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Vocal Process Avulsion
Vocal Process Avulsion Scott S. Harris, Reena Gupta, Mary J. Hawkshaw, and Robert T. Sataloff, Philadelphia, Pennsylvania Summary: Vocal process avulsion is a rare condition in which laryngeal trauma causes a separation of the vocal process from the body of the arytenoid cartilage. Typically symptoms are dysphonia and shortness of breath during phonation. Strobovideolaryngoscopy, laryngeal electromyography, and laryngeal computed tomography are helpful in establishing this important and sometimes elusive diagnosis. Several treatment modalities have been reported with varying success. We report four new cases, review four cases reported previously by the senior author, and suggest approaches to diagnosis and optimal treatment of vocal process avulsion. Key Words: Vocal process avulsion–Vocal fold avulsion–Dysphonia–Laryngeal trauma–Vocal fold trauma. INTRODUCTION Vocal process avulsion is a rare condition in which laryngeal trauma causes a separation of the vocal process from the body of the arytenoid cartilage. The trauma may be because of either external or internal forces. Most internal laryngeal injuries are iatrogenic, caused by intubation or flexible or rigid endoscopy.1,2 As with all laryngeal injuries, airway management is the first priority, and the index of suspicion for airway compromise in patients who have sustained laryngeal trauma must be high. This is especially true in sedated, unconscious, or severely injured patients who may not exhibit the classical symptoms of dyspnea, dysphonia, and/or dysphagia. Vocal process avulsion itself does not cause airway obstruction usually, but hematoma associated with the causative trauma may. In such cases, obtaining an airway via oral tracheal intubation must be carried out with expert skill to avoid further damage to an already injured larynx, and a tracheotomy should be considered. The complexity of managing these patients is increased by the possible presence of anatomic rearrangement, mucosal damage, and decreased visibility.3 If the patient does not present in acute distress, or once the patient is stable and alert, laryngeal function can be assessed. Appropriate evaluations may include fiberoptic laryngoscopy, strobovideolaryngoscopy, laryngeal electromyography (LEMG), and laryngeal computed tomography (CT). The differential diagnosis for posttraumatic dysphonia includes, but is not limited to, vocal fold paralysis/paresis, arytenoid subluxation/ dislocation, vocal fold hematoma, and vocal process avulsion. Presentation of four new cases, together with review and reconsideration of four cases we reported previously, has led to our current practice regarding diagnosis and treatment of vocal process avulsion. NEW CASES Case 1 A 16-year-old female presented with chronic hoarseness, deep voice quality, vocal fatigue, decreased projection, and shortness Accepted for publication May 7, 2010. From the Department of Otolaryngology – Head and Neck Surgery, Drexel University College of Medicine, Philadelphia, Pennsylvania. Address correspondence and reprint requests to Robert Thayer Sataloff, MD, DMA, FACS, Department of Otolaryngology – Head and Neck Surgery, Drexel University College of Medicine, 1721 Pine Street, Philadelphia, PA 19103-6771. E-mail: rtsataloff@ phillyent.com Journal of Voice, Vol. 25, No. 5, pp. 638-645 0892-1997/$36.00 Ó 2011 The Voice Foundation doi:10.1016/j.jvoice.2010.05.001
of breath, which she described as running out of air before completing a sentence. Her symptoms were exacerbated by prolonged speaking, dehydration, increased phlegm, and generalized fatigue. She had a history of prolonged intubation at the age of 14 years after a severe allergic reaction to intravenous immunoglobulin treatment for an undifferentiated connective tissue disease. Subsequently, she underwent tracheotomy and was decannulated 2 months later, at which time she noticed her present symptoms. The patient initially sought treatment elsewhere. Her symptoms persisted despite allergy and laryngopharyngeal reflux (LPR) treatment. Her past medical history was significant for asthma. When we initially evaluated the patient, her voice was moderately hoarse, moderately breathy, soft, and low in pitch. Strobovideolaryngoscopy revealed moderate supraglottic hyperfunction and LPR. Most significantly, the vocal process of the right arytenoid cartilage appeared to be moving freely (Figure 1). The avulsion resulted in laxity and foreshortening of the vocal fold, and glottic insufficiency and sluggish