AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 3 61–3 6 3
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Multilevel airway stenosis in patients with granulomatosis with polyangiitis (Wegener’s)☆,☆☆ Elizabeth Guardiani, MD a,⁎, 1 , Hassan Sheikh Moghaddas, MD b, 2 , Jonathan Lesser, MD d, 2 , Franco Resta-Flarer, MD d, 2 , Andrew Blitzer, MD, DDS c, 3 , Faiz Bhora, MD e, 3 , Robert Lebovics, MD c, 3 a
Department of Otorhinolaryngology-Head and Neck Surgery, University of Maryland School of Medicine Department of Surgery, York Hospital, York, PA c Department of Otolaryngology-Head and Neck Surgery, Mt. Sinai-Roosevelt Hospital, New York, NY d Department of Anesthesiology, Mt. Sinai-Roosevelt Hospital, New York, NY e Department of Surgery, Mt Sinai-Roosevelt Hospital, New York, NY b
ARTI CLE I NFO
A BS TRACT
Article history:
Objectives: To describe the presentation and clinical course of subglottic stenosis (SGS), in
Received 3 November 2014
particular the development of concurrent airway lesions, in patients with Granulomatosis with Polyangiitis (Wegener’s) (GPA). Materials and methods: Retrospective review of clinical data from all patients presenting to our institution from 2000 to 2012 with SGS and GPA. Results: Thirty-five patients were identified. The average age at diagnosis was 33 years old. Eleven patients (31%) presented with SGS as part their initial manifestation of GPA. The remaining patients developed SGS later, at a median of 2.5 years from diagnosis (range 6 months to 14 years). Twelve patients (34%) were noted to have multilevel airway involvement. Seven patients (20%) had documentation of cricoarytenoid joint fixation and vocal cord immobility. This was typically progressive in nature and occurred at an average of two years following the diagnosis of SGS. Six patients (17%) had mid/distal tracheal stenosis and four (11%) had bronchial stenosis. The majority of patients (86%) had evidence of concurrent sinonasal involvement, ten patients (29%) had evidence of otologic involvement and eight (23%) had ocular involvement. Conclusions: Cricoarytenoid joint fixation and distal stenosis occur not infrequently in patients with GPA and SGS, resulting in progressive multilevel airway stenosis in about one third of patients. It is critical to identify multilevel stenosis when managing the airways of these patients. © 2015 Elsevier Inc. All rights reserved.
☆
Financial disclosures: none. Conflict of interest: none. ⁎ Corresponding author at: 16 S. Eutaw St. Suite 500, Baltimore, MD 21201. E-mail address: [email protected] (E. Guardiani). 1 Data analysis, drafting of manuscript. 2 Data analysis, critical revision of manuscript. 3 Conception and design, critical revision of manuscript.
☆☆
http://dx.doi.org/10.1016/j.amjoto.2014.12.010 0196-0709/© 2015 Elsevier Inc. All rights reserved.
362
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY–H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 3 61 –3 6 3
1.
Introduction
Granulomatosis with polyangiitis (Wegener’s) (GPA) is a multisystem disease characterized by necrotizing granulomatous inflammation and vasculitis affecting approximately 3 in 100,000 individuals in the United States [1]. GPA classically involves the upper airway, lung and kidneys. Diagnosis is typically made by the presence of necrotizing granulomatous inflammation of the upper respiratory tract and small to medium size vessel vasculitis on histology and/or anti-neutrophil cytoplasmic antibody (ANCA) serologies. Otolaryngologic manifestations occur in 87%–92% of patients with GPA, often as the presenting symptom [2,3]. The most common head and neck manifestation is sinonasal disease, occurring in 85% of patients, followed by otitis media (44% of patients) [2,3]. Subglottic stenosis (SGS) is a less common, but a life-threatening manifestation of GPA, especially if not identified and correctly managed. The incidence of subglottic stenosis in GPA has been estimated to be 8%–23% and occurs more commonly in younger patients [2–4]. It may occur in isolation as the presenting symptom or as a latestage manifestation of disease [5]. Stenosis is often limited to the subglottis/proximal trachea, but may extend into the distal trachea and bronchi. Involvement of the glottic and supraglottic larynx may also occur, in particular cricoarytenoid joint fixation, but its incidence is not well defined [3,6]. In general, the course of SGS has been found to run independently of the systemic disease course of GPA [7,8]. In this study we aim to characterize the clinical presentation of SGS in GPA, in particular the incidence of multilevel airway disease, including distal tracheal, bronchial and glottic involvement, which has not been well established.
