Logopedics Phoniatrics Vocology, 2015; 40: 93–95
LPV FORUM
A classification system for airway compromise due to bilateral vocal fold mobility impairment
S. A. REZA NOURAEI & GURI S. SANDHU The National Centre for Airway Reconstruction, Department of ENT Surgery, Charing Cross Hospital, London W6 8RF, UK
Abstract We present a system for classification of bilateral vocal fold mobility impairment. Type 1 obstructions are caused by bilateral laryngeal denervation, most commonly due to bilateral recurrent laryngeal nerve palsy. Type 2 obstructions are caused by crico-arytenoid joint ankylosis. Type 3 obstructions are due to inter-arytenoid granulation tissue. Type 4 lesions are caused by mature inter-arytenoid scar tissue and type 5 lesions are complex or total laryngeal stenoses. Key words: Bilateral vocal fold mobility impairment, bilateral vocal palsy
Airway compromise due to bilateral vocal fold mobility impairment in adduction is a challenging condition to treat. Unlike the subglottis and the trachea that are relatively static structures, the larynx performs multiple dynamic physiological functions. It provides sphincteric protection against pulmonary ingress of alimentary tract contents, it regulates ventilatory airflow on a breath-by-breath basis, and it acts as a flutter valve for phonation (1). As a result, restoration of one function can come at the expense of deteriorations in others (2,3). Cotton and Myer previously suggested a paediatric laryngeal stenosis classification based on estimates of the degree of cross-sectional obstruction (4). We have found a general classification system based on underlying aetiology to be more useful for treatment selection and prognostication in this condition (Figure 1). Type I stenoses are a spectrum of neurogenic conditions whose commonest cause is bilateral recurrent laryngeal nerve palsy and whose commonest aetiology is thyroid surgery (5,6). These patients can be treated with arytenoidectomy and may, in highly selected cases, be candidates for laryngeal neurorrhaphy, nerve transfer, or laryngeal pacing (7). Type II stenoses are caused by cricoarytenoid joint ankylosis (8). The most common aetiology in our experience is rheumatoid arthritis, but joint
ankylosis can also result from intubation or trauma. Patients with a history of laryngeal denervation with fixed cricoarytenoid joints are classified as IIa. Type II stenosis can respond to a combination of arytenoidectomy and laryngeal balloon dilation. Types III, IV, and V stenoses are most commonly caused by endolaryngeal intubation (9). Type III stenoses are seen soon after endolaryngeal intubation. If untreated, they can progress to type IV stenoses. These lesions respond very well to laser granulation tissue reduction, intralesional steroid therapy, and balloon dilation. Type IV stenoses are caused by vocal fold fixation due to interarytenoid scarring. They are further classified based on whether the scar affects the anterior or posterior interarytenoid region. Patients with type IVa lesions can respond well to scar division and balloon dilation of the larynx. Treatment delay can, however, lead to permanent cricoarytenoid joint ankylosis. In type IVb lesions the scar causes interarytenoid coalescence, leading to a high incidence of interarytenoid scar reformation and stenosis recurrence. Type V lesions are exceptionally challenging to treat. It is hoped that in the fullness of time laryngeal transplantation may become a safe and clinically acceptable procedure and become a viable treatment option for highly selected patients within
Correspondence: S. A. R. Nouraei, The National Centre for Airway Reconstruction, Department of ENT Surgery, Charing Cross Hospital, London W6 8RF, UK. E-mail: [email protected] (Received 27 December 2013 ; accepted 1 March 2014 ) ISSN 1401-5439 print/ISSN 1651-2022 online © 2014 Informa UK, Ltd. DOI: 10.3109/14015439.2014.902498
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S. A. R. Nouraei & G. S. Sandhu
Figure 1. A classification system for airway compromise due to vocal fold mobility impairment. Type I stenoses are caused by laryngeal paralysis or neuromuscular dysfunction. They are also referred to as bilateral laryngeal paralysis or bilateral vocal fold palsy. Type II stenoses are caused by primary cricoarytenoid joint ankylosis. Extrusion of degenerated cricoarytenoid joint contents is seen during arytenoidectomy (right image). Type III stenoses are seen soon after extubation. In these patients, bilateral vocal fold mobility impairment is caused by interarytenoid granulation. Type IV stenoses are most commonly caused by endotracheal intubation. In type IVa stenoses the scar affects the anterior interarytenoid region, and in type IVb the scar affects the posterior interarytenoid region. Type V stenoses refer to complex or total laryngeal stenoses. Patients with type Va stenoses have relatively normal underlying cartilaginous frameworks, and patients with Vb stenoses have underlying cartilaginous abnormalities.
this subgroup. In the meantime, reasonable laryngeal function can often, but not always, be preserved with regular treatments. Declaration of interest: The authors report no conflicts of interest. References 1. Negus VE. The comparative anatomy and physiology of the larynx. New York: Hafner; 1949.
