Vocal Fold Paralysis Secondary to Phonotrauma *Travis A. L. Klein, †Joy E. Gaziano, and *Marion B. Ridley, *yTampa, Florida Summary: A unique case of acute onset vocal fold paralysis secondary to phonotrauma is presented. The cause was forceful vocalization by a drill instructor on a firearm range. Imaging studies revealed extensive intralaryngeal and retropharyngeal hemorrhage. Laryngoscopy showed a complete left vocal fold paralysis. Relative voice rest was recommended, and the patient regained normal vocal fold mobility and function after approximately 12 weeks. Keywords: Phonotrauma–Vocal fold paralysis–Voice rest. INTRODUCTION Numerous risk factors can predispose an individual to laryngeal injury, especially the vocal demands of an individual’s occupation.1–3 We describe a rarely reported case of complete vocal fold paralysis secondary to phonotrauma. The occupational risk factors associated with phonotrauma and the role of vocal rest in its treatment are reviewed. CASE REPORT A 45-year-old male was referred to our clinic with acute onset of hoarseness 1 month prior during a period of forceful vocalization as a drill instructor in the county sheriff’s department. Two days later he experienced progressive throat and neck pain and dysphagia. He noted tenderness and bruising of his anterior lower neck, which extended onto his upper chest. He was otherwise in excellent health and was not taking any anticoagulants, antiplatelet agents, or nutritional supplements. At the time of his initial examination, there was no tenderness or palpable swelling in the neck, and laryngeal crepitus was normal. Laryngoscopy showed the left true vocal fold fixed in a paramedian position. Review of the computed tomographic (CT) scans of the neck and chest with contrast performed 3 days after the injury revealed increased soft tissue density consistent with hematoma in the left paraglottic and retropharyngeal spaces; however, there was no discrete accumulation requiring surgical drainage (Figure 1). The trachea and esophagus were deviated to the right, and there was increased soft tissue density in the subcutaneous tissues of the upper chest, neck, and mediastinum (Figure 2). Gastrografin esophagram revealed no evidence of esophageal perforation. A follow-up CT without contrast 6 weeks after injury revealed that the paraglottic and retropharyngeal hematoma had almost completely resolved. Eight weeks after injury the patient reported substantial improvement in vocal quality, although he did have decreased vocal stamina toward the end of each day. Videostroboscopy revealed a persistent left vocal fold paralysis in paramedian position with good Accepted for publication August 26, 2013. From the *Department of Otolaryngology-Head and Neck Surgery, University of South Florida Morsani College of Medicine, Tampa, Florida; and the yJoy McCann Culverhouse Center for Esophageal and Swallowing Disorders, Department of Internal Medicine, University of South Florida Morsani College of Medicine, Tampa, Florida. Address correspondence and reprint requests to Marion B. Ridley, Department of Otolaryngology-Head and Neck Surgery, University of South Florida Morsani College of Medicine, 12901 Bruce B. Downs Boulevard MDC 73, Tampa, FL 33612. E-mail: [email protected] Journal of Voice, Vol. 28, No. 1, pp. 129.e9-129.e11 0892-1997/$36.00 Ó 2014 The Voice Foundation. All rights reserved http://dx.doi.org/10.1016/j.jvoice.2013.08.014
approximation by the right vocal fold. There was compensatory lateromedial and anteroposterior supraglottic compression. Vocal fold vibration was asymmetric with the left preceding the right, but vocal fold vibration was periodic with normal amplitude of vibration and mucosal wave. Voice quality was perceptually normal, and acoustic assessment revealed a speaking fundamental frequency of 102 Hz (within normal limits), maximum sustained phonation time of 18.5 seconds (reduced), and normal amplitude and frequency perturbation measures. Sixteen weeks after the injury the patient reported continued improvement in vocal quality and stamina. He had returned to work as a drill instructor on modified duty with outdoor drill instruction limited to 15–20 minutes. He reported no vocal fatigue or increased vocal effort after an 8-hour workday consisting of classroom instruction and telephone duties. On repeat videostroboscopy the left vocal fold demonstrated near-normal mobility; however, there remained a subtle lag in abduction on the left. Symmetry of vocal fold vibration had returned to normal. Acoustic voice measurements were unchanged with a persistently reduced maximum sustained phonation time (20 seconds). Short-term voice therapy to instruct in safe ways to project the voice and to reinforce voice conservation measures was begun. Use of a personal voice amplifier for use on the firearms range and for lengthy periods of forceful phonation was recommended. The patient gradually returned to unrestricted duty without any further voice complaints. DISCUSSION This report represents an unusual case of vocal fold paralysis caused by phonotrauma. Sudden forceful vocalization caused hemorrhage and edema in the paraglottic space and the soft tissues of the neck. The etiology of the vocal fold paralysis was mechanical, neurogenic, or both. The extensive amount of blood and edema in the laryngeal muscles could have resulted in mechanical impairment of vocal fold mobility or the paralysis could have been due to neuropraxia of the recurrent laryngeal nerve or its terminal branches from the pressure of the hematoma and swelling in the neck. Electromyogram might have distinguished between these two mechanisms of vocal fold paralysis but would not have changed the plan of treatment. The near-complete return of vocal fold function between 8 and 16 weeks after the injury is consistent with either mechanism of injury. Phonotrauma is a laryngeal injury caused by phonation. It is well established that vocal abuse or overuse can produce laryngeal inflammation and vocal fold hemorrhage4; however, vocal
129.e10
FIGURE 1. CT scan of the neck with contrast demonstrating left intralaryngeal and retropharyngeal hematoma (arrows).
