Orbital infarction syndrome after multiple percutaneous sclerotherapy sessions for facial low‑flow vascular malformation: A case report and literature review.

Vision loss following sclerotherapy for facial vascular malformations (VMs) is a rare but detrimental complication. Here, we report a case of an 11‑year‑old boy with acute onset blepharoptosis, ophthalmoplegia, and blindness in his right eye after the 14th sclerotherapy session (percutaneous intralesional injection of sodium tetradecyl sulfate) for a right facial low‑flow VM without orbital involvement. Computed tomography angiography revealed no contrast enhancement in the right ophthalmic artery, superior ophthalmic vein, or extraocular muscles. He presented with the hallmarks of orbital infarction syndrome: Clear signs of anterior and posterior segment ischemia and disrupted arterial flow to the extraocular muscles. His blepharoptosis and eye movement improved 4 months later; however, he remained blind, and phthisis bulbi developed eventually. Thus, sclerotherapy for facial VM—even without orbital involvement––may result in severe ocular and orbital complications.

Early vitreomacular separation with delayed macular hole closure after ocriplasmin treatment.

Based on the indications, one‑third to one‑half of patients can achieve full‑thickness macular hole (FTMH) closure with or without the separation of vitreomacular adhesion (VMA) within 28 days of ocriplasmin treatment. The authors report the case of a 63‑year‑old man with early VMA separation and delayed FTMH closure after ocriplasmin treatment. Four weeks posttreatment, the posterior vitreous detachment occurred at the optic disk, and the macular hole (MH) started decreasing thereafter. MH closure was finally achieved at 10 weeks posttreatment, leaving minimal subretinal fluid. The patient’s vision improved from 0.8 LogMAR (pretreatment) to 0.3 LogMAR (12 weeks posttreatment). This case suggests that FTMH closure can be achieved within 28 days of ocriplasmin treatment.