2. Woodman DG, Pollack D. Bilateral abductor paralysis; the postoperative care and speech therapy following arytenoidectomy. Trans Am Laryngol Rhinol Otol Soc. 1950; 54th Meeting:448–58. 3. Yilmaz T, Suslu N, Atay G, Ozer S, Gunaydin RO, Bajin MD. Comparison of voice and swallowing parameters after endoscopic total and partial arytenoidectomy for bilateral abductor vocal fold paralysis: a randomized trial. JAMA Otolaryngol Head Neck Surg. 2013;139:712–18. 4. Cotton RT, Myer CM. Contemporary surgical management of laryngeal stenosis in children. Am J Otolaryngol. 1984; 5:360–8.
Classification of bilateral vocal fold immobility 5. Al-Fattah HA, Hamza A, Gaafar A, Tantawy A. Partial laser arytenoidectomy in the management of bilateral vocal fold immobility: a modification based on functional anatomical study of the cricoarytenoid joint. Otolaryngol Head Neck Surg. 2006;134:294–301. 6. Gardner GM, Smith MM, Yaremchuk KL, Peterson EL. The cost of vocal fold paralysis after thyroidectomy. Laryngoscope. 2013;1231455–63. 7. Li M, Chen S, Zheng H, Chen D, Zhu M, Wang W, et al. Reinnervation of bilateral posterior cricoarytenoid
95
muscles using the left phrenic nerve in patients with bilateral vocal fold paralysis. PLoS One. 2013;8: e77233. 8. Eckel HE, Wittekindt C, Klussmann JP, Schroeder U, Sittel C. Management of bilateral arytenoid cartilage fixation versus recurrent laryngeal nerve paralysis. Ann Otol Rhinol Laryngol. 2003;112:103–8. 9. McCombe AW, Philips DE, Rogers JH. Inter-arytenoid glottic bar following intubation. J Laryngol Otol. 1990; 104:727–9.
Copyright of Logopedics Phoniatrics Vocology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
LPV FORUM
A classification system for airway compromise due to bilateral vocal fold mobility impairment
S. A. REZA NOURAEI & GURI S. SANDHU The National Centre for Airway Reconstruction, Department of ENT Surgery, Charing Cross Hospital, London W6 8RF, UK
Abstract We present a system for classification of bilateral vocal fold mobility impairment. Type 1 obstructions are caused by bilateral laryngeal denervation, most commonly due to bilateral recurrent laryngeal nerve palsy. Type 2 obstructions are caused by crico-arytenoid joint ankylosis. Type 3 obstructions are due to inter-arytenoid granulation tissue. Type 4 lesions are caused by mature inter-arytenoid scar tissue and type 5 lesions are complex or total laryngeal stenoses. Key words: Bilateral vocal fold mobility impairment, bilateral vocal palsy
Airway compromise due to bilateral vocal fold mobility impairment in adduction is a challenging condition to treat. Unlike the subglottis and the trachea that are relatively static structures, the larynx performs multiple dynamic physiological functions. It provides sphincteric protection against pulmonary ingress of alimentary tract contents, it regulates ventilatory airflow on a breath-by-breath basis, and it acts as a flutter valve for phonation (1). As a result, restoration of one function can come at the expense of deteriorations in others (2,3). Cotton and Myer previously suggested a paediatric laryngeal stenosis classification based on estimates of the degree of cross-sectional obstruction (4). We have found a general classification system based on underlying aetiology to be more useful for treatment selection and prognostication in this condition (Figure 1). Type I stenoses are a spectrum of neurogenic conditions whose commonest cause is bilateral recurrent laryngeal nerve palsy and whose commonest aetiology is thyroid surgery (5,6). These patients can be treated with arytenoidectomy and may, in highly selected cases, be candidates for laryngeal neurorrhaphy, nerve transfer, or laryngeal pacing (7). Type II stenoses are caused by cricoarytenoid joint ankylosis (8). The most common aetiology in our experience is rheumatoid arthritis, but joint