right vocal fold motion. The left true vocal fold appeared normal. Objective voice analysis indicated irregularity and instability of vocal fold vibration that increased with sustained phonation, and inadequate glottal closure. LEMG revealed 30% reduced recruitment in the distribution of the left (contralateral) superior laryngeal nerve (SLN) and 30–40% reduced recruitment in the left recurrent laryngeal nerve (RLN). No right-sided neurological abnormalities were noted. Noncontrast CT revealed slight asymmetry of the vocal process, but the avulsion could not be visualized. In the operating room, right vocal process avulsion was confirmed by palpation. The body of the arytenoid cartilage and vocal process contact surfaces were abraded through an incision. The fractured segment was then reduced with a figureof-eight 4-0 chromic suture, which approximated the vocal process with the body of the arytenoid cartilage. Five mouse units of botulinum toxin were injected into the right thyroarytenoid muscle to help control muscle forces that might distract the repair in the postoperative period. Evaluation of the patient 3 months after the procedure revealed complete vocal fold closure and equal vocal process height (Figure 2). The patient was satisfied with her voice and reported nearly complete resolution of her presenting complaints. Case 2 A 40-year-old white female cantor and director of a church choir presented with an inability to sing and with dysphonia.
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FIGURE 1. Stroboscopic view of larynx on initial evaluation showing the right vocal process protruding medially, separated, and displaced anteriorly from the body of the arytenoid cartilage.
Her symptoms began 2 weeks after intubation for sinus surgery, when she first attempted to sing postoperatively. As she attempted to sing in her upper register, she heard or felt a ‘‘pop’’ in her throat, and then stopped singing. Since then, she had experienced hoarseness that had improved slightly, but she noted persistent cracking of her speaking voice, loss of range, and diminished quality of her head voice. Before presentation to our office, she was examined by an otolaryngologist who told her that she had reflux and a cyst on her right vocal fold. She was placed on omeprazole twice daily. She noticed no improvement, and she stopped the medication after 3 months of treatment. She presented to us for a second opinion before undergoing surgery for the presumed cyst. Her past medical history was significant for seasonal allergies and nasal polyps for which she had been placed long term on 5 mg prednisone every other day. Laryngoscopy, strobovideolaryngoscopy, and complex voice analysis revealed slight hoarseness, a low-pitched voice, LPR, and mild supraglottic hyperfunction. The right vocal fold was higher than the left. The vocal process of the right arytenoid cartilage was bulging medially within the vocal fold, and it moved freely on phonation (Figure 3A and B). There was also sluggish
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FIGURE 2. Stroboscopic view of larynx 3 mo after endoscopic reduction with open suture fixation and with botulinum toxin injection. right adduction and abduction, intermittently incomplete closure, and increased waveform. Posterior to the vocal process, but anterior to the arytenoid cartilage, the vocal fold exhibited hypodynamic vibration and an area of persistent failure of glottic closure. LEMG revealed right SLN paresis with 20% reduced recruitment response, and poor relaxation at rest suggesting muscle tension dysphonia. CT scan of the neck with contrast did not show the injury well enough to be helpful clinically. Initial treatment included preoperative voice therapy, lansoprazole, ranitidine, and reevaluation in 6 weeks. Her symptoms had not improved significantly, but there was decreased evidence of LPR. She agreed to undergo surgery but has not proceeded, so far. Case 3 This 65-year-old male experienced sudden voice change after yelling at the age of 14 years. He noted vocal fatigue, odynophonia, and deepness of his voice. He had not sought treatment during the intervening 51 years. However, he was considering to become a teacher and felt he would be unable to do so with his current voice condition.
FIGURE 3. A. Stroboscopic view of larynx showing that the right vocal fold was higher than the left; the vocal process of the right arytenoid cartilage was bulging medially within the vocal fold. B. Vocal process of the right arytenoid cartilage displaced anteriorly during phonation.
