Pathophysiology Study of Filler-Induced Blindness

A number of authors have proposed retrograde arterial embolism as the responsible mechanism for filler-induced blindness. However, no previous human study has substantiated this proposed mechanism. The aim of this study was to investigate the pathophysiology of filler-induced blindness using a fresh cadaver perfusion technique. A fresh cadaver head perfusion model that simulates both physiologic blood pressure and flow rate of the carotid artery, ophthalmic artery, and supratrochlear artery was used. The common carotid artery was cannulated and the internal jugular vein exposed for open venous drainage. A plasma-based perfusate was circulated through the cadaver head, which was connected to a perfusion system consisting of a roller pump, preload reservoir, and pressure monitor. The hyaluronic acid filler mixed with methylene blue was injected into the cannulated superficial branch of the supratrochlear artery. Cadaver dissection, angiographic study, and histology were used to investigate filler-induced blindness. Cannulation of the superficial branch of the supratrochlear artery was successful in all six cadavers. Emboli to the ophthalmic artery was successfully demonstrated in the three out of 6 fresh cadaver heads. The C-arm angiogram documented a cut-off sign in the ophthalmic artery due to hyaluronic acid filler emboli. An average intravascular volume of the intraorbital part of the supratrochlear artery was 50.0 L. The average depth of location of the superficial branch of the supratrochlear artery from the epidermal surface was 1.5 mm. Our cadaveric study demonstrated that retrograde hyaluronic acid filler emboli to the ophthalmic artery could be produced by the cannulation of the supratrochlear artery. The superficial location of the supratrochlear artery, the rich vasculature surrounding it, and the variability in the anatomy make this possible.