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Invited Commentary
December 15, 2016

Nasal Reconstruction in the Vasculopathic Patient—Saddle Up

Author Affiliations
  • 1Division of Facial Plastic & Reconstructive Surgery, Department of Otolaryngology–Head and Neck Surgery, Indiana University School of Medicine, Indianapolis
JAMA Otolaryngol Head Neck Surg. Published online December 15, 2016. doi:10.1001/jamaoto.2016.3491

Saddle nose deformity ranks high among the burden of disease in patients diagnosed with systemic vascular disorders. Nearly one-quarter of patients diagnosed with granulomatosis with polyangiitis (GPA) develop this deformity.1 The process contributes to the overall cosmetic, mental, and functional toll taken on by a patient. It is only in the last several decades that literature has surfaced highlighting surgical interventions for vasculitis-induced saddle nose deformity.

Approach to the saddle nose deformity in reconstructive rhinoplasty calls for careful suture and grafting techniques to achieve a desired cosmetic and functional outcome. Acquired causes include sinonasal trauma, previous septorhinoplasty, and cocaine abuse. Granulomatosis with polyangitis, however, requires a more thoughtful approach in that the disease process predisposes the patient to higher rates of complications and failure. The primary complications include resorption or extrusion of grafting material. Conclusions and consensus from the literature have remained scattered, though techniques to increase the likelihood of successful reconstruction have been published.

The primary question in performing surgery on a patient with autoimmune vascular disease is the risk of exacerbating the condition, which may lead to graft failure and leave the patient in worse condition postoperatively. Classically, a patient should be in remission at the time of intervention to optimize the chance of success. However, previous studies2 have shown that surgery does not induce flare-ups or accelerate the course of the disease. In this issue of JAMA Otolaryngology–Head & Neck Surgery, Ezzat et al3 calculate postoperative flare-ups at an 11% rate, occurring 2 months postoperatively at the earliest. The timing ranged from 2 months to 25 months from surgery, supporting the hypothesis that surgery does not directly cause disease flare-up. Additionally, only 2 of the 5 documented cases of flare-ups resulted in graft failure.3

In our experience, approach to the saddle nose deformity requires a multidimensional grafting technique. The importance of establishing both the dorsum and strong tip support cannot be stressed enough. Daniel et al4 provide a comprehensive classification guide for the saddle nose deformity, which is used in the review by Ezzat et al3 when feasible. Most of these deformities present as type 3 and above, which calls for reestablishing dorsal contour along with tip support, projection, and rotation. While dorsal onlay grafts and columellar strut grafts remain options, we have found that the calvarial L-strut—or similar L-struts using autologous materials—may give superior results and is our method of choice for these reconstructions.

The L-strut graft type is advocated because it achieves these outcomes through a previously described extramucosal approach.5 Avoiding mucosal incisions is recommended to prevent a local disease flare-up, which may contribute to reconstructive failure. Fewer incisions with fewer grafts ultimately provide a less traumatic approach. This is achieved through an open rhinoplasty approach through intravestibular marginal incisions. This provides access to the medial alar crura, which may be released from one another to ultimately allow insertion of a columella strut graft through a pocket along the nasal spine. The dorsum is then favorably accessed from here as well. Ezzat et al3 concisely present a myriad of techniques and materials available to the facial plastic surgeon for surgery on patients with GPA. Their review shows substantial support of the aforementioned technique, noting only 6% graft failure with the L-strut technique vs 21% and 38% with dorsal onlay and columellar strut grafts, respectively. It is important to note that most surgeons (93%) use autografts as opposed to allograft material in this patient population. This is our institutional preference as well, given that the risk of graft failure and complications appears to be higher in patients with inflammatory disease.

Numerous grafting materials are available to the surgeon, including autografts, allografts, and alloplastic grafts. Alloplastic implants in the setting of vasculitis-induced nasoseptal disease are generally avoided due to a higher risk of extrusion and infection. The reconstructive surgeon should be wary of using such materials in patients with inflammatory disease. Though the review by Ezzat et al3 is limited in statistical analysis, it supports overall higher failure rates associated with allografts and alloplastic grafts. Costal cartilage is favored among cases available for review in the literature. In the setting of GPA, however, cartilage more so than bone is classically targeted in the disease, increasing concern for potential resorption of rib cartilage over calvarial bone.6 This inference seems to be supported among the data collected by the authors, who found a higher rate of complications, including resorption and infection, with rib cartilage (19%) over calvarial bone (11%).

The outcome from primary reconstructive rhinoplasty in patients with GPA in the aggregate data revealed an 83% success rate with 2 cases of subsequent secondary rhinoplasty, elevating the overall success rate to 84%. Though no statistical significance was drawn from these 44 cases, it provides a scaffold on which to build a methodical approach to surgical therapy. Functional outcomes were not measured in the aggregate data. However, previous studies have shown, when documented, that nearly all patients will endorse some improvement in nasal breathing.2

We commend Ezzat et al3 and their achievements in aggregating and reviewing this data. The reconstruction of the nose in vasculopathic patients has been perpetuated as conventionally high risk and commonly avoided as such. It is reinforced here that with the proper surgical techniques, reconstructive surgery remains a viable option. Though an overall complication rate of 20% was found, a number of the grafts and techniques described have the potential to reduce this complication rate.

When considering surgical intervention for nasal deformity in patients with GPA, Ezzat et al3 along with others2,5 provide valuable information and potential recommendations to optimize successful saddle nose reconstruction in this technically challenging operation.

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Article Information

Corresponding Author: Taha Z. Shipchandler, MD, Division Director, Facial Plastic & Reconstructive Surgery, Residency Program Director, Department of Otolaryngology–Head and Neck Surgery, Indiana University School of Medicine, 1120 W Michigan St, Ste 200, Indianapolis, IN 46202-5230 (tshipcha@iupui.edu).

Published Online: December 15, 2016. doi:10.1001/jamaoto.2016.3491

Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.

References
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Congdon  D, Sherris  DA, Specks  U, McDonald  T.  Long-term follow-up of repair of external nasal deformities in patients with Wegener’s granulomatosis. Laryngoscope. 2002;112(4):731-737.
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Ezzat  WH, Compton  RA, Basa  KC, Levi  J.  Reconstructive techniques for the saddle nose deformity in granulomatosis with polyangiitis: a systematic review  [published online December 15, 2016]. JAMA Otolaryngol Head Neck Surg. doi:10.1001/jamaoto.2016.3484
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Daniel  RK, Brenner  KA.  Saddle nose deformity: a new classification and treatment. Facial Plast Surg Clin North Am. 2006;14(4):301-312, vi.
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Shipchandler  TZ, Chung  BJ, Alam  DS.  Saddle nose deformity reconstruction with a split calvarial bone L-shaped strut. Arch Facial Plast Surg. 2008;10(5):305-311.
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Kesel  N, Köhler  D, Herich  L,  et al.  Cartilage destruction in granulomatosis with polyangiitis (Wegener’s granulomatosis) is mediated by human fibroblasts after transplantation into immunodeficient mice. Am J Pathol. 2012;180(5):2144-2155.
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