fold paralysis secondary to phonotrauma has only rarely been reported. Forceful vocalization by the generation of high subglottic pressure and hard glottal attacks can produce greatly increased shear forces on the vocal folds. High vocal demand in occupations requiring aggressive vocal behaviors such as screaming or yelling can result in vocal injury. Individual factors can predispose to phonotrauma, including female sex; hormonal influences; stress; medications, such as corticosteroids, aspirin, and other nonsteroidal anti-inflammatory drugs; tobacco smoke; and inflammatory conditions, such as upper respiratory infection or allergy.4–8 Environmental factors such as background noise, poor ambient acoustics, the distance among speakers, and poor air quality may compound the risk.2,3 Aggressive vocalization in the setting of poor acoustic conditions and poor air quality is most hazardous.9,10 Because of the prevalence of occupational phonotrauma risk factors, an understanding of preventative measures and appropriate clinical treatment options is crucial. The treatment of phonotraumatic laryngeal injuries is dependent on the mechanism of injury and the resulting laryngeal abnormality. Some injuries are treated conservatively with modified voice rest, whereas others may require surgery to restore the anatomic integrity of the larynx. Harris et al11 reported a series of eight
Journal of Voice, Vol. 28, No. 1, 2014
cases of traumatic vocal process avulsion, one of which was due to phonotrauma. This case was treated conservatively with voice therapy and antireflux measures, however, in most of the other cases, which were due to intubation or external trauma, endoscopic microlaryngeal repositioning of the avulsed vocal process with suturing to the body of the arytenoid cartilage was performed. Behlau et al10 reported a case of vocal fold disruption from phonotrauma in an actor in which the mucosa of the vocal fold was detached along its length from anterior to posterior but was left attached to the vocal process. The case was treated conservatively with voice rest and therapy, and the actor’s voice returned to its preinjury state. Voice rest after laryngeal injury is inherently reasonable but clinically unproven.12 Historically, vocal rest has been the primary treatment for many voice problems, and its effectiveness as an adjunct to the healing process has been validated through physiological models.13,14 However, there are also data to suggest that low physiological levels of mechanical forces are in fact beneficial to tissue healing by attenuation of the inflammatory response.14–17 In a recent survey of members of the American Academy of Otolaryngology-Head and Neck Surgery regarding voice rest after laryngeal microsurgery, a majority of the respondents favored either complete or relative voice rest although one-fifth of the respondents were unlikely to recommend even relative voice rest (defined as significantly reduced vocal demands).18 The lack of a clinical standard of care on this issue reflects a paucity of well-controlled studies regarding the efficacy of voice rest in postoperative patients or in those who have sustained phonotrauma. The present case was managed conservatively with voice rest given the fact that there was no gross anatomic disruption of the larynx and no definable collection of blood or fluid to be drained.
CONCLUSION This rare case of vocal fold paralysis caused by phonotrauma was the result of extensive hemorrhage into the paraglottic and retropharyngeal soft tissues of the neck. The mechanism of injury was mechanical, preventing vocal fold mobility; neuropraxia, impairing axonal conduction along the recurrent laryngeal nerve or its terminal branches; or a combination of both. CT scans of the neck and chest showed no discrete collection of blood or fluid that required surgical drainage, and the hematoma resolved gradually in a few weeks. Relative voice rest was recommended during this period with avoidance of abusive vocal behaviors such as yelling, screaming, and loud or excessive talking. Vocal fold mobility recovered and the patient’s voice returned to its premorbid state without additional intervention. Relative voice rest is a prudent course of action in this condition. REFERENCES
FIGURE 2. CT scan of the chest with contrast showing the trachea and esophagus deviated to the right and a small amount of air in the esophagus (arrow).
