In the current study, nine eyes with extramacular BRVO showed retinal swelling in the macular area with foveal SRD. Macular swelling was predominantly observed in the outer plexiform layer while the inner layer of the retina often retained relatively normal physiologic structure. Using timedomain OCT, Takahashi et al14
previously reported four cases of foveal SRD associated with extramacular BRVO. The authors speculated that the leakage from the extramacular BRVO traveled to the macula through the subretinal space and formed the SRD beneath the fovea. In the current study, however, we could not detect any subretinal connections between the area affected by BRVO and the foveal SRD, even with sequential thin sectioning using spectral-domain OCT.
The eyes from two of the patients in the study showed a small break on the external surface of the detached neurosensory retina near the fovea. In these eyes, the break seemed to allow fluid that had accumulated within the outer retina to flow into the subretinal space. Recent advances in OCT resolution and contrast have facilitated the detection of breaks on the external surface of the neurosensory retina in eyes with diabetic macular edema,17
retinal arterial macroaneurysms,18
and retinal vein occlusions.10
Although it may be an uncommon feature associated with SRD, we could not detect any apparent breaks on the external surface of the retina in the remaining eyes. Small breaks on the external surface of the retina may be one possible mechanism for causing focal SRD beneath the fovea. Simple diffusion of intraretinal fluid into the subretinal space may represent a more common cause of foveal SRD associated with extramacular BRVO.19
It is not known why focal SRD associated with extramacular BRVO invariably occurs beneath the fovea. Previously, Taki et al20
reported a case of macular edema caused by an extramacular BRVO that improved after vitrectomy. However, none of the eyes from the patients reviewed in this study showed vitreomacular traction in the macular area. Tsujikawa et al10
reported that Müller cell cone traction plays a role in the formation of small pointed foveal SRD in eyes with retinal vein occlusion. They reported that small pointed SRD extends to become dome-shaped SRD, which resembles the SRD observed in our study patients. Müller cell cones, which are believed to serve as plugs that bind the photoreceptor cells to the foveola,21
extend outward and form the internal limiting membrane at the foveal area.22
In eyes with extramacular BRVO, leakage from the affected retinal capillaries travels preferentially through the outer plexiform layer and causes retinal edema mainly within Henle’s layer. At the fovea, however, Müller cell cones serve to maintain the integrity of the foveal structure and consequently cause traction with the inner and outer segments of the foveal photoreceptors, which results in foveal SRD. In the current study, none of the records reviewed reported focal SRD outside the fovea. Because patients may not have had symptoms arising from the focal SRD formed outside the fovea, we cannot deny the possibility that some patients had this type of SRD.
Of the nine eyes in this study, two had a final visual acuity of less than 0.5. Visual prognosis of eyes with extramacular BRVO is better than those with macular BRVO, even if they have SRD under the fovea. In the current study, the mean total retinal thickness in the fovea was 413 ± 80 μm. However, most of the patients reviewed had relatively normal neurosensory retinal thickness in the fovea (mean ± standard deviation; 179 ± 68 μm). The formation of SRD under the fovea may contribute to retaining the integrity of the foveal structure. Unless SRD develops under the fovea, fluid extending into the fovea may form large foveal cystoid spaces, leading to severe visual dysfunction.24
SRD may occasionally regress spontaneously, but focal laser photocoagulation often results in immediate regression. In the current study, all eyes showed hyperreflective foci in the outer retina, most frequently along the inner boundary of the outer plexiform layer and external limiting membrane. It is reported that hyperreflective foci are mainly small lipid exudates left after the absorption of intraretinal fluid.25
Foveal accumulation of the hard exudate may cause destruction of the foveal structure and lead to poor visual prognosis.13
Limitations of the current study include its retrospective nature and small sample size. In addition, when extramacular BRVO causes no macular complications, patients rarely present ocular symptoms. Thus, it is difficult to estimate the risk of macular complications when BRVO occurs outside the vascular arcade. Furthermore, in all of our patients, leakage from the BRVO extended towards the macula, even if BRVO occurred in the inferior quadrant. The reason for this preferential fluid extension is unclear. Therefore, although the leakage from extramacular BRVO may extend in various directions, we only reviewed cases with extramacular BRVO that had macular complications.