DOI: 10.1097/PRS.0b013e3181d5152e

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PMID: 20440131

Issn Print: 0032-1052

Publication Date: 2010/05/01


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Alar Necrosis after Facial Injection of Hyaluronic Acid

Benjamin Burt; Tanuj Nakra; David K. Isaacs; Robert A. Goldberg

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Excerpt

A 46-year-old man requested aesthetic enhancement of his nasolabial folds. Local anesthetic block of the infraorbital nerves was achieved using 2% lidocaine with 1:100,000 epinephrine. One cubic centimeter of hyaluronic acid gel (Juvéderm; Allergan, Inc., Irvine, Calif.) was injected into both nasolabial folds through a transcutaneous and superior gingivobuccal sulcus approach. Successful effacement of the nasolabial folds was achieved. The patient tolerated the procedure well and there were no immediate postinjection complications.
On postinjection day 1, the patient reported right-sided alar pain during the prior night. The external skin of the right ala appeared dusky with poor capillary return, but the nasal mucosa was intact.
Over the ensuing days, epidermal sloughing was seen from the right nasofacial angle over the right alar region to the soft triangle. The lateral crus of the alar cartilage was not involved. Granulation tissue and epithelium emanated from the sebaceous pores at postinjection day 3 (Fig. 1). The affected area was completely epithelialized without contour abnormality at postinjection week 1. Complete recovery without contour abnormality or skin change was seen at postinjection month 3 (Fig. 1).
Delayed injection necrosis through vascular compression from hyaluronic acid has been described previously.1 Glabellar injection necrosis has been described and averted with hyaluronidase.2 This is the first report describing skin necrosis in the alar region.
The vascular supply to the superior aspect of the nose is through the angular artery, whereas the infraorbital artery supplies most of the inferior portion. Both arteries and their respective branches have abundant anastomoses. The angular artery turns sharply in this region and is vulnerable to being clamped shut by extravascular pressure and occluded by actual intraarterial injection. Deep anatomy that may be vulnerable includes the medial and lateral crura of the alar cartilage, extending to the triangular cartilage. Despite the abundant blood supply to the nose, vascular compromise can occur, as evidenced by poor healing in smokers.
The mechanism of ischemia following filler injection may relate to vascular compression by increased tissue pressure, or to intravascular injection; the delayed onset of ischemia in this case likely favors a compressive mechanism.
Hyaluronidase dissolves the peptide bonds in the long-chain proteins within hyaluronic acid, increasing the mobility of the injected viscoelastic and allowing it to disperse more freely as oligoproteins through the tissue. Early injection of hyaluronidase might avert the onset of ischemic necrosis because of compression by hyaluronic acid. The lack of full-thickness alar necrosis in this case may have been predictive of a favorable outcome with observation alone.
Tissue necrosis is a feared complication of filler injections. The glabella and nasal ala may be vulnerable regions because of vascular anatomy. These cases are rare, and treatment recommendations are based on theoretical mechanisms and anecdotal reports. Massage and topical vasodilators have been shown to significantly increase blood flow in internal mammary artery grafts.3 In the case of hyaluronic acids, hyaluronidase injections offer another treatment option, and their immediate use should be considered for emergency treatment of postinjection ischemia.
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