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FIGURE 4. Stroboscopic view of larynx shows the right vocal process bulging anteriorly. It overlaps and is higher than the left vocal process. On physical examination, his voice was somewhat pressed. Strobovideolaryngoscopy revealed right true vocal fold bowing, the right true vocal fold at a higher level than the left, and right incomplete vocal process avulsion (Figure 4). There was also sluggish right adduction and abduction, and increased waveform. Posterior to the vocal process but anterior to the arytenoid cartilage the vocal fold vibration was hypodynamic. Signs of LPR were present. Reflux treatment and voice therapy were prescribed. On follow-up examination approximately 6 weeks later, he reported an improvement of his symptoms through voice therapy. Because of the stability (51 years) and baseline functionality of his voice, and the risks of anesthesia and surgery, the patient opted not to undergo surgical correction and has remained satisfied with his voice. Case 4 A 46-year-old female secretary presented with a 1-year history of dysphonia. She reported that her vocal difficulties began approximately 2 weeks after undergoing septoplasty. She denied vocal difficulties before the surgery and had no dysphonia during the first 2 weeks after septoplasty. She denied any awareness of difficulties regarding her intubation and she denied any previous history of laryngeal trauma. Her dysphonia had been worsening gradually. She complained of hoarseness, vocal fatigue, voice breaks, weak voice, decreased projection, decreased ability to produce a loud volume, postnasal drip, throat clearing, and occasional odynophonia. Six months after her septoplasty, she discussed her vocal difficulties with her otolaryngologist. He referred her to a gastroenterologist who performed upper endoscopy that reportedly revealed signs of gastritis but no Barrett’s metaplasia. She was treated with Carafate. She had also been started on Nexium 40 mg once daily. Strobovideolaryngoscopy revealed a gravely and deep voice, left vocal fold avulsion, left vocal fold paresis, LPR, and muscle tension dysphonia. The left vocal process appeared more anterior than the right, and there was laxity in the left vocal
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FIGURE 5. Strobovideolaryngoscopy shows that the left vocal process appears more anterior than the right. There is also left vocal fold laxity, shortening, and thickening. fold with vocal fold shortening and thickening (Figure 5). Her reflux finding score was 11. LEMG revealed a left RLN paresis with 40–50% reduced recruitment response and left SLN paresis with 30% reduced recruitment response; the right side was normal. Two weeks preoperatively, she was given 3.75 mouse units of Botox into the left thyroarytenoid muscle. She underwent microdirect laryngoscopy with open reduction and internal fixation of her left vocal process avulsion. At the time of surgery, palpation confirmed separation between the vocal process and the body of the left arytenoid. The vocal process was found anteriorly displaced approximately 3 mm (Figure 6). Suture (4-0 chromic) was passed through the body of the arytenoid and the vocal process in a figure-of-eight to restore longitudinal tension and approximate the vocal process and body of the arytenoid cartilage. PREVIOUSLY PUBLISHED CASES Of the four cases previously published by the senior author (R.T.S.),4,5 three had satisfactory voice improvement at least 6 months after surgery. These patients came from long distances and were lost to follow up thereafter. One patient was followed-up for approximately 4 years but has since died of unrelated causes. Case 5 A 69-year-old white male retired teacher presented with a several year history of dysphonia, which worsened after intubation for cervical spine fusion 4 years earlier. He complained of hoarseness, vocal fatigue, decreased ability to project, a choking sensation when speaking, and the inability to maintain pitch. His voice was worse in the morning and after extensive voice use. We observed moderate-to-severe hoarseness and a pressed voice quality with moderate supraglottic hyperfunction. The vocal process of the left arytenoid cartilage jutted medially at a 45 angle toward the midline, and it moved into alignment with the rest of the vocal fold with pressure from the opposite vocal fold. Additionally, the left vocal fold was high, short,
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FIGURE 7. Stroboscopic view of larynx. The left vocal process overlaps the right vocal process and is angled toward midline.
FIGURE 6. A. Intraoperative photograph of Case 4. Suture needle passed through the body of the left arytenoid. The needle is resting over the white, avulsed vocal process. B. The other needle of this double-ended suture is being passed through the avulsed vocal process in preparation for tying the suture in a figure-of-eight, to bring the vocal process in approximation with the body of the arytenoid cartilage. C. The suture has been tied, and the vocal process has been reattached to the arytenoid. Longitudinal tension along the vocal fold edge has been restored.
and bowed; and there was a pattern of ‘‘scissoring’’ with left vocal fold overlapping the right side on phonation (Figure 7). LEMG revealed 30% reduced recruitment in the distribution of the right SLN.