2.
Materials and methods
The Institutional Review Board at St. Luke’s-Roosevelt Hospital Center (Now Mt. Sinai-Roosevelt Hospital) approved this retrospective study. The records of all patients presenting to the senior author (RL) at the Head and Neck Surgical Group at St. Luke’sRoosevelt Hospital Center from 2000 to 2012 with a diagnosis of GPA and SGS were reviewed. Patients were included in the study if they had significant subglottic stenosis, defined as requiring at least one surgical intervention and compelling evidence of GPA by histological findings and/or positive ANCA serologies. SGS and proximal tracheal stenosis were grouped together when describing the airway lesions. Patients in whom the diagnosis of GPA was uncertain or whose medical records were incomplete or did not include information on the initial presentation of GPA were excluded. Clinical history, demographics, age at diagnosis, time to development of SGS, sites of GPA involvement, physical exam findings, endoscopy findings, pathology and laboratory studies were reviewed and compiled into a database.
3.
Results
A total of thirty-five patients, twenty-four female and eleven male, with GPA and SGS were identified. The average age at diagnosis of GPA
was 33 years old. Diagnosis was made by tissue biopsy alone in six patients, ANCA serologies in nine patients and a combination of both in twenty patients. The most common site for a diagnostic biopsy was the lung (11 patients), followed by nasal mucosa (9 patients) and subglottic/tracheal mucosa (4 patients) (Table 1). In eleven patients (31%), SGS was the presenting manifestation of GPA. Eight of these patients were also noted to have concurrent sinonasal disease at the time of presentation and none had evidence of severe systemic disease. The remaining twenty-four patients developed SGS later in their disease course, at a median of 2.5 years from diagnosis (range 6 months to 14 years). Twelve patients (34%) were noted to have multilevel airway involvement. Eight patients (23%) developed vocal fold immobility throughout their disease course. One patient with late onset SGS had a unilateral paralysis seven years prior to the onset of SGS that was found to be of neurologic etiology on laryngeal electromyography. The remaining seven patients (20%) had progressive cricoarytenoid joint fixation and inflammation accompanying their subglottic stenosis. Vocal fold fixation was unilateral in two patients and bilateral in five patients. The diagnosis of vocal cord fixation ranged from concurrent to the time of diagnosis of SGS to ten years following the onset of SGS, at a median of two years following diagnosis of SGS. In addition to proximal stenosis, six patients (17%) had mid/distal tracheal stenosis and four of those patients also had bronchial stenosis (Table 2). All patients with the exception of one juvenile male had other head and neck manifestations of GPA. The majority of patients (86%) had evidence of concurrent sinonasal involvement at some point in their disease, ten patients (29%) had evidence of otologic involvement and eight (23%) had ocular involvement.
4.
Discussion
While GPA is a relatively rare disease, it should remain high in the differential diagnosis in any patient with SGS, especially in those without a clear history of airway trauma. GPA is generally felt to occur either as limited disease, wherein the upper respiratory tract is most commonly affected and there is lack of significant pulmonary, renal or other systemic involvement, or as severe disease, where there is multisystem
Table 1 – Demographics and method of diagnosis. No of patients (%) a
Patient characteristic Gender Male Female Age at Diagnosis, years SGS as part of initial presentation Serology ANCA positive ANCA negative +Histologic diagnosis of GPA Lung Sinonasal Subglottis/trachea Renal Chest wall lesion GPA = Granulomatosis with Subglottic stenosis. a Except where indicated.
Polyangiitis
11 24 33 11
(31) (69) (7–58) (31)
29 6 26 11 9 4 1 1
(83) (17) (74) (31) (26) (11) (3) (3)
(Wegener’s);
SGS =
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 3 61–3 6 3
Table 2 – Sites of airway involvement. Affected airway site Subglottis CA joint Mid/distal Trachea Bronchial Multilevel Stenosis SG + CA joint SG + DT SG + DT + bronchial SG + CA joint + DT + bronchial
No. of patients (%) 35 7 6 4 12 6 2 3 1
(100) (20) (16) (11) (34) (17) (6) (9) (3)
SG = subglottis; CA = cricoaryenoid; DT = mid/distal trachea.