1. Fritzell B. Voice disorders and occupations. Logoped Phoniatr Vocol. 1996; 21:7–12. 2. Williams NR. Occupational groups at risk of voice disorders: a review of the literature. Occup Med (Lond). 2003;53:456–460.
Travis A.L. Klein, et al
Vocal Fold Paralysis Secondary to Phonotrauma
3. Vilkman E. Voice problem at work: a challenge for occupational safety and health arrangement. Folia Phoniatr Logop. 2000;52:120–125. 4. Sataloff RT, Hawkshaw MJ. Vocal fold hemorrhage. In: Sataloff RT, ed. Professional Voice. 3rd ed. The Science and Art of Clinical Care, 2005; Vol 3. San Diego, CA: Plural Publishing; 2005:1291–1307. 5. Kiese-Himmel C, Pralle L, Kruse E. Psychological profiles of patients with laryngeal contact granulomas. Eur Arch Otorhinolaryngol. 1998;255: 296–301. 6. Butler JE, Hammond TH, Gray SD. Gender-related differences of hyaluronic acid distribution in the human vocal fold. Laryngoscope. 2001;111: 907–911. 7. Hamdan AL, Sibai A, Youssef M, Deeb R, Zaitoun F. The use of a screening questionnaire to determine the incidence of allergic rhinitis in singers with dysphonia. Arch Otolaryngol Head Neck Surg. 2006;132:547–549. 8. Krecicki T, Zalesska-Krecicka M, Pastuszek P, Rak J, MorawskaKochman M, Zatonski M. Treatment of Reinke’s edema among different professional groups: presentation of results. Int J Occup Med Environ Health. 2004;17:279–284. 9. Behlau M. Acute vocal trauma. In: Proceedings XXVth World Congress of the International Association of Logopedics and Phoniatrics, Montreal, Canada. Folia Phoniatr Logop. 2001;53:231.
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10. Behlau M, Oliveira G, Pontes P. Vocal fold self-disruption after phonotrauma on a lead actor: a case presentation. J Voice. 2009;23:726–732. 11. Harris SS, Gupta R, Hawkshaw MJ, Sataloff RT. Vocal process avulsion. J Voice. 2011;25:638–645. 12. Kaufman JA, Blalock PD. Is voice rest never indicated? J Voice. 1989;13: 79–81. 13. Cho SH, Kim HT, Lee IJ, Kim MS, Park HJ. Influence of phonation on basement membrane zone recovery after phonomicrosurgery: a canine model. Ann Otol Rhinol Laryngol. 2000;109:658–666. 14. Ishikawa K, Thibeault S. Voice rest versus exercise: a review of the literature. J Voice. 2010;24:379–387. 15. Branski RC, Perera P, Verdolini K, Rosen CA, Hebda PA, Agaewal S. Dynamic biomechanical strain inhibits IL-1 beta-induced inflammation in vocal fold fibroblasts. J Voice. 2006;20:432–442. 16. Li NYK, Verdolini K, Clermont G, Mi Q, Rubinstein EN, et al. A patientspecific in silico model of inflammation and healing tested in acute vocal fold injury. PLoS One. 2008;3:e2789. 17. Kutty JK, Webb K. Engineering therapies for the vocal fold lamina propria. Tissue Eng Part B Rev. 2009;15:249–262. 18. Behrman A, Sulica L. Voice rest after microlaryngoscopy: current opinion and practice. Laryngoscope. 2003;113:2182–2186.