The patient’s reflux medications were optimized, which improved his reflux findings substantially. Voice therapy resulted in partial, improvement in his symptoms. Under microdirect laryngoscopy, the diagnosis of vocal process avulsion was confirmed by palpation. Autologous fat was injected into the left vocal fold in an attempt to secure placement of the avulsed segment yielding better contact with the arytenoid cartilage. The fast was positioned to try to reduce the vocal process and hold it in place against the arytenoid. Fat was also injected laterally to medialize the vocal fold, but overinjection was avoided to prevent distraction (displacement of the vocal process). One month postoperatively, the patient’s voice was improved, and strobovideolaryngoscopy demonstrated substantial improvement in glottic closure. He underwent repeat lipoinjection for medialization several months later because of excessive resorption, but the vocal process position remained better after the first procedure. Postoperatively, he continued to demonstrate improved glottic closure, although his voice was still somewhat hoarse. He therefore underwent a third injection medialization, this time bilaterally with Radiesse. This intervention resulted in a poorer voice quality. Strobovideolaryngoscopy with magnification revealed persistent scissoring of the vocal processes with left over right, but the level mismatch was improved, as was glottic closure. There was also mucosal stiffness after Radiesse injection. Over time, despite voice therapy, his voice continued to worsen. His laryngeal examination demonstrated increasing flaccidity and atrophy in right true vocal fold, and diplophonia. Case 6 A 28-year-old male with no prior voice complaints presented with dysphonia after intubation for removal of a benign stomach mass. He also noted dysphagia, later confirmed as including aspiration on barium swallow. An arytenoid dislocation was diagnosed at another facility, and the patient presented after an attempt at operative reduction. Strobovideolaryngoscopy demonstrated normal arytenoid motion on the right and decreased (but not absent) vocal fold motion on the left. Glottic closure was incomplete. The right
642 vocal process was slightly higher than the left. It was also displaced anteriorly, turned slightly medially, and obviously separated from the body of the arytenoid cartilage (Figure 8). LEMG revealed 50% reduced recruitment in the left RLN, 30–40% reduced recruitment in the right RLN, and 10–20% reduced recruitment in the right SLN. The right vocal process avulsion was confirmed by intraoperative palpation. Autologous lipoinjection was performed on the left to ameliorate aspiration symptoms. Palpation of the right vocal process suggested fibrous union with the body of the arytenoid cartilage. It was suspected that adequate reduction would occur without distracting forces; therefore, botulinum toxin was injected into the vocalis muscle but suture was not placed. Two weeks postoperatively, the patient’s voice was stronger despite the Botulinum toxin. Examination showed expected right true vocal fold sluggishness and flaccidity. Left vocal fold movement was normal. The right vocal process was persistently higher than the left. Three months postopertively, his voice was still slightly hoarse but improved; a result that persisted for 7 months. However, at 13 months, his voice worsened and laryngeal examination demonstrated glottic insufficiency despite improvement in vocal process height and position. Bilateral thyroplasty was performed. This resulted in improved glottic closure, essentially equal vocal process height, and voice improvement. No further treatment was required. Case 7 A 24-year-old male with no prior voice complaints suffered a blow to the neck from an elbow while wrestling, resulting in dysphonia. Strobovideolaryngoscopy revealed decreased abduction and adduction of the right vocal fold, angulation of the right vocal process medially, and separation of the vocal process from the body of the arytenoid cartilage by 3–4 mm. Laryngeal electromyogram showed 40% reduced recruitment in the distribution of the right RLN. Cricoarytenoid joint CT showed a fracture in the posterolateral aspect of the cricoid cartilage and elevation of the right cricoarytenoid joint, but it
FIGURE 8. Stroboscopic view of larynx. The right vocal process is slightly higher than the left, displaced anteriorly and separated from the body of the arytenoid cartilage, and turned slightly medially.
