Table 1.
Patient clinical characteristics among follow-ups.
Fig 1.
Left-eye SD-OCT of patient 1 throughout disease evolution.
A. Attached vitreous at the level of the vitreoretinal interface with punctate hyperreflective vitreous cells, a loss of foveal architecture, an epiretinal membrane, disruption of inner retinal layers and hyper-reflective material within outer retinal layers. B. Full-thickness involvement corresponding to retinochoroidal lesion. C. epiretinal membrane, central irregular hyper-reflective material within the zone of RPE atrophy. D. Macular atrophy with an epiretinal membrane, hyper-reflective points within outer retinal layers, and irregularity of RPE.
Fig 2.
A-D. Color fundus photography follow-up of patient 2. A. Left eye color fundus photography at initial presentation showing disc pallor, an active creamy yellowish PORT lesion in the parafoveal area. B. Disc pallor improvement, PORT lesion starts becoming hyperpigmented. C and D. Disc pallor is no longer notable, and the PORT lesion is reduced in size and appears more pigmented at two months of follow-up. E-L. SD-OCT scan follow-up of the same patient. E. SD-OCT scan demonstrating vitreous cells, foveal architectural loss, subretinal fluid pocket with white material accumulations and disruption of the ellipsoid zone. F. Atrophy of outer retinal layers. G. Thinning of outer retinal layers. H. Disruption of the ellipsoid zone and atrophy of RPE. I. Foveal thinning, subretinal disruption with hyper-reflective material in outer retinal layers, and backscattering. J. Foveal atrophy, ellipsoid disruption, RPE atrophy, and backscattering. K. Important foveal atrophy, ellipsoid zone disruption and backscattering. L. Atrophic scarring at the fovea with central loss of the ellipsoid zone and hyperreflective backscattering. M-N. Fundus autofluorescence follow-up of the same patient. M. Hypo-autofluorescence area in the perifovea corresponding to PORT lesion with a hyper-autofluorescent superonasal edge. N. At the 10-month follow-up, shows a hypo-autofluorescence in the perifovea corresponding to the PORT lesion with a hyper-autofluorescent superonasal edge and a mottled hyper-autofluorescence between the disc and the PORT lesion.
Fig 3.
A. SD-OCT shows a PORT lesion with epiretinal membrane, full-thickness involvement, and central ellipsoid disruption. B. SD-OCT shows a PORT lesion after three months of treatment, retinochoroidal atrophy with backscattering corresponds to an earlier retinochoroiditis lesion. C. Fundus autofluorescence demonstrates mottled hypoautofluorescence of PORT lesion in perifoveal area.
Fig 4.
SD-OCT follow-up of patient 4.
A. SD-OCT shows loss of architectural foveal with small mound of deep hyper-reflective material within zone RPE atrophy and photoreceptor disruption. B. SD-OCT demonstrates foveal architecture irregularity because of the presence of a smaller amount of hyper-reflective material in the fovea with RPE atrophy and photoreceptor disruption.
Fig 5.
A. Fundus photography of RE showing a superotemporal retinochoroidal scar and superior perifoveal white-yellowish PORT lesion (arrow). B. Green line demonstrates the location of SD-OCT image through an old chorioretinal scar with areas of irregular RPE and atrophy with visualization of Bruch’s membrane.
Fig 6.
Multimodal assessment of patient 7.
A. SD-OCT demonstrates a lesion with full-thickness involvement and hyper-reflective material at the outer retinal layers. B. Fundus photograph shows healed retinochoroiditis with pigmentation temporal to the fovea. C. Autofluorescence shows hypo-autofluorescence of PORT lesions.
Fig 7.
Multimodal imaging of patient 8.
A. Green line demonstrates location of SD-OCT image: irregular thinning of the ellipsoid zone, RPE atrophy and photoreceptor disruption. B. Right eye widefield fundus photography shows a retinochoroidal scar between the fovea and inferotemporal arcade. C. Left eye widefield fundus photography shows mild vitritis, disc pallor, a retinochoroidal scar at the inferonasal arcade, and a focal yellowish lesion at the edge of a healing retinochoroiditis lesion in the superonasal area.