PMC10149671_01
Serial ultrawide-field fundus photographs. (A) Initial presentation showed diffuse perivascular sheathing with frosted branch angiitis appearance. (B) Initial fluorescein angiography revealed multiple segmental phlebitis (yellow arrow) with occlusive arteritis (white arrow) and retinal non-perfusion (orange arrow). The visual acuity was 0.025 (both eyes). (C) Four weeks later, partial resolution of the perivasculitis following systemic corticosteroid and antiviral treatment was seen; however, aggravated Purtscher-like retinopathy was demonstrated (white arrow). (D) Twenty-one weeks after initial visit and 8 weeks following HBOT, alleviated vascular leakage, however, with extensive macular and midperipheral retinal non-perfusion was shown. The visual acuity was 0.16 (both eyes). (E) Nineteen weeks after initial visit, reduced Purtscher fleckens was note. Frosted branch angiitis almost completely resolved following combined corticosteroid, antiviral agent, and immunosuppressive medications. (F) Thirty-nine weeks after initial visit and 26 weeks following HBOT as well as 15 weeks after retinal photocoagulation, there were vascular leakage with few vitreous hemorrhage. The visual acuity was 0.1 (right) and 0.16 (left).
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F1
Necrotizing retinitis was not observed (Figures 1A, B). Although the bilateral FBA and macular edema gradually alleviated (Figures 1C, 2B) after several weeks of medical treatment, the BCVA improvement was minimal (0.05, right eye; counting finger, left eye) (Table 1). Persistent macular ischemia, with clinical presentations of profound PuR and compatible ischemic hyperreflective changes on OCT (Figures 1C, 2C), was identified to be the main cause of poor vision. FBA treatment and corticosteroid tapering (Figure 3). Follow-up fundus photograph and fluorescein angiography performed 21 weeks after the initial visit and 8 weeks following HBOT revealed almost completely resolution of FBA and decrease in size of PuR, but extensive macular and mid-peripheral retinal ischemia (Figures 1D, E). Therefore, retinal photocoagulation on the non-perfusion area was performed 13 weeks after the initiation of HBOT to prevent further neovascular complications, such as vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma (Figure 1F).
Serial changes in OCT. (A) Initial OCT showed profound macular edema with combine intraretinal and subretinal fluid. (B) Two weeks after initial visit, partial resolution of the macular edema; however, hyperreflective change could be noted at the inner and middle retinal layers. The visual acuity was 0.1 (right) and 0.05 (left). (C) Eleven weeks after initial visit, complete resolution of the macular edema. CFT 156 mum (right) and 147 mum (left). The visual acuity was 0.05 (right) and counting finger 30 cm (left). (D) Seventeen weeks after initial visit and 4 weeks following HBOT. Slightly reduce hyperreflectivity at the left eye could be noted. The visual acuity was 0.1 (both). (E) Twenty-one weeks after initial visit and 8 weeks following HBOT. Extensive retinal thinning with ellipsoid zone loss was noted. The visual acuity was 0.16 (both). (F) Twenty-eight weeks after initial visit and 15 weeks following HBOT. Reduced inner retinal thinning was noted. The visual acuity was 0.16 (right) and 0.2 (left). (G) Forty-three weeks after initial visit and 30 weeks following HBOT. Reduced inner retinal thinning was noted. The visual acuity was 0.05 (right) and 0.16 (left). (H) Sixty weeks after initial visit and 47 weeks following HBOT. Reduced inner retinal thinning was noted. The visual acuity was 0.1 (right) and 0.16 (left).
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F2
OCT revealed profound macular edema with intraretinal fluid, subretinal fluid, and inner to middle retinal layer hyperreflectiveness (Figure 2A). Although the bilateral FBA and macular edema gradually alleviated (Figures 1C, 2B) after several weeks of medical treatment, the BCVA improvement was minimal (0.05, right eye; counting finger, left eye) (Table 1). Persistent macular ischemia, with clinical presentations of profound PuR and compatible ischemic hyperreflective changes on OCT (Figures 1C, 2C), was identified to be the main cause of poor vision.
Treatment timeline. ATA, atmosphere absolute; HBOT, hyperbaric oxygen therapy; qd, every day; q12h, every 12 hours; qod, every other day; qw, every week. *Treatment protocol: 2.0 ATA for 75 min per session, 1 session per day, 5 days per week.
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F3
The patient was initially prescribed prednisolone (40 mg/day), valaciclovir (500 mg every 12 h), and acetylsalicylic acid (100 mg every other day) (Figure 3). FBA treatment and corticosteroid tapering (Figure 3). Follow-up fundus photograph and fluorescein angiography performed 21 weeks after the initial visit and 8 weeks following HBOT revealed almost completely resolution of FBA and decrease in size of PuR, but extensive macular and mid-peripheral retinal ischemia (Figures 1D, E).