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was unremarkable at the site of the avulsion. Avulsion of the vocal process was confirmed by microdirect laryngoscopy. Right cordotomy allowed by reapproximation with 4-0 chromic figure-of-eight suture placement through the body of the arytenoid cartilage and the avulsed vocal process. Botulinum toxin was injected into right thyroarytenoid muscle. Dramatic voice improvement was appreciated postoperatively.5 He was lost to follow up after 6 months. Case 8 This 26-year-old male had no voice complaints before motor vehicle collision 5 years before evaluation. During the accident, he struck his neck on the steering wheel. Nasotracheal intubation was performed in the emergency room. He was diagnosed with laryngeal fracture and ‘‘degloving injury of the left arytenoid.’’ An otolaryngologist sutured the mucosa through a laryngofissure and subsequently performed a laryngoplasty. The patient underwent voice therapy, but he remained hoarse. Four months later, he had a vocal fold Teflon injection with some voice improvement, but it remained soft, hoarse, and fatigued easily. Repeat Teflon injection at 6 months did not result in significant change. His voice was stable for the next 3.5 years until he was referred to our practice. Strobovideolaryngoscopy revealed a Teflon granuloma laterally in the ventricle. The left true vocal fold was erythematous, and the vocal process was 3–4 mm below the right vocal process, allowing the right vocal fold to overlap the left on adduction. Both arytenoids were mobile, but movement was diminished on the left. He had suffered avulsion of the left vocal process, and the thyroarytenoid muscle had contracted anteriorly. Much of the Teflon was removed, and the vocal process was sutured to the arytenoid at an appropriate height. His voice improved somewhat. However, as expected, it was not restored to normal because of the Teflon granuloma and muscle atrophy. He did not return for recommended postoperative care. DISCUSSION Vocal process avulsion is a traumatic separation of the vocal process from the body of the arytenoid cartilage. Although few cases have been reported in the literature (Table 1), this injury requires specialized management for satisfactory voice outcome. The junction of the vocal process of the arytenoid and the arytenoid cartilage may be vulnerable because of the separate embryological origins of its components and the fragility of the structures.3 Vocal fold instability after vocal process avulsion leads to hoarseness and breathiness. It is possible that the junction between the vocal process and body of the arytenoid cartilage may be more vulnerable in younger people. If this is so, it might be because of immaturity of the cartilaginous framework; but there are no data to shed light on this question. It is interesting to note that of the cases we compiled, combined with the cases in the literature we reviewed, seven out of the 11 cases reported were 30 years old or younger.4,6–9 This unusual condition may be confused easily with arytenoid cartilage dislocation. The most common mechanisms of
Age (y)
Mode of Injury
Abraham et al, 20096
_
13
Clothes line injury from a tree branch
Knapp et al, 20007
_
15
Anterior neck trauma from slip and fall onto a log
Wohl, 19968
_
Newborn Intubation
Diagnostic Process
Treatment
Outcome
(Continued )
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Return to normal Oral antibiotics and steroids Aphonia and hemoptysis / voice quality with pre-/postoperatively. Direct Transnasal videostroboscopy— slight left-sided atrophy visualization under operating Incomplete glottis closure, and phase asymmetry microscope with bilateral vertical fold mismatch. Right true at 6 mo suture reapproximation. vocal fold—irregularity with Botulinum toxin injection into decreased mobility and mucosal left thyroarytenoid muscle wave. Left true vocal fold— irregularity with decreased mobility, no mucosal wave / CT—Small focus of air in left glottis soft tissue at the site of suspected laceration / Direct laryngoscopy—Bilateral vocal process fractures Decannulated post-op Tracheostomy, DL, bronchoscopy, Hoarseness and small amount day 5, good glottic and esophagoscopy and laryngeal of hemoptysis. supraglottic airway fracture repair. DL revealed No airway distress. CT scan avulsion of right arytenoid revealed small thyroid cartilage cartilage with laceration overlying fracture and disruption of the mucosa, repositioned and mucosa of the right supraglottic repaired. Avulsion and mucosal airway. laceration with 6-0 chromic gut. Flexible laryngoscopy revealed Repair of laryngeal fracture by right arytenoid edema and false open cervical approach with vocal fold laceration causing simple interrupted closure using inability to visualize the right prolene sutures true vocal fold. The left true vocal fold is intact and mobile. Blunt probe and fine tip Postop granuloma Postextubation biphasic stridor suction catheter alignment, repaired at 4 wk 1 Flexible laryngoscopy—left-sided 8 mo—Normal, followed by sedation and glottic soft-tissue encroachment paralysis for 72 h symmetric vocal fold into the glottic airway / growth and mobility. Direct laryngoscopy—‘‘Gouge Grossly normal voice injury’’ extending the posterior portion of the membranous left vocal fold to the superior arcuate line. Lateral extension through the vocalis muscle and into the medial aspect of the thyroarytenoid muscle. A triangular wedge of muscle with attached vocal fold ‘‘flopping’’ into the laryngeal airway