ankylosis can also result from intubation or trauma. Patients with a history of laryngeal denervation with fixed cricoarytenoid joints are classified as IIa. Type II stenosis can respond to a combination of arytenoidectomy and laryngeal balloon dilation. Types III, IV, and V stenoses are most commonly caused by endolaryngeal intubation (9). Type III stenoses are seen soon after endolaryngeal intubation. If untreated, they can progress to type IV stenoses. These lesions respond very well to laser granulation tissue reduction, intralesional steroid therapy, and balloon dilation. Type IV stenoses are caused by vocal fold fixation due to interarytenoid scarring. They are further classified based on whether the scar affects the anterior or posterior interarytenoid region. Patients with type IVa lesions can respond well to scar division and balloon dilation of the larynx. Treatment delay can, however, lead to permanent cricoarytenoid joint ankylosis. In type IVb lesions the scar causes interarytenoid coalescence, leading to a high incidence of interarytenoid scar reformation and stenosis recurrence. Type V lesions are exceptionally challenging to treat. It is hoped that in the fullness of time laryngeal transplantation may become a safe and clinically acceptable procedure and become a viable treatment option for highly selected patients within
Correspondence: S. A. R. Nouraei, The National Centre for Airway Reconstruction, Department of ENT Surgery, Charing Cross Hospital, London W6 8RF, UK. E-mail: [email protected] (Received 27 December 2013 ; accepted 1 March 2014 ) ISSN 1401-5439 print/ISSN 1651-2022 online © 2014 Informa UK, Ltd. DOI: 10.3109/14015439.2014.902498
94
S. A. R. Nouraei & G. S. Sandhu
Figure 1. A classification system for airway compromise due to vocal fold mobility impairment. Type I stenoses are caused by laryngeal paralysis or neuromuscular dysfunction. They are also referred to as bilateral laryngeal paralysis or bilateral vocal fold palsy. Type II stenoses are caused by primary cricoarytenoid joint ankylosis. Extrusion of degenerated cricoarytenoid joint contents is seen during arytenoidectomy (right image). Type III stenoses are seen soon after extubation. In these patients, bilateral vocal fold mobility impairment is caused by interarytenoid granulation. Type IV stenoses are most commonly caused by endotracheal intubation. In type IVa stenoses the scar affects the anterior interarytenoid region, and in type IVb the scar affects the posterior interarytenoid region. Type V stenoses refer to complex or total laryngeal stenoses. Patients with type Va stenoses have relatively normal underlying cartilaginous frameworks, and patients with Vb stenoses have underlying cartilaginous abnormalities.
this subgroup. In the meantime, reasonable laryngeal function can often, but not always, be preserved with regular treatments. Declaration of interest: The authors report no conflicts of interest. References 1. Negus VE. The comparative anatomy and physiology of the larynx. New York: Hafner; 1949.
2. Woodman DG, Pollack D. Bilateral abductor paralysis; the postoperative care and speech therapy following arytenoidectomy. Trans Am Laryngol Rhinol Otol Soc. 1950; 54th Meeting:448–58. 3. Yilmaz T, Suslu N, Atay G, Ozer S, Gunaydin RO, Bajin MD. Comparison of voice and swallowing parameters after endoscopic total and partial arytenoidectomy for bilateral abductor vocal fold paralysis: a randomized trial. JAMA Otolaryngol Head Neck Surg. 2013;139:712–18. 4. Cotton RT, Myer CM. Contemporary surgical management of laryngeal stenosis in children. Am J Otolaryngol. 1984; 5:360–8.
Classification of bilateral vocal fold immobility 5. Al-Fattah HA, Hamza A, Gaafar A, Tantawy A. Partial laser arytenoidectomy in the management of bilateral vocal fold immobility: a modification based on functional anatomical study of the cricoarytenoid joint. Otolaryngol Head Neck Surg. 2006;134:294–301. 6. Gardner GM, Smith MM, Yaremchuk KL, Peterson EL. The cost of vocal fold paralysis after thyroidectomy. Laryngoscope. 2013;1231455–63. 7. Li M, Chen S, Zheng H, Chen D, Zhu M, Wang W, et al. Reinnervation of bilateral posterior cricoarytenoid
95
muscles using the left phrenic nerve in patients with bilateral vocal fold paralysis. PLoS One. 2013;8: e77233. 8. Eckel HE, Wittekindt C, Klussmann JP, Schroeder U, Sittel C. Management of bilateral arytenoid cartilage fixation versus recurrent laryngeal nerve paralysis. Ann Otol Rhinol Laryngol. 2003;112:103–8. 9. McCombe AW, Philips DE, Rogers JH. Inter-arytenoid glottic bar following intubation. J Laryngol Otol. 1990; 104:727–9.
Copyright of Logopedics Phoniatrics Vocology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
