Background: Blindness following facial filler procedures, although rare, is devastating, usually acute, permanent, and attributed to an ophthalmic artery embolus. However, blindness may be delayed for up to 2 weeks, sometimes following injection at remote sites, suggesting alternative pathways and pathogenesis. Methods: Seeking solutions, fresh cadaver radiographic lead oxide injection, dissection, and histologic studies of the orbital and facial pathways of the ophthalmic angiosome, performed by the ophthalmic artery and vein, both isolated and together, and facial artery perfusions, were combined with total body archival arterial and venous investigations. Results: These revealed (1) arteriovenous connections between the ophthalmic artery and vein in the orbit and between vessels in the inner canthus, allowing passage of large globules of lead oxide; (2) the glabella, inner canthi, and nasal dorsum are the most vulnerable injection sites because ophthalmic artery branches are anchored to the orbital rim as they exit, a plexus of large-caliber avalvular veins drain into the orbits, and arteriovenous connections are present; (3) choke anastomoses between posterior and anterior ciliary vessels supplying the choroid and eye muscles may react with spasm to confine territories impacted with ophthalmic artery embolus; (4) true anastomoses exist between ophthalmic and ipsilateral or contralateral facial arteries, without reduction in caliber, permitting unobstructed embolus from remote sites; and (5) ophthalmic and facial veins are avalvular, allowing reverse flow. Conclusion: The authors’ study has shown potential arterial and venous pathways for filler embolus to cause blindness or visual field defects, and is supported clinically by a review of the case literature of blindness following facial filler injection.

These findings provide the anatomical basis for the observed reliability of longitudinal flaps in the leg. The superficial cutaneous nerves of the leg, especially the saphenous and medial sural cutaneous nerves, are paralleled by a vascular axis on or beside the nerve comprising long perforator branches connected usually but not always by large-caliber true anastomotic connections. This emphasizes the importance of understanding the characteristics of interperforator anastomoses when designing and raising flaps.

We present 3 patients undergoing revisional implant surgery more than 20 years after congenital breast asymmetry correction. All of them had Poland syndrome. In 2 patients, the parietal pleura was inadvertently damaged during capsulectomy, resulting in a pneumothorax in one patient and implant loss in the other. The loss followed a copious accumulation of fluid around the implant, possibly due to a (persistent) communication with the pleural cavity. In the first case the pneumothorax was successfully treated intraoperatively. The third patient suffered no complications during surgery. Predisposing factors for pleural damage during revisional implant surgery for congenital breast asymmetry are discussed, in addition to the merits of total capsulectomy during implant exchange. It is concluded that surgeons should aim to minimize the possibility of pleural damage during this surgery and should proceed with caution when performing total capsulectomy in at-risk patients.