Vocal Process Avulsion
Sex
Author
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TABLE 1. Review of Literature
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Outcome
Decannulated, adequate airway, no aspiration/ dysphagia, weak voice with R TVF paralysis
Diagnostic Process
Treatment
MVA 14 _ Wootten et al, 20099
Mode of Injury Age (y) Sex Author
TABLE 1 (Continued )
Diagnostic modalities not described—Vertical thyroid cartilage fracture creating laryngofissure, unequal true vocal fold height, right arytenoid rotation with true vocal fold vulsion from vocal process, cricothyroid membrane tear, cricoid fracture, and pharyngeal tear
Emergent tracheotomy; suture fixation of cricoid fracture, completion of laryngofissure with suturepexy of the right true vocal fold and prolapsed glottic and subglottic mucosa over Aboulker Stent, repair of pharynx and cricothyroid membrane
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injury in both conditions are intubation and external laryngeal trauma.3,7,10 The differential diagnosis must also include vocal fold paresis and paralysis, which are much more common. Similar symptoms of all these conditions dictate that comprehensive evaluation should be performed to establish an accurate diagnosis. Various approaches to diagnosis and treatment have been reported (Table 1). On the basis of these reports and our experience, we rely primarily on strobovideolaryngoscopy supplemented by LEMG. Intraoperative palpation provides the most definitive assessment. CT scan sometimes provides important information about surrounding structures that may have been injured, but it has not provided useful images of vocal process avulsion. Perhaps, technological improvements will eventually remedy this deficiency. Strobovideolaryngoscopy is valuable to confirm the position and hypermobility of the avulsed vocal process and detect functional consequences and related injuries. LEMG can help differentiate vocal fold paresis/paralysis from anatomical and structural defects. A normal or mildly reduced recruitment pattern would imply intact neuromuscular function, making primary paresis or paralysis an unlikely cause of substantial movement impairment or dysphonia.11 If the diagnosis is still unclear, laryngeal CT may be useful primarily to rule out other diagnoses. Laryngeal CT may help diagnose arytenoid cartilage dislocation and identify fractures of the cartilaginous framework, although fractures of un-ossified cartilage in children and young adults may be missed.10,11 CT may be helpful in diagnosis of vocal fold paralysis also, although a CT suggestive of vocal fold paralysis is not definitively diagnostic.12,13 All of our patients undergo objective voice analysis and are advised to undergo pre- and postoperative voice therapy to eliminate compensatory hyperfunction and optimize safe phonation. It is important to recognize that even in newborns, intubation may result in vocal process avulsion. Wohl recommends conservative management with observation, with vocal fold realignment via gentle tissue manipulation to recreate normal anatomical position under laryngoscopic visualization. He advises that this should be followed by 72 hours of tissue immobilization achieved by sedation and paralysis, with the infant remaining intubated with an uncuffed endotracheal tube. In severe cases, or if realignment fails, suture placement or open repair may be considered. Treatment of older children and adults may begin with a trial of voice therapy to eliminate compensatory hyperfunction and optimize safe phonation. When results are unsatisfactory, surgery may be performed. Surgical approaches include closed reduction using fat injection to force the vocal process posteriorly, stabilizing it against the body of the arytenoid; botulinum toxin injection, and endoscopic open reduction and suture of the fracture. A combination of these procedures may also be used. In the author’s (R.T.S.) experience, endoscopic reduction and suture have produced the best and long-lasting results. Botulinum toxin can be injected into the thyroarytenoid muscle, causing temporary paralysis of the muscle that would tend to pull the
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vocal process away from its sutured position. Botulinum toxin can be used intraoperatively or several days preoperatively. This allows reduced tension during healing; occasionally botulinum toxin injection alone may be therapeutic.8
ertheless, the best voice quality and most durable results are achieved with open reduction and suture fixation, which we now consider our primary approach to this challenging problem for most patients.