approximation by the right vocal fold. There was compensatory lateromedial and anteroposterior supraglottic compression. Vocal fold vibration was asymmetric with the left preceding the right, but vocal fold vibration was periodic with normal amplitude of vibration and mucosal wave. Voice quality was perceptually normal, and acoustic assessment revealed a speaking fundamental frequency of 102 Hz (within normal limits), maximum sustained phonation time of 18.5 seconds (reduced), and normal amplitude and frequency perturbation measures. Sixteen weeks after the injury the patient reported continued improvement in vocal quality and stamina. He had returned to work as a drill instructor on modified duty with outdoor drill instruction limited to 15–20 minutes. He reported no vocal fatigue or increased vocal effort after an 8-hour workday consisting of classroom instruction and telephone duties. On repeat videostroboscopy the left vocal fold demonstrated near-normal mobility; however, there remained a subtle lag in abduction on the left. Symmetry of vocal fold vibration had returned to normal. Acoustic voice measurements were unchanged with a persistently reduced maximum sustained phonation time (20 seconds). Short-term voice therapy to instruct in safe ways to project the voice and to reinforce voice conservation measures was begun. Use of a personal voice amplifier for use on the firearms range and for lengthy periods of forceful phonation was recommended. The patient gradually returned to unrestricted duty without any further voice complaints. DISCUSSION This report represents an unusual case of vocal fold paralysis caused by phonotrauma. Sudden forceful vocalization caused hemorrhage and edema in the paraglottic space and the soft tissues of the neck. The etiology of the vocal fold paralysis was mechanical, neurogenic, or both. The extensive amount of blood and edema in the laryngeal muscles could have resulted in mechanical impairment of vocal fold mobility or the paralysis could have been due to neuropraxia of the recurrent laryngeal nerve or its terminal branches from the pressure of the hematoma and swelling in the neck. Electromyogram might have distinguished between these two mechanisms of vocal fold paralysis but would not have changed the plan of treatment. The near-complete return of vocal fold function between 8 and 16 weeks after the injury is consistent with either mechanism of injury. Phonotrauma is a laryngeal injury caused by phonation. It is well established that vocal abuse or overuse can produce laryngeal inflammation and vocal fold hemorrhage4; however, vocal
129.e10
FIGURE 1. CT scan of the neck with contrast demonstrating left intralaryngeal and retropharyngeal hematoma (arrows).
fold paralysis secondary to phonotrauma has only rarely been reported. Forceful vocalization by the generation of high subglottic pressure and hard glottal attacks can produce greatly increased shear forces on the vocal folds. High vocal demand in occupations requiring aggressive vocal behaviors such as screaming or yelling can result in vocal injury. Individual factors can predispose to phonotrauma, including female sex; hormonal influences; stress; medications, such as corticosteroids, aspirin, and other nonsteroidal anti-inflammatory drugs; tobacco smoke; and inflammatory conditions, such as upper respiratory infection or allergy.4–8 Environmental factors such as background noise, poor ambient acoustics, the distance among speakers, and poor air quality may compound the risk.2,3 Aggressive vocalization in the setting of poor acoustic conditions and poor air quality is most hazardous.9,10 Because of the prevalence of occupational phonotrauma risk factors, an understanding of preventative measures and appropriate clinical treatment options is crucial. The treatment of phonotraumatic laryngeal injuries is dependent on the mechanism of injury and the resulting laryngeal abnormality. Some injuries are treated conservatively with modified voice rest, whereas others may require surgery to restore the anatomic integrity of the larynx. Harris et al11 reported a series of eight
Journal of Voice, Vol. 28, No. 1, 2014
cases of traumatic vocal process avulsion, one of which was due to phonotrauma. This case was treated conservatively with voice therapy and antireflux measures, however, in most of the other cases, which were due to intubation or external trauma, endoscopic microlaryngeal repositioning of the avulsed vocal process with suturing to the body of the arytenoid cartilage was performed. Behlau et al10 reported a case of vocal fold disruption from phonotrauma in an actor in which the mucosa of the vocal fold was detached along its length from anterior to posterior but was left attached to the vocal process. The case was treated conservatively with voice rest and therapy, and the actor’s voice returned to its preinjury state. Voice rest after laryngeal injury is inherently reasonable but clinically unproven.12 Historically, vocal rest has been the primary treatment for many voice problems, and its effectiveness as an adjunct to the healing process has been validated through physiological models.13,14 However, there are also data to suggest that low physiological levels of mechanical forces are in fact beneficial to tissue healing by attenuation of the inflammatory response.14–17 In a recent survey of members of the American Academy of Otolaryngology-Head and Neck Surgery regarding voice rest after laryngeal microsurgery, a majority of the respondents favored either complete or relative voice rest although one-fifth of the respondents were unlikely to recommend even relative voice rest (defined as significantly reduced vocal demands).18 The lack of a clinical standard of care on this issue reflects a paucity of well-controlled studies regarding the efficacy of voice rest in postoperative patients or in those who have sustained phonotrauma. The present case was managed conservatively with voice rest given the fact that there was no gross anatomic disruption of the larynx and no definable collection of blood or fluid to be drained.
