This study sought to investigate macular microvascular changes on OCTA imaging after scleral buckling for RRD, showing a postoperative reduction in vessel density of the superficial capillary plexus in both macula-on and macula-off RRDs. Postoperative vessel density of deep capillary plexus seems to be impaired in eyes affected by macula-off RRD, while it seems to be unchanged in macula-on RRDs.
Microvascular alterations in retinal and choroidal circulation occurring in RRD eyes have been long studied.6,9,18 Before the advent of OCTA, other tools had been used.6,18 Scanning laser Doppler flowmetry showed a decrease in macular flow in RRD eyes.18 Such vascular changes have been supposed to be related to a reversible vasoconstriction, which could be secondary to tissue hypoxia.9,19 In macula-off detachments, biological composition of subretinal fluid has been assumed to affect oxygen diffusion due to an increase of inflammatory mediators.9,12,20 Consequently, microvascular changes and photoreceptor alterations are likely to occur in the macula and might not be fully restored even after anatomical re-attachment.10,14,21 These alterations, in turn, may determine functional defects, such as suboptimal visual recovery, color vision impairment and persistent metamorphopsia.9,21,22
The introduction of OCTA imaging represented a significant breakthrough in the assessment of retinal microcirculation. Several studies have explored macular microvascular alterations on OCTA imaging following RRD repair surgery.10–17, 23 Most available evidence is on vitrectomy cases.12, 14–17,23 A few reports included both scleral buckling and vitrectomy cases. Barca et al found an augmentation in the FAZ area in the SB group compared with the vitrectomy group.10 Tsen et al found no difference in the FAZ area and vessel density between eyes with and without a buckle.11 Nam et al found a greater vessel density reduction in vitrectomy cases compared with SB cases.13 However, to the best of our knowledge, no study has specifically focused on microvascular alterations on OCTA following scleral buckling for RRD.
According to the majority of studies on vitrectomy cases, vessel density of macular capillary plexi, both deep and superficial, is reduced after RRD surgery.10,11,13,14,16,17,23 Hong et al analyzed macular vessel density of 31 eyes at 6 months from vitrectomy for RRD, including both macula-on and macula-off cases.15 Their study showed no difference in mean vessel density of both DCP and SCP between RRD eyes and controls. These findings seem to be in disagreement with those reported by most studies, but need to be looked at in more detail. A possible explanation for these controversial results is the fact that vessel density seems to increase on a long-term follow-up. Some authors described a significantly reduced vessel density in the early post-operative period, which progressively increased throughout long-term follow-up.10,13 Indeed, vessel density seems to be comparable between RRD eyes and controls between 6-to-12 months post-operatively.10,13 Such a tendency could explain why Hong et al15 were unable to prove microvascular alterations at 6 months after RRD surgery.
Our findings showed that vessel density featured a similar increasing trend over a 6-month follow-up after scleral buckling surgery for RRD. In eyes with macula-on RRD, baseline vessel density was reduced in the superficial capillary plexus compared with controls; following SB procedure, SCP vessel density increased over a 6-month period. In eyes with macula-off RRD, baseline OCTA was not available; in this group, vessel density in the deep capillary plexus significantly improved from month 1 to month 6 postoperatively.
Barca et al hypothesized that the impairment of vessel density of the superficial capillary plexus in eyes with macula-on RRD might be related to the fact that the SCP is the first vascular layer affected in case of a rapid increase of vascular resistance secondary to a recent retinal detachment.10 The superficial capillary plexus is characterized by a greater density of smooth muscle and arterioles compared with the deep plexus. Consequently, vasoconstriction driven by tissue hypoxia is supposed to be stronger in the superficial plexus.10 The improvement of SCP vessel density following successful RRD repair seems to confirm this hypothesis. Our findings in the macula-on cohort corroborated this. Furthermore, our correlation analysis between axial length change and vessel density provides a new insight in the pathogenetic mechanism leading to microvascular alterations. In the macula-on cohort, mean change of axial length negatively correlated with mean change of SCP vessel density. This means that the greater the postoperative increase in axial length, the deeper the reduction of vessel density. A greater increase in axial length is secondary to a tighter encircling band. Scleral buckling procedure included an evacuative puncture with external fluid drainage in all cases. The encircling band is likely to be tighter in cases with a greater amount of subretinal fluid because post-drainage hypotony is usually dealt with by tightening the band. On this basis, our assumption is that a greater increase in axial length could be associated with a larger amount of subretinal fluid. Consequently, we might speculate that the larger the amount of subretinal fluid, the greater the impairment of SCP vessel density. This corroborates the hypothesis of vasoconstriction in the macular SCP secondary to an increase of vascular resistance due to peripheral hypoxia in the detached retina. However, we cannot rule out that this inverse correlation between axial length increase and vessel density change could be a consequence of mechanical damage of the retinal microvascular network caused by the surgery itself. D’Aloisio et al reported a reduction in iris perfusion on anterior segment OCTA after scleral buckling procedure.7 The author speculated that these alterations could be related to mechanical stress on vessels due to surgical maneuvers and encircling band application.7
We found a reduction of vessel density in both superficial and deep capillary plexi in the macula-off group at 6 months after SB surgery. The deep capillary plexus has been shown to be more vulnerable to hypoxic injury.14 Vascular alterations of this layer are typical of chronic diseases, such as diabetic retinopathy.24 In the context of retinal detachment, a detached macula usually means a less recent onset compared with macula-on RRDs. The fact that DCP vessel density is reduced in the macula-off group could be secondary either to damage induced by the subretinal fluid or to microvascular alterations related to a longer disease duration. The increase of DCP vessel density during the follow-up might indicate that successful surgery removed the causative factor of such microvascular injury. However, the understanding of this mechanisms is limited by the lack of baseline scans.
Several limitations characterized the present study. First, the retrospective design might have introduced some bias. However, the strict eligibility criteria should have reduced this risk. Second, the sample size was relatively small. A larger population would have allowed additional analyses and to further investigate which clinical variables might have an influence on vessel density. Nonetheless, we included a total of 37 eyes and all surgeries were performed by the same vitreoretinal consultant. With regard to OCTA imaging, our software did not provide two different values of FAZ area for the deep and the superficial capillary plexi, but only one value including both layers.
In conclusion, our analyses showed that vessel density on OCTA is reduced following scleral buckling surgery for RRD. These microvascular alterations, to some extent, are similar to those reported after vitrectomy and could be a consequence of the disease rather than the surgical procedure. Axial length increase seems to be associated with worse vessel density outcome. Whether this is secondary to the presence of a greater amount of subretinal fluid at baseline or to mechanical damage caused by the encircling band needs to be further investigated. Larger studies are warranted to better understand which mechanisms lead to such a microvascular impairment and which clinical variables might have an influence on it.