CONCLUSION Strobovideolaryngoscopy is the mainstay of diagnosis of vocal process avulsion. Findings that support the diagnosis include visualization of the vocal process moving freely in vocal fold, bulging medially within the vocal fold, and occasional correction of vocal process angulation with pressure from the contralateral vocal. The vocal process may also be seen to move freely on phonation. There may be movement abnormalities anterior to the avulsed segment, particularly on abduction, and decreased mucosal wave between the vocal process and body is common. Confirmation is achieved with intraoperative palpation, appreciating the defect between the vocal process and the body of the arytenoid cartilage. Voice therapy alone was insufficient to restore acceptable voice in most of our cases. Endoscopic reduction with suture fixation with or without botulinum toxin injection proved most successful in reestablishing union between the arytenoid body and the vocal process, but currently we prefer preoperative Botulinum toxin injection. If avulsion is incomplete, suture fixation may not always be necessary, and botulinum toxin injection to achieve chemical tenotomy may be sufficient to allow healing. Autologious fat injection also may result in voice improvement, but it has not been as successful as vocal process suture. Assessment of long-term outcomes in our cases was confounded by the co-existence of paresis and other vocal fold abnormalities (as is usually the case). However, improvement in voice and increased function was achieved in all of the reported cases. Nev-
REFERENCES 1. Blanc VF, Tremblay NAG. The complications of tracheal intubation: a new classification with a review of literature. Anesth Analg. 1974;53: 202–213. 2. Whited RE. A prospective of laryngotracheal sequelae in long-term intubation. Laryngoscope. 1984;94:367–377. 3. Heman-Ackah YD, Sataloff RT. Laryngotracheal trauma. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care. 3rd ed. San Diego, CA: Plural Publishing, Inc.; 2005:1315–1340. 4. Rubin AD, Hawkshaw MJ, Sataloff RT. Vocal process avulsion. J Voice. 2005;19:702–706. 5. Sataloff RT, Heuer RJ, Hawkshaw MJ, Spiegel JR. Vocal fold avulsion. Ear Nose Throat J. 1995;74:230. 6. Abraham RF, Shapshay SM, Galati L. Botulinum-assisted endoscopic repair of traumatic vocal fold avulsion; endoscopic repair. Ear Nose Throat J. In press. 7. Knapp JF, Johnson PS, Kirse D, Barnett T. Case record of Children’s Mercy Hospital: a 15-year-old hoarseness following neck trauma. Pediatr Emerg Care. 2000;16:364–366. 8. Wohl DL. Traumatic vocal fold avulsion injury in a newborn. J Voice. 1995; 10:106–108. 9. Wootten CT, Bromwich MA, Myer CM. Trends in blunt laryngotracheal trauma in children. Int J Pediatr Otorhinolaryngol. 2009;73:1071–1075. 10. Rubin AD, Hawkshaw MJ, Moyer CA, et al. Arytenoid cartilage dislocation: a 20-year experience. J Voice. 2005;19:687–701. 11. Sataloff RT, Praneetvatakul P, Heuer RJ, et al. Laryngeal electromyography: clinical application. J Voice. 2010;24:228–234. 12. Chin SC, Edelstein S, Chen CY, Som PM. Using CT to localize side and level of vocal cord paralysis. Am J Roentgenol. 2003;180:1165–1170. 13. Kim BS, Ahn KJ, Park YH, Hahn ST. Usefulness of laryngeal phonation CT in the diagnosis of vocal cord paralysis. Am J Roentgenol. 2008;190: 1376–1379.