CONCLUSION This rare case of vocal fold paralysis caused by phonotrauma was the result of extensive hemorrhage into the paraglottic and retropharyngeal soft tissues of the neck. The mechanism of injury was mechanical, preventing vocal fold mobility; neuropraxia, impairing axonal conduction along the recurrent laryngeal nerve or its terminal branches; or a combination of both. CT scans of the neck and chest showed no discrete collection of blood or fluid that required surgical drainage, and the hematoma resolved gradually in a few weeks. Relative voice rest was recommended during this period with avoidance of abusive vocal behaviors such as yelling, screaming, and loud or excessive talking. Vocal fold mobility recovered and the patient’s voice returned to its premorbid state without additional intervention. Relative voice rest is a prudent course of action in this condition. REFERENCES
FIGURE 2. CT scan of the chest with contrast showing the trachea and esophagus deviated to the right and a small amount of air in the esophagus (arrow).
1. Fritzell B. Voice disorders and occupations. Logoped Phoniatr Vocol. 1996; 21:7–12. 2. Williams NR. Occupational groups at risk of voice disorders: a review of the literature. Occup Med (Lond). 2003;53:456–460.
Travis A.L. Klein, et al
Vocal Fold Paralysis Secondary to Phonotrauma
3. Vilkman E. Voice problem at work: a challenge for occupational safety and health arrangement. Folia Phoniatr Logop. 2000;52:120–125. 4. Sataloff RT, Hawkshaw MJ. Vocal fold hemorrhage. In: Sataloff RT, ed. Professional Voice. 3rd ed. The Science and Art of Clinical Care, 2005; Vol 3. San Diego, CA: Plural Publishing; 2005:1291–1307. 5. Kiese-Himmel C, Pralle L, Kruse E. Psychological profiles of patients with laryngeal contact granulomas. Eur Arch Otorhinolaryngol. 1998;255: 296–301. 6. Butler JE, Hammond TH, Gray SD. Gender-related differences of hyaluronic acid distribution in the human vocal fold. Laryngoscope. 2001;111: 907–911. 7. Hamdan AL, Sibai A, Youssef M, Deeb R, Zaitoun F. The use of a screening questionnaire to determine the incidence of allergic rhinitis in singers with dysphonia. Arch Otolaryngol Head Neck Surg. 2006;132:547–549. 8. Krecicki T, Zalesska-Krecicka M, Pastuszek P, Rak J, MorawskaKochman M, Zatonski M. Treatment of Reinke’s edema among different professional groups: presentation of results. Int J Occup Med Environ Health. 2004;17:279–284. 9. Behlau M. Acute vocal trauma. In: Proceedings XXVth World Congress of the International Association of Logopedics and Phoniatrics, Montreal, Canada. Folia Phoniatr Logop. 2001;53:231.
129.e11
10. Behlau M, Oliveira G, Pontes P. Vocal fold self-disruption after phonotrauma on a lead actor: a case presentation. J Voice. 2009;23:726–732. 11. Harris SS, Gupta R, Hawkshaw MJ, Sataloff RT. Vocal process avulsion. J Voice. 2011;25:638–645. 12. Kaufman JA, Blalock PD. Is voice rest never indicated? J Voice. 1989;13: 79–81. 13. Cho SH, Kim HT, Lee IJ, Kim MS, Park HJ. Influence of phonation on basement membrane zone recovery after phonomicrosurgery: a canine model. Ann Otol Rhinol Laryngol. 2000;109:658–666. 14. Ishikawa K, Thibeault S. Voice rest versus exercise: a review of the literature. J Voice. 2010;24:379–387. 15. Branski RC, Perera P, Verdolini K, Rosen CA, Hebda PA, Agaewal S. Dynamic biomechanical strain inhibits IL-1 beta-induced inflammation in vocal fold fibroblasts. J Voice. 2006;20:432–442. 16. Li NYK, Verdolini K, Clermont G, Mi Q, Rubinstein EN, et al. A patientspecific in silico model of inflammation and healing tested in acute vocal fold injury. PLoS One. 2008;3:e2789. 17. Kutty JK, Webb K. Engineering therapies for the vocal fold lamina propria. Tissue Eng Part B Rev. 2009;15:249–262. 18. Behrman A, Sulica L. Voice rest after microlaryngoscopy: current opinion and practice. Laryngoscope. 2003;113:2182–2186.