involvement. SGS occurs more commonly in the limited form of the disease, but can also occur in severe disease [9]. In our series, SGS was part of the initial presentation of GPA in one third of patients. It is important to distinguish these patients from idiopathic SGS as they tend to have a more persistent disease course, are poorer candidates for open laryngotracheal reconstruction and, as highlighted here, may go onto develop additional sites of stenosis [10]. The involvement of other head and neck sites can help guide the diagnosis towards GPA as patients with limited disease often have negative ANCA serologies and subglottic tissue is notoriously unreliable for a pathologic diagnosis of GPA [7,9]. Our study found a relatively high incidence of multilevel airway involvement (34%). One in five patients had evidence of cricoarytenoid joint involvement and subsequent vocal cord fixation, more commonly bilateral. This was often progressive and typically occurred after the onset of subglottic stenosis. This is an important consideration in the management of these patients, as bilateral vocal cord immobility will likely decrease the success rate of any endoscopic or open airway procedure [11]. In our series of patients, 4/5 patients with bilateral vocal cord fixation required a tracheotomy. We also found significant comorbidity of distal tracheal and bronchial disease (16% and 11% respectively). All of the bronchial lesions occurred in concert with distal tracheal lesions. Similar to cricoarytenoid joint involvement, distal tracheal/bronchial involvement was typically progressive and occurred after the onset of SGS. It is important that patients with GPA and SGS undergo bronchoscopy at the time of any intervention as failure to recognize these distal lesions may preclude success of the procedure. Also, these lesions will not be managed with tracheostomy so routine tracheobronchoscopy in tracheostomy dependent patients should be performed to evaluate for any distal lesions.
5.
363
Conclusions
GPA is an important cause of subglottic stenosis with a unique clinical course. Cricoarytenoid joint fixation and distal airway disease occur not infrequently, resulting in progressive, multilevel airway stenosis in about one third of patients.
Acknowledgments The authors would like to acknowledge Dr. Monica Rodriguez for her assistance in data collection.
REFERENCES
[1] Cotch MF, Hoffman GS, Yerg DE, et al. The epidemiology of Wegener's granulomatosis. Estimates of the five-year period prevalence, annual mortality, and geographic disease distribution from population-based data source. Arthritis Rheum 1996;39:87–92. [2] Lebovics RS, Hoffman GS, Leavitt RY, et al. The management of subglottic stenosis in patients with Wegener’s granulomatosis. Laryngoscope 1992;102:1341–5. [3] Martinez Del Pero M, Rasmussen N, Chaudhry A, et al. Structured clinical assessment of the ear nose and throat in patients with granulomatosis with polyangiitis (Wegener’s). Eur Arch Otorhinolaryngol 2013;270:345–54. [4] Waxman J, Bose WJ. Laryngeal manifestations of Wegener’s granulomatosis: case reports and review of the literature. J Rheumatol 1986;13:408–11. [5] Solans-Laque R, Bosch-Gil JA, Canela M, et al. Clinical features and therapeutic management of subglottic stenosis in patients with Wegener’s granulomatosis. Lupus 2008;17:832–6. [6] Eckel HE, Wittekindt C, Klussman JP, et al. Management of bilateral arytenoid cartilage fixation versus recurrent laryngeal nerve paralysis. Ann Otol Rhinol Laryngol 2003;112:103–8. [7] Gluth M, Shinners P, Kasperbauer J. Subglottic stenosis associated with Wegener’s granulomatosis. Laryngoscope 2003;113:1304–7. [8] Langford C, Sneller M, Hallahan C, et al. Clinical features and therapeutic management of subglottic stenosis in patients with Wegener’s granulomatosis. Arthritis Rheum 1996;39:1754–60. [9] Stone J. Limited versus severe Wegener’s granulomatosis: baseline data on patients in the Wegener’s granulomatosis etanercept trial. Arthritis Rheum 2003;48:2299–309. [10] Taylor S, Clayburgh D, Rosenbaum J, et al. Clinical manifestations and treatment of idiopathic and Wegener granulomatosis-associated subglottic stenosis. JAMA Otolaryngol Head Neck Surg 2013;139:76–81. [11] Morcillo A, Wins R, Gomez-Caro A, et al. Single-staged laryngotracheal reconstruction for idiopathic tracheal stenosis. Ann Thorac Surg 2013;95:433–9.
