less resolved. For practices focused on early DR detection, a 3×3mm protocol is the better choice for DCP assessment.

DCP segmentation errors: The boundary between SCP and DCP is set by the software at the IPL/INL interface. In eyes with significant retinal thickening (diabetic macular edema, for example), boundary tracking can fail — the DCP slab boundaries may shift into the SCP layer or into the OPL. Always confirm slab boundaries with the B-scan overlay when DCP findings seem inconsistent with the clinical picture.

Layer	Key Boundaries	FAZ Size	Earliest Pathology
SCP	ILM → IPL	Smaller (reference FAZ)	FAZ enlargement, arcade NPA (moderate DR)
DCP	INL → OPL	Slightly larger than SCP	Perivenular capillary dropout (early NPDR)

Outer Retina: Avascular in Health

The outer retina — spanning the outer plexiform layer through the ellipsoid zone and into the photoreceptor outer segment zone — contains no blood vessels in a healthy eye. The photoreceptors are nourished entirely by diffusion from the choriocapillaris through the RPE. This metabolic arrangement is why the photoreceptors are the retinal cells most vulnerable to outer retinal or choroidal vascular compromise.

On OCTA, the outer retina slab should appear uniformly dark. The absence of decorrelation signal in this layer is not a finding to report — it is the expected normal result. The outer retina slab's clinical purpose is entirely the detection of abnormal flow, which in this layer means one of two things: choroidal neovascularization (CNV) or projection artifact from the overlying vascular layers.

CNV on the outer retina slab: When a neovascular membrane grows from the choroid into or through the RPE, the vessels carrying blood into that membrane produce decorrelation signal in the outer retina slab. The signal pattern varies by CNV type — Type 1 (sub-RPE) may appear as a subtle irregular network; Type 2 (sub-retinal) appears as a more prominent vascular tangle above the RPE line. The outer retina slab is therefore the primary screening slab for CNV detection in AMD monitoring. Any unexpected flow here should trigger a systematic evaluation: check the B-scan for structural correlate, confirm projection removal was applied, and assess the choriocapillaris slab for complementary findings.

Projection artifact in the outer retina slab: Flow signal from the SCP and DCP projects through the outer retina during OCTA acquisition, creating false decorrelation signal at the locations directly below the superficial vessels. This is the most clinically significant OCTA artifact because it directly mimics CNV. The key distinguishing feature: projection artifact follows the exact topographic pattern of the overlying superficial vasculature — if the outer retina "flow" matches the arcade pattern visible on the SCP slab, it is projection, not CNV. Projection removal algorithms address this, but always compare the algorithm-corrected and uncorrected outer retina slabs side by side.

Outer retina slab in other diseases: In macular telangiectasia type 2 (MacTel), abnormal neovascularization originating from the inner retina extends into the outer retina — the outer retina slab shows characteristic vessels in the parafoveal region temporal to the FAZ. In high myopia, lacquer cracks can be associated with CNV that appears in the outer retina slab. Wherever RPE integrity is disrupted, monitor the outer retina slab for new flow.

Choriocapillaris: Flow Voids and Clinical Meaning

The choriocapillaris is a sheet-like network of large-diameter capillaries lying immediately beneath the RPE and Bruch's membrane. It is the sole blood supply to the outer retina and photoreceptors. Despite its clinical importance, the choriocapillaris has historically been difficult to study in vivo — structural OCT shows the choroidal-RPE complex but cannot resolve individual CC lobules. OCTA changes this.

On OCTA, the choriocapillaris slab appears as a relatively uniform, high-flow sheet with scattered small dark spots — the physiologic flow voids that represent the spaces between CC lobule units. Normal CC flow voids are small, scattered, and distributed without topographic pattern. They are not clinically significant.

Pathological flow voids: Geographic Atrophy

In geographic atrophy (GA), RPE cell loss is accompanied by — and preceded by — loss of the underlying choriocapillaris. OCTA studies have demonstrated that choriocapillaris flow voids appear at the site of future GA before RPE loss is visible on structural OCT. This makes choriocapillaris OCTA a potential early biomarker for GA progression — one of the most compelling clinical arguments for OCTA in AMD monitoring beyond CNV detection.

On the CC slab, GA appears as a well-defined, focal area of complete flow void — a dark region surrounded by normal CC flow. The shape and size of the CC void typically matches the area of RPE loss on the structural OCT within a few months. In early GA, the CC void may be slightly larger than the visible RPE atrophy — the "CC leading edge" of atrophy expansion.

Differentiating pathological voids from artifact:

• Signal attenuation artifact: If the overlying RPE is disrupted (drusen, pigment clumping, media opacity), less light reaches the CC — the CC appears dark not because flow is absent but because signal is blocked. This is a signal attenuation artifact, not true flow void. Cross-reference with B-scan: true CC dropout has no overlying RPE to attenuate signal. Signal attenuation shows structural RPE above the dark zone.
• Segmentation artifact: If the RPE boundary is misidentified (a common error in advanced AMD, high myopia, or CNV), the CC slab boundaries shift and the image may show the choroidal stroma or sclera instead of the CC. Always confirm RPE segmentation on the B-scan overlay.

OCTA Layer	Disease to Look For First	Normal vs Abnormal Rule
SCP	Proliferative DR (NVE/NVD), RVO vein pattern, FAZ area	Dark NPA zones = non-perfusion; irregular tufts = NVE
DCP	Early NPDR (perivenular dropout), ischemic maculopathy	Perivenular dark spots = pericyte loss; expanded FAZ = ischemia
Outer Retina	CNV (AMD, myopia, MacTel, trauma)	Should be dark; any flow = CNV or projection artifact
Choriocapillaris	Geographic atrophy, pachychoroid NV, CC dropout	Focal large void = GA or CC atrophy; scattered small = normal