OCT Angiography reveals changes in foveal vessel architecture and foveal flow in central serous chorioretinopathy.

Abstract

Central serous chorioretinopathy (CSC) represents one of the most common vision-threatening retinopathies after age-related macular degeneration, diabetic retinopathy and retinal vein occlusion. It is characterized by an accumulation of subretinal fluid (SRF) sometimes in association with a retinal pigment epithelium (RPE) detachment. The exact pathophysiological mechanism is still a matter of debate. Nevertheless, based on multimodal imaging numerous authors have postulated that a hyperpermeable choroid and a dysfunctional RPE cause the accumulation of SRF (Daruich et al. 2015). So far, the information on secondary effects on retinal vessels in this disease is limited. With the advent of optical coherence tomography angiography (OCT-A), a novel non-invasive depth-selective imaging tool, an enhanced visualization of retinal blood flow and the foveal avascular zone (FAZ) has become available. We included 16 CSC patients that showed characteristic chorioretinal alterations in the affected eye and no morphological or functional change in the fellow eye based on spectral domain OCT and fluorescence angiography (FA). Optical coherence tomography angiography imaging was conducted with a commercial OCT-system (AngioVue, RTVue XR Avanti SD-OCT; Optovue, Fremont, CA, USA ). The device obtains volumetric scans of 304 × 304 A-scans at 70 000 A-scans per second using a light source centred on 840 nm. The software offers automated segmentation of retinal layers as well as a quantification of flow density in the superficial layers of the retina defined as flow per volume in percent (AngioAnalytics, Optovue). In both the affected eye and the non-affected fellow eye of CSC patients, the flow density in the foveal (FDfov) region of a foveally-centred Early Treatment Diabetic Retinopathy Study grid was measured and compared to data of age-matched healthy control eyes. Besides, the FAZ was determined in both eyes of CSC patients using a manual measurement tool of the software (Fig. 1). Interestingly, both, affected eyes and non-affected fellow eyes of CSC patients showed a significantly higher mean FDfov (35.66% ± 4.02%; 36.09% ± 4.77%) in the superficial plexus compared to healthy controls (32.22% ± 3.94%). In addition, the FAZ was significantly smaller in CSC patients compared to healthy controls in the superficial plexus (CSC eyes affected, non-affected fellow eyes, controls: 0.15 ± 0.07 mm2; 0.15 ± 0.07 mm2; 0.21 ± 0.06 mm2; Fig. 1). We hypothesize that the decrease in the FAZ and the increase in flow in eyes of CSC patients may be interpreted as a reaction to pathological changes due to CSC such as accumulation of SRF. Continuous SRF impedes nourishment of the photoreceptor layer from the choriocapillaris and may stimulate an increase in retinal flow density (Eperon et al. 1975). Second, in contrast to many other macular diseases with accumulated SRF, the inner blood retina barrier is presumably not affected by CSC pathology and may be capable of inducing regulatory mechanisms such as vasodilatation to resorb SRF. With regards to the affected eye, the findings in the fellow eyes of CSC patients suggest that such compensatory changes in the retinal vessels may be centrally induced. Another explanation might be that clinically non-affected fellow eyes are in fact affected by the disease, however, changes are not yet accessible to current imaging methods. Optical coherence tomography angiography is a nascent technology, yet, experience and data on clinical image interpretation in CSC is growing (Costanzo et al. 2015; Teussink et al. 2015). Obviously, this preliminary study is also limited by the small sample size. In conclusion, OCT-A reveals an increase in retinal flow density and a decrease in the FAZ in affected eyes as well as unaffected fellow eyes of CSC patients. This may be interpreted as an adaptation of foveal retinal vessels in response to pathological CSC changes such as perfusion changes in the choriocapillaris, disintegrity of the RPE and subsequent accumulation of SRF.