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Multilevel airway stenosis in patients with granulomatosis with polyangiitis (Wegener’s)☆,☆☆ Elizabeth Guardiani, MD a,⁎, 1 , Hassan Sheikh Moghaddas, MD b, 2 , Jonathan Lesser, MD d, 2 , Franco Resta-Flarer, MD d, 2 , Andrew Blitzer, MD, DDS c, 3 , Faiz Bhora, MD e, 3 , Robert Lebovics, MD c, 3 a
Department of Otorhinolaryngology-Head and Neck Surgery, University of Maryland School of Medicine Department of Surgery, York Hospital, York, PA c Department of Otolaryngology-Head and Neck Surgery, Mt. Sinai-Roosevelt Hospital, New York, NY d Department of Anesthesiology, Mt. Sinai-Roosevelt Hospital, New York, NY e Department of Surgery, Mt Sinai-Roosevelt Hospital, New York, NY b
ARTI CLE I NFO
A BS TRACT
Article history:
Objectives: To describe the presentation and clinical course of subglottic stenosis (SGS), in
Received 3 November 2014
particular the development of concurrent airway lesions, in patients with Granulomatosis with Polyangiitis (Wegener’s) (GPA). Materials and methods: Retrospective review of clinical data from all patients presenting to our institution from 2000 to 2012 with SGS and GPA. Results: Thirty-five patients were identified. The average age at diagnosis was 33 years old. Eleven patients (31%) presented with SGS as part their initial manifestation of GPA. The remaining patients developed SGS later, at a median of 2.5 years from diagnosis (range 6 months to 14 years). Twelve patients (34%) were noted to have multilevel airway involvement. Seven patients (20%) had documentation of cricoarytenoid joint fixation and vocal cord immobility. This was typically progressive in nature and occurred at an average of two years following the diagnosis of SGS. Six patients (17%) had mid/distal tracheal stenosis and four (11%) had bronchial stenosis. The majority of patients (86%) had evidence of concurrent sinonasal involvement, ten patients (29%) had evidence of otologic involvement and eight (23%) had ocular involvement. Conclusions: Cricoarytenoid joint fixation and distal stenosis occur not infrequently in patients with GPA and SGS, resulting in progressive multilevel airway stenosis in about one third of patients. It is critical to identify multilevel stenosis when managing the airways of these patients. © 2015 Elsevier Inc. All rights reserved.
☆
Financial disclosures: none. Conflict of interest: none. ⁎ Corresponding author at: 16 S. Eutaw St. Suite 500, Baltimore, MD 21201. E-mail address: [email protected] (E. Guardiani). 1 Data analysis, drafting of manuscript. 2 Data analysis, critical revision of manuscript. 3 Conception and design, critical revision of manuscript.
☆☆
http://dx.doi.org/10.1016/j.amjoto.2014.12.010 0196-0709/© 2015 Elsevier Inc. All rights reserved.
362
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY–H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 3 61 –3 6 3
1.
Introduction
Granulomatosis with polyangiitis (Wegener’s) (GPA) is a multisystem disease characterized by necrotizing granulomatous inflammation and vasculitis affecting approximately 3 in 100,000 individuals in the United States [1]. GPA classically involves the upper airway, lung and kidneys. Diagnosis is typically made by the presence of necrotizing granulomatous inflammation of the upper respiratory tract and small to medium size vessel vasculitis on histology and/or anti-neutrophil cytoplasmic antibody (ANCA) serologies. Otolaryngologic manifestations occur in 87%–92% of patients with GPA, often as the presenting symptom [2,3]. The most common head and neck manifestation is sinonasal disease, occurring in 85% of patients, followed by otitis media (44% of patients) [2,3]. Subglottic stenosis (SGS) is a less common, but a life-threatening manifestation of GPA, especially if not identified and correctly managed. The incidence of subglottic stenosis in GPA has been estimated to be 8%–23% and occurs more commonly in younger patients [2–4]. It may occur in isolation as the presenting symptom or as a latestage manifestation of disease [5]. Stenosis is often limited to the subglottis/proximal trachea, but may extend into the distal trachea and bronchi. Involvement of the glottic and supraglottic larynx may also occur, in particular cricoarytenoid joint fixation, but its incidence is not well defined [3,6]. In general, the course of SGS has been found to run independently of the systemic disease course of GPA [7,8]. In this study we aim to characterize the clinical presentation of SGS in GPA, in particular the incidence of multilevel airway disease, including distal tracheal, bronchial and glottic involvement, which has not been well established.
