PMC8077460_01
Multimodal imaging specifically for diseases of the pachychoroid disease spectrum. On EDI-OCT (a) thinning in sattler's and choriocapillaris layer, pathologically dilated veins in the Haller's layer and increased choroidal thickening can be visualized. b BAF reveals a shallow hyper-reflectivity inferior to the fovea, indicating the presence of former subretinal fluid accumulation forming a gravitational tract (arrowhead  ). OCT, optical coherence tomography; BAF, blue autofluorescence.
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F1
On NIR and SD-OCT, the left eye presented with a serous neurosensory detachment of the fovea with elongated photoreceptors and an underlying shallow, irregular, vascularized PED (shown in Fig. 1a). Mean subfoveal choroidal thickness was 266 mum (shown in Fig. 1a). An ill-defined gravitational tract of 4,322 mum diameter horizontally and 4,844 mum vertically was seen on BAF (shown in Fig. 1b).
Vessel imaging. On fluorescein angiography (a-c), only faint late leakage and mostly staining can be visualized. On ICG (d-f) and even better on OCT-A (g), the borders of the type 1 CNV can be visualized. OCT, optical coherence tomography; OCT-A, OCT angiography; ICG, indocyanine green angiography.
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F2
OCT-A (shown in Fig. 2). Only faint leakage was observed from the CNV.
Time course of central retinal thickness, subretinal fluid accumulation, and structural PED changes on OCT. a OCT on the day of presentation (after 29 aflibercept injections) shows a serous detachment of the fovea with elongated photoreceptors and an underlying shallow PED. b OCT 6 weeks after spironolactone administration shows a decrease in subfoveal fluid by 51%. PED growth was noted on the nasal and temporal CNV borders in the parafoveal region. c OCT 12 weeks after spironolactone administration shows a further decrease in subfoveal fluid by 90%, while further CNV growth at the PED borders can be noted, partially penetrating the retinal pigment epithelium with deposition of SHRM (*) atop the now type II CNV borders. d OCT 17 weeks after spironolactone administration and 5 weeks after a further anti-VEGF (aflibercept) injection, a complete resolution of subretinal fluid is achieved. anti-VEGF, anti-vascular endothelial growth factor; PED, pigment epithelium detachment; OCT, optical coherence tomography; SHRM, subretinal hyper-reflective material.
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F3
Within 6 weeks, subfoveal fluid significantly diminished by 51% from 108 to 55 mum (shown in Fig. 3b) and by 90% to 12 mum after 12 weeks (shown in Fig. 3c). Simultaneously to the reduction in subretinal fluid and choroidal thickness, at week 6 the PED was noted to grow on the nasal and temporal CNV borders in the parafoveal region, partially penetrating the retinal pigment epithelium, defining conversion into a type 2 CNV (shown in Fig. 3b). Fig. 3c), CNV growth and RPE penetration continued, along with newly diagnosed subretinal hyper-reflective material atop the type II CNV borders (shown in Fig. 3c). FAG and OCT-A confirmed the diagnosis of a type II CNV. As a consequence, the type 2 segments of the CNV regressed below the RPE, the PED returned to its original configuration, and subretinal fluid disappeared (shown in Fig. 3d).