PMC9968801_01
Typical manifestations and resolution of SO. One week after the first PPV, residual vitreous hemorrhage and a yellowish supertemporal lesion were found in the right eye on the initial arrival at our hospital (A), although the ocular fundus was apparently normal in the left eye (B). Two weeks after the second PPV, mutton-fat keratic precipitates (C,D) and serous retinal detachment (E,F) were found in both eyes. OCT scanning revealed subretinal fluids and elongation of the outer segments (G,H). The UWFA showed delayed perfusion in the early phase, staining of the optic disc, and multi-lake fluorescence accumulation in both eyes (I-L). After 1 week of oral corticosteroids, the patient returned and the subretinal fluids were completely reabsorbed on ultrawide-field photographs (M,N) and OCT (O,P).
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The ocular examination revealed that the temporal mass was linked to a pair of dilated vessels, however, the persistent vitreous hemorrhage obscured further details, and the left eye was apparently normal (Figures 1A,B). Mutton-fat keratic precipitates were also found bilaterally (Figures 1C,D). Ultrawide-field photographs showed multifocal serous detachments of the retina in the posterior hole bilaterally (Figures 1E,F). OCT (Spectralis, Heidelberg Engineering Inc., Germany) scans revealed the loss of choroidal vascular architecture, bacillary detachment, and subretinal fluids in both eyes (Figures 1G,H). United Kingdom) was ordered based on the suspicion of SO. UWFA revealed hyperfluorescence of the temporal RCHs in the early phase in the right eye (Figure 1I). Delayed choroidal perfusion reflected by the choroidal hypofluorescence and multiple bilateral hyperfluorescent pinpoints in the posterior hole were found in the left eye (Figure 1J). In the late phase, the staining of the optic discs and increased subretinal pooling of fluorescence leaked from the initial pinpoints were also found (Figures 1K,L). After about 1 week of treatment, the serous retinal detachments resolved bilaterally (Figures 1M,N). However, the borders of the subfoveal choroid were still undetectable on enhanced depth imaging (EDI)-OCT (Figures 1O,P).
Comparison of the subfoveal choroidal thicknesses after the first PPV and after corticosteroid treatment. Five weeks after the first PPV, the subfoveal choroidal thicknesses of the right and left eyes were 572 and 458 mum, respectively (A,B). Three months after the second PPV being treated with oral corticosteroid, the subfoveal choroidal thicknesses of the right and left eyes decreased to 369 and 290 mum, respectively (C,D).
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B scan through the fovea revealed the macular epiretinal membrane in the right eye and bilateral increased subfoveal choroidal thickness (OD = 572 mum; OS = 458 mum, Figures 2A,B). In the present case, the choroidal thickness after corticosteroid treatment was smaller than the previous thickness (OD = 369 mum; OS = 290 mum, Figures 2C,D).
Choroidal vascular changes detected by OCTA after the first PPV and after corticosteroid treatment. Five weeks after the first PPV, the en-face OCTA slabs of the retina were mainly normal for both eyes (A,I), except for the shadowing effects of the vitreous hemorrhage in the right eye. However, the en-face OCTA slabs of both the choriocapillaris (B,J) and choroid (C,K) showed scattered dark spots (White arrows, yellow boxes in the corners of the panel contain magnified views). The B scan images (D,L) were taken along the level of the yellow line through the dark dots, which confirmed flow voids in the choriocapillaris and inner choroid layer (Yellow boxes in the corners of the panel contain magnified views). The choroid en-face structural slab of the left eye also showed an absence of choroidal vessels in the parapapillary area (M, yellow arrows). Three months after the second PPV and sustained oral corticosteroid treatment, the OCTA examination was repeated for both eyes. The retinal angiographies were still normal (E,N), the dark dots at the choriocapillaris (F,O), and choroid (G,P) levels disappeared at the corresponding locations. The follow-up B scans (H,Q) at the positions where the dark dots had been (yellow lines) demonstrated the recovery of the bloodstream signal (Yellow boxes in the corners of the panel contain magnified views). The choroidal vessels also reoccurred on the follow-up choroid en-face structural slab of the left eye (R, yellow arrows).
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Five weeks after the first PPV, OCTA images at the level of the retina were generally normal bilaterally, except for the dilated supratemporal vein with tortuosity that was linked to the RCH beyond the scope of the posterior 12 mm x 12 mm (Figures 3A,I). However, at the levels of both the choriocapillaris and choroid, there was a scattering of dots of flow void (Figures 3B,C,J,K, refer to yellow boxes for magnified view). The B scan through these dark spots (Figures 3B,C,J,K, yellow lines) confirmed the absence of the bloodstream signal beneath the RPE-Bruch membrane (Figures 3D,L, refer to yellow boxes for magnified view). After 3 months of oral administration of prednisone, there were still no obvious retinal vascular changes (Figures 3E,N). However, the flow void dots at the levels of both the choriocapillaris and choroid disappeared (Figures 3F,G,O,P, refer to yellow boxes for magnified view). The B scan through the positions corresponding to where the flow voids had been indicated the reappearance of blood stream signal (Figures 3H,Q, refer to yellow boxes for magnified view). Moreover, on the en-face structural images of the choroid, the choroidal vessels in the parapapillary atrophic area reappeared 3 months after the second PPV (Figure 3R, yellow arrow), whereas 5 weeks after the first PPV, the vessel was absent in this position (Figure 3M, yellow arrow).
Timeline summarizing the progression of SO. The key events or multimodal imaging examination results in the progression of SO are indicated by short lines along the timeline.
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The timeline in Figure 4 summarizes the key events and time intervals during the progression of SO.