2.
Materials and methods
The Institutional Review Board at St. Luke’s-Roosevelt Hospital Center (Now Mt. Sinai-Roosevelt Hospital) approved this retrospective study. The records of all patients presenting to the senior author (RL) at the Head and Neck Surgical Group at St. Luke’sRoosevelt Hospital Center from 2000 to 2012 with a diagnosis of GPA and SGS were reviewed. Patients were included in the study if they had significant subglottic stenosis, defined as requiring at least one surgical intervention and compelling evidence of GPA by histological findings and/or positive ANCA serologies. SGS and proximal tracheal stenosis were grouped together when describing the airway lesions. Patients in whom the diagnosis of GPA was uncertain or whose medical records were incomplete or did not include information on the initial presentation of GPA were excluded. Clinical history, demographics, age at diagnosis, time to development of SGS, sites of GPA involvement, physical exam findings, endoscopy findings, pathology and laboratory studies were reviewed and compiled into a database.
3.
Results
A total of thirty-five patients, twenty-four female and eleven male, with GPA and SGS were identified. The average age at diagnosis of GPA
was 33 years old. Diagnosis was made by tissue biopsy alone in six patients, ANCA serologies in nine patients and a combination of both in twenty patients. The most common site for a diagnostic biopsy was the lung (11 patients), followed by nasal mucosa (9 patients) and subglottic/tracheal mucosa (4 patients) (Table 1). In eleven patients (31%), SGS was the presenting manifestation of GPA. Eight of these patients were also noted to have concurrent sinonasal disease at the time of presentation and none had evidence of severe systemic disease. The remaining twenty-four patients developed SGS later in their disease course, at a median of 2.5 years from diagnosis (range 6 months to 14 years). Twelve patients (34%) were noted to have multilevel airway involvement. Eight patients (23%) developed vocal fold immobility throughout their disease course. One patient with late onset SGS had a unilateral paralysis seven years prior to the onset of SGS that was found to be of neurologic etiology on laryngeal electromyography. The remaining seven patients (20%) had progressive cricoarytenoid joint fixation and inflammation accompanying their subglottic stenosis. Vocal fold fixation was unilateral in two patients and bilateral in five patients. The diagnosis of vocal cord fixation ranged from concurrent to the time of diagnosis of SGS to ten years following the onset of SGS, at a median of two years following diagnosis of SGS. In addition to proximal stenosis, six patients (17%) had mid/distal tracheal stenosis and four of those patients also had bronchial stenosis (Table 2). All patients with the exception of one juvenile male had other head and neck manifestations of GPA. The majority of patients (86%) had evidence of concurrent sinonasal involvement at some point in their disease, ten patients (29%) had evidence of otologic involvement and eight (23%) had ocular involvement.
4.
Discussion
While GPA is a relatively rare disease, it should remain high in the differential diagnosis in any patient with SGS, especially in those without a clear history of airway trauma. GPA is generally felt to occur either as limited disease, wherein the upper respiratory tract is most commonly affected and there is lack of significant pulmonary, renal or other systemic involvement, or as severe disease, where there is multisystem
Table 1 – Demographics and method of diagnosis. No of patients (%) a
Patient characteristic Gender Male Female Age at Diagnosis, years SGS as part of initial presentation Serology ANCA positive ANCA negative +Histologic diagnosis of GPA Lung Sinonasal Subglottis/trachea Renal Chest wall lesion GPA = Granulomatosis with Subglottic stenosis. a Except where indicated.
Polyangiitis
11 24 33 11
(31) (69) (7–58) (31)
29 6 26 11 9 4 1 1
(83) (17) (74) (31) (26) (11) (3) (3)
(Wegener’s);
SGS =
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 3 61–3 6 3
Table 2 – Sites of airway involvement. Affected airway site Subglottis CA joint Mid/distal Trachea Bronchial Multilevel Stenosis SG + CA joint SG + DT SG + DT + bronchial SG + CA joint + DT + bronchial
No. of patients (%) 35 7 6 4 12 6 2 3 1
(100) (20) (16) (11) (34) (17) (6) (9) (3)
SG = subglottis; CA = cricoaryenoid; DT = mid/distal trachea.
