This prospective study evaluated the OCT-A derived retinal FI values of subjects undergoing routine phacoemulsification cataract surgery at baseline as well as after the procedure. Following cataract extraction, there was a significant increase in the FI measures obtained from the superficial plexus as well as deep retinal plexus, with the greatest changes occurring in the latter. In contrast, no significant changes in FI measures were noted in the outer retinal layer and choriocapillaris. As can be expected in conjunction with improved media clarity, a significant improvement in SSI values was also noted following surgery.
The most significant change in FI was measured in the deep retinal plexus. Indeed, previous studies have reported an increased perfusion of the inner plexuses following cataract surgery.[21] Yu et al. reported a significant increase in OCT-A derived flow indices in both superficial and deep capillary plexuses following cataract surgery among a cohort of 12 patients.[21] Interestingly, Pilotto et al. reported a temporary increase in vascular area density and vessel density index in both the intermediate and deep capillary plexuses, but not the superficial plexus.[22] The increased measures, noted in 9 patients, appeared one day following surgery, but normalized one week postoperatively.[22] In our study, OCT-A derived measures of macular blood flow were not obtained during the first postoperative week, whereas emphasis was placed on the 4-8 week postoperative period, when the occurrence of pseudophakic CME is most frequently encountered.[3] Perhaps, differences in the OCT-A machines and postoperative care regimens employed in the aforementioned study may explain the seemingly contradicting results. The results of our study are supported by those of Zhoa et al. who employed the same OCT-A system and reported an increase in the total vessel density, representing measures from all retinal layers combined, as well as a decrease in FAZ area following cataract surgery.[18] The rise in the macular FI measures found in the current study could be attributed to the secretion of pro-inflammatory factors from the anterior segment, which migrate through the Cloquet canal to the posterior ocular segment. Such inflammatory cytokines may induce vasodilation which leads to an increase in vascular flow within the retinal capillary plexus and explains the elevation in FI found in our study.[3]
Recent studies employing enhanced depth imaging (EDI)-OCT demonstrated macular choroidal thickening following cataract surgery.[10–12] This technique involves acquisition of cross sectional macular images enabling enhanced visualization of the choroidal layers. However, EDI-OCT does not provide direct assessment of the choroidal vascular blood flow. In our current study no postoperative changes in the FI from the choriocapillaris were depicted on OCT-A. This discrepancy in results may be due to the development of choroidal leakage manifesting as choroidal thickening on EDI-OCT, yet not visualized on OCT-A technology as the flow is typically too slow. Alternatively, the changes may result from alterations occurring in deeper layers of the choroid which are not imaged on OCT-A. Previous studies evaluating changes in flow using OCT-A after cataract surgery did not consistently report data regarding the outer layers.[18, 21] Pilotto et al. reported an insignificant increase in choroidal thickness following surgery, but did not report on blood flow or perfusion measures in this vascular layer.[22] The authors postulated that a local choroidal inflammatory response may contribute to choroidal thickening detected at 1 month in their study.
Several studies, including the PREMED study[23] have reported on the successful prevention of pseudophakic CME using bromofenac 0.09% and dexamethasone 0.1% eye drops. It is of interest whether these treatments may impact the changes in FI measures identified in the current study following phacoemulsification cataract surgery. In the current study no patients developed pseudophakic CME and thus a comparison between patients with or without this condition was not performed. Future studies examining a correlation between changes in flow measures and the development of pseudophakic CME will perhaps identify risk factors for this condition. Future studies examining a correlation between changes in FI and the development of pseudophakic CME may identify risk factors for this condition and assess the etiologic role of such a rise in causing pseudophakic CME.
Despite its prospective nature, our study has several limitations, first of which is its relatively small sample size. However, repeated OCT-A images obtained longitudinally from the same patients before and after surgery allowed for a paired analysis with an adequate power, compared to a non-paired analysis. Larger studies may be warranted to validate our findings. An additional potential limitation is that due to the inherent nature of this study, baseline SSI values among eyes with cataract were considerably lower compared to the corresponding values obtained after surgery from the same eyes, thus potentially compromising the quantitative measures obtained at baseline and affecting our results. To address this limitation, only patients with an SSI value of 40 or higher at baseline were included in our study. This cut-off is in consistency with previous studies of eyes with potential media opacities. [18–20]
Altogether, our prospective OCT-A imaging study demonstrates a significant increase in the macular blood flow among eyes undergoing routine cataract extraction, with FI measures from the superficial and deep retinal plexuses demonstrating the largest changes. These findings corroborate evidence from structural imaging and histopathological studies, and support the vascular etiology of pseudophakic CME.