PMC9938398_01
At presentation, the fundus photograph showed parafoveal and post-hyaloid hemorrhage (a) and optical coherence tomography (OCT) demonstrated alterations at the macular area, such as slight thickening of the macula, loss of fovea depression, disruption, and migration of the retinal pigment epithelium (RPE) and alterations of the outer retina including attenuation of the ellipsoid zone, external limiting membrane, and outer nuclear layer and disruption of photoreceptors' inner segment/outer segment (IS/OS) junction (b). At the 1-month follow-up visit, the patient presented with a full-thickness macular hole that was evident in the fundus photograph (c) and OCT (d).
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F1
Ophthalmological examination of the right eye demonstrated an unremarkable anterior segment, lens, intraocular pressure, and vitreous, while fundoscopic examination revealed parafoveal and post-hyaloid hemorrhage (Fig. 1a). Optical coherence tomography (OCT) showed a slight thickening of the macula, loss of fovea depression, disruption and migration of the retinal pigment epithelium (RPE), and alterations of the outer retina including attenuation of the ellipsoid zone, external limiting membrane, and outer nuclear layer and disruption of photoreceptors' inner segment/outer segment junction (Fig. 1b). After 1 month, fundoscopy disclosed the formation of a full-thickness macular hole (FTMH) (Fig. 1c), which was also confirmed by OCT (Fig. 1d).
At 6 months, fundus photograph (a) and OCT (b) show macular hole closure with disruption and migration of the retinal pigment epithelium (RPE). Fluorescein angiography (FAG) demonstrated window defects due to the RPE alterations at the macula (c) and indocyanine green angiography showed normal choroidal vasculature (d). One and a half year later, the patient presented with RPE alterations on the fundus photograph (e), while intraretinal and subretinal fluids were present on the OCT (f). Early (g) and late (h) phase of FAG revealed leakage which corresponded to classic choroidal neovascularization.
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F2
Notwithstanding the fact that functional outcomes were satisfactory, fundus examination (Fig. 2a) depicted a distorted retinal morphology and structure, along with disruption of the RPE. OCT illustrated disruption and migration of the RPE (Fig. 2b), while intravenous fluorescein angiography (Fig. 2c) demonstrated associated window defects due to the RPE alterations at the macula, confirming chronicity, and indocyanine green angiography showed normal choroidal vasculature (Fig. 2d). Fundus examination revealed alterations at the level of the RPE (Fig. 2e). OCT of the macula demonstrated a central subretinal hyper-reflective region along with intraretinal and subretinal fluid that corresponded to signs indicating CNV (Fig. 2f). Fluorescein angiography displayed leakage which corresponded to the CNV lesion, confirming the diagnosis of classic CNV (Fig. 2g).
Two weeks after the diagnosis of choroidal neovascularization, the patient came back with subretinal blood at the macular area, as shown at the fundus photograph (a) along with extensive intraretinal and subretinal fluid, as shown on OCT (b). The patient was treated with intravitreal ranibizumab injection. At the 4-week visit after the injection, fundus image (c) and OCT (d) illustrated absorption of blood, as well as intraretinal and subretinal fluid, with residual neovascular scarred tissue. OCT images (e, f) at 8-year of follow-up remained stable.
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F3
Fundoscopic examination revealed extensive subretinal blood (Fig. 3a), while OCT imaging was worse than that of the previous visit (Fig. 3b). OCT illustrated absorption of the intraretinal and subretinal fluid with residual neovascular scarred tissue at the foveal area (Fig. 3d), which was also evident at the fundoscopy (Fig. 3c). The patient's condition has remained stable during a follow-up period of 8 years (Fig. 3e, f).