involvement. SGS occurs more commonly in the limited form of the disease, but can also occur in severe disease [9]. In our series, SGS was part of the initial presentation of GPA in one third of patients. It is important to distinguish these patients from idiopathic SGS as they tend to have a more persistent disease course, are poorer candidates for open laryngotracheal reconstruction and, as highlighted here, may go onto develop additional sites of stenosis [10]. The involvement of other head and neck sites can help guide the diagnosis towards GPA as patients with limited disease often have negative ANCA serologies and subglottic tissue is notoriously unreliable for a pathologic diagnosis of GPA [7,9]. Our study found a relatively high incidence of multilevel airway involvement (34%). One in five patients had evidence of cricoarytenoid joint involvement and subsequent vocal cord fixation, more commonly bilateral. This was often progressive and typically occurred after the onset of subglottic stenosis. This is an important consideration in the management of these patients, as bilateral vocal cord immobility will likely decrease the success rate of any endoscopic or open airway procedure [11]. In our series of patients, 4/5 patients with bilateral vocal cord fixation required a tracheotomy. We also found significant comorbidity of distal tracheal and bronchial disease (16% and 11% respectively). All of the bronchial lesions occurred in concert with distal tracheal lesions. Similar to cricoarytenoid joint involvement, distal tracheal/bronchial involvement was typically progressive and occurred after the onset of SGS. It is important that patients with GPA and SGS undergo bronchoscopy at the time of any intervention as failure to recognize these distal lesions may preclude success of the procedure. Also, these lesions will not be managed with tracheostomy so routine tracheobronchoscopy in tracheostomy dependent patients should be performed to evaluate for any distal lesions.
5.
363
Conclusions
GPA is an important cause of subglottic stenosis with a unique clinical course. Cricoarytenoid joint fixation and distal airway disease occur not infrequently, resulting in progressive, multilevel airway stenosis in about one third of patients.
Acknowledgments The authors would like to acknowledge Dr. Monica Rodriguez for her assistance in data collection.
REFERENCES
[1] Cotch MF, Hoffman GS, Yerg DE, et al. The epidemiology of Wegener's granulomatosis. Estimates of the five-year period prevalence, annual mortality, and geographic disease distribution from population-based data source. Arthritis Rheum 1996;39:87–92. [2] Lebovics RS, Hoffman GS, Leavitt RY, et al. The management of subglottic stenosis in patients with Wegener’s granulomatosis. Laryngoscope 1992;102:1341–5. [3] Martinez Del Pero M, Rasmussen N, Chaudhry A, et al. Structured clinical assessment of the ear nose and throat in patients with granulomatosis with polyangiitis (Wegener’s). Eur Arch Otorhinolaryngol 2013;270:345–54. [4] Waxman J, Bose WJ. Laryngeal manifestations of Wegener’s granulomatosis: case reports and review of the literature. J Rheumatol 1986;13:408–11. [5] Solans-Laque R, Bosch-Gil JA, Canela M, et al. Clinical features and therapeutic management of subglottic stenosis in patients with Wegener’s granulomatosis. Lupus 2008;17:832–6. [6] Eckel HE, Wittekindt C, Klussman JP, et al. Management of bilateral arytenoid cartilage fixation versus recurrent laryngeal nerve paralysis. Ann Otol Rhinol Laryngol 2003;112:103–8. [7] Gluth M, Shinners P, Kasperbauer J. Subglottic stenosis associated with Wegener’s granulomatosis. Laryngoscope 2003;113:1304–7. [8] Langford C, Sneller M, Hallahan C, et al. Clinical features and therapeutic management of subglottic stenosis in patients with Wegener’s granulomatosis. Arthritis Rheum 1996;39:1754–60. [9] Stone J. Limited versus severe Wegener’s granulomatosis: baseline data on patients in the Wegener’s granulomatosis etanercept trial. Arthritis Rheum 2003;48:2299–309. [10] Taylor S, Clayburgh D, Rosenbaum J, et al. Clinical manifestations and treatment of idiopathic and Wegener granulomatosis-associated subglottic stenosis. JAMA Otolaryngol Head Neck Surg 2013;139:76–81. [11] Morcillo A, Wins R, Gomez-Caro A, et al. Single-staged laryngotracheal reconstruction for idiopathic tracheal stenosis. Ann Thorac Surg 2013;95:433–9.