of breath, which she described as running out of air before completing a sentence. Her symptoms were exacerbated by prolonged speaking, dehydration, increased phlegm, and generalized fatigue. She had a history of prolonged intubation at the age of 14 years after a severe allergic reaction to intravenous immunoglobulin treatment for an undifferentiated connective tissue disease. Subsequently, she underwent tracheotomy and was decannulated 2 months later, at which time she noticed her present symptoms. The patient initially sought treatment elsewhere. Her symptoms persisted despite allergy and laryngopharyngeal reflux (LPR) treatment. Her past medical history was significant for asthma. When we initially evaluated the patient, her voice was moderately hoarse, moderately breathy, soft, and low in pitch. Strobovideolaryngoscopy revealed moderate supraglottic hyperfunction and LPR. Most significantly, the vocal process of the right arytenoid cartilage appeared to be moving freely (Figure 1). The avulsion resulted in laxity and foreshortening of the vocal fold, and glottic insufficiency and sluggish right vocal fold motion. The left true vocal fold appeared normal. Objective voice analysis indicated irregularity and instability of vocal fold vibration that increased with sustained phonation, and inadequate glottal closure. LEMG revealed 30% reduced recruitment in the distribution of the left (contralateral) superior laryngeal nerve (SLN) and 30–40% reduced recruitment in the left recurrent laryngeal nerve (RLN). No right-sided neurological abnormalities were noted. Noncontrast CT revealed slight asymmetry of the vocal process, but the avulsion could not be visualized. In the operating room, right vocal process avulsion was confirmed by palpation. The body of the arytenoid cartilage and vocal process contact surfaces were abraded through an incision. The fractured segment was then reduced with a figureof-eight 4-0 chromic suture, which approximated the vocal process with the body of the arytenoid cartilage. Five mouse units of botulinum toxin were injected into the right thyroarytenoid muscle to help control muscle forces that might distract the repair in the postoperative period. Evaluation of the patient 3 months after the procedure revealed complete vocal fold closure and equal vocal process height (Figure 2). The patient was satisfied with her voice and reported nearly complete resolution of her presenting complaints. Case 2 A 40-year-old white female cantor and director of a church choir presented with an inability to sing and with dysphonia.
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FIGURE 1. Stroboscopic view of larynx on initial evaluation showing the right vocal process protruding medially, separated, and displaced anteriorly from the body of the arytenoid cartilage.
Her symptoms began 2 weeks after intubation for sinus surgery, when she first attempted to sing postoperatively. As she attempted to sing in her upper register, she heard or felt a ‘‘pop’’ in her throat, and then stopped singing. Since then, she had experienced hoarseness that had improved slightly, but she noted persistent cracking of her speaking voice, loss of range, and diminished quality of her head voice. Before presentation to our office, she was examined by an otolaryngologist who told her that she had reflux and a cyst on her right vocal fold. She was placed on omeprazole twice daily. She noticed no improvement, and she stopped the medication after 3 months of treatment. She presented to us for a second opinion before undergoing surgery for the presumed cyst. Her past medical history was significant for seasonal allergies and nasal polyps for which she had been placed long term on 5 mg prednisone every other day. Laryngoscopy, strobovideolaryngoscopy, and complex voice analysis revealed slight hoarseness, a low-pitched voice, LPR, and mild supraglottic hyperfunction. The right vocal fold was higher than the left. The vocal process of the right arytenoid cartilage was bulging medially within the vocal fold, and it moved freely on phonation (Figure 3A and B). There was also sluggish
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FIGURE 2. Stroboscopic view of larynx 3 mo after endoscopic reduction with open suture fixation and with botulinum toxin injection. right adduction and abduction, intermittently incomplete closure, and increased waveform. Posterior to the vocal process, but anterior to the arytenoid cartilage, the vocal fold exhibited hypodynamic vibration and an area of persistent failure of glottic closure. LEMG revealed right SLN paresis with 20% reduced recruitment response, and poor relaxation at rest suggesting muscle tension dysphonia. CT scan of the neck with contrast did not show the injury well enough to be helpful clinically. Initial treatment included preoperative voice therapy, lansoprazole, ranitidine, and reevaluation in 6 weeks. Her symptoms had not improved significantly, but there was decreased evidence of LPR. She agreed to undergo surgery but has not proceeded, so far. Case 3 This 65-year-old male experienced sudden voice change after yelling at the age of 14 years. He noted vocal fatigue, odynophonia, and