Pathophysiology Study of Filler-Induced Blindness

Pathophysiology Study of Filler-Induced Blindness Abstract Background 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. Objectives The aim of this study was to investigate the pathophysiology of filler-induced blindness using a fresh cadaver perfusion technique. Methods A fresh cadaver head perfusion model that simulates both physiologic blood pressure and flow rate of the carotid artery, ophthalmic artery, 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. Results 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 six 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 µl. The average depth of location of the superficial branch of the supratrochlear artery from the epidermal surface was 1.5 mm. Conclusions 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. © 2018 The American Society for Aesthetic Plastic Surgery, Inc. Reprints and permission: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Aesthetic Surgery Journal Oxford University Press

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Publisher
Mosby Inc.
Copyright
© 2018 The American Society for Aesthetic Plastic Surgery, Inc. Reprints and permission: journals.permissions@oup.com
ISSN
1090-820X
eISSN
1527-330X
D.O.I.
10.1093/asj/sjy141
Publisher site
See Article on Publisher Site

Abstract

Abstract Background 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. Objectives The aim of this study was to investigate the pathophysiology of filler-induced blindness using a fresh cadaver perfusion technique. Methods A fresh cadaver head perfusion model that simulates both physiologic blood pressure and flow rate of the carotid artery, ophthalmic artery, 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. Results 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 six 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 µl. The average depth of location of the superficial branch of the supratrochlear artery from the epidermal surface was 1.5 mm. Conclusions 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. © 2018 The American Society for Aesthetic Plastic Surgery, Inc. Reprints and permission: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

Aesthetic Surgery JournalOxford University Press

Published: Jun 5, 2018

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