Botulinum toxin–induced blepharoptosis: Anatomy, etiology, prevention, and therapeutic options. (11th August 2021)

• Record Type: Journal Article
• Authors: Nestor, Mark S.; Han, Haowei; Gade, Anita; Fischer, Daniel; Saban, Yves; Polselli, Roberto
• Is Part Of: Journal of cosmetic dermatology. Volume 20:Number 10(2021)
• Page Start: 3133
• Page End: 3146
• Publication Date: 2021-08-11
• Subjects: anatomy -- blepharoptosis -- botulinum toxin -- eyelid -- ptosis -- review; Skin -- Diseases -- Treatment -- Periodicals; Lasers in surgery -- Periodicals; Skin -- Pathophysiology -- Periodicals; Surgery, Plastic -- Periodicals; 616.5
• DOI: 10.1111/jocd.14361
• Languages: English
• ISSNs: 1473-2130

Abstract

Abstract: Background: Botulinum toxin A (BoNT‐A) has grown tremendously in aesthetic dermatology since 2002 when the United States Food and Drug Administration (FDA) first approved its use for treating moderate‐to‐severe glabellar lines. Blepharoptosis, due to local spread of toxin, is a reported side effect of BoNT‐A which, although rare, more frequently occurs among inexperienced practitioners. Objectives: The purpose of this review is to highlight the causes and management of eyelid ptosis secondary to BoNT‐A administration including new anatomic pathways for BoNT‐A spread from the brow area to the levator palpebrae superioris muscle. Methods: A literature search was conducted using electronic databases (PubMed, Science Direct, MEDLINE, Embase, CINAHL, EBSCO) regarding eyelid anatomy and the underlying pathogenesis, presentation, prevention, and treatment of eyelid ptosis secondary to BoNT‐A. Anatomic dissection has been performed to assess the role of neurovascular pedicles and supraorbital foramen anatomic variations. Results: Blepharoptosis occurs due to weakness of the levator palpebrae superioris muscle. Mean onset is 3–14 days after injection and eventually self‐resolves after the paralytic effect of BoNT‐A wanes. Administration of medications, such as oxymetazoline hydrochloride or apraclonidine hydrochloride eye drops, anticholinesterase agents, or transdermal BoNT‐A injections to the pre‐tarsal orbicularis, can at least partially reverse eyelid ptosis. Anatomic study shows that a supraorbital foramen may be present in some patients and constitutes a shortcut from the brow area directly into the orbital roof, following the supraorbital neurovascular pedicle. Conclusion: Providers should understand the anatomy and be aware of the causes and treatment for blepharoptosis when injecting BoNT‐A for the reduction of facial wrinkles. Thorough anatomic knowledge of the supraorbital area and orbital roof is paramount to preventing incorrect injection into "danger zones, " which increase the risk of eyelid ptosis.