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Introduction Vascular occlusion secondary to hyaluronic acid fillers represents a severe complication requiring prompt intervention. While consensus guidelines often advocate high-dose pulsed hyaluronidase, empirical low-dose protocols remain underexplored in real-world clinical settings. The aim of this study is to report our clinical experience using targeted low-dose hyaluronidase in patients presenting with facial vascular occlusion, alongside an untreated case documenting the natural history and sequelae of prolonged ischemia. Cases description We conducted a retrospective case series of seven patients presenting with filler-induced vascular occlusion. One patient presented with established irreversible damage and received no enzymatic intervention, serving as an observational reference. Two representative cases exhibiting established necrotic eschars were described in detail, alongside four additional cases managed following prolonged ischemia. Intervention and outcomes Six patients underwent targeted infiltration of compounded bovine hyaluronidase (100 IU/mL; total doses 200–275 IU, titrated according to anatomical territory and extent of tissue compromise) combined with standardized adjunctive supportive care. In the untreated case, delayed presentation culminated in full-thickness scalp necrosis and permanent cicatricial alopecia. Among the six treated patients, including cases presenting after an extended delay, targeted low-dose hyaluronidase halted ischemic progression and resulted in complete clinical recovery without permanent structural tissue loss, provided that a consolidated necrotic eschar had not developed prior to intervention. Conclusion This case series illustrates the clinical course of filler-induced ischemia, reinforcing the risk of irreversible tissue destruction in untreated presentations. Furthermore, our findings suggest that a targeted low-dose hyaluronidase regimen, titrated by territory and combined with supportive therapy, may achieve favorable resolution in facial vascular compromise even following delayed presentation, provided that a necrotic eschar has not already become consolidated. Further controlled investigations are warranted.
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Barber-García et al. (2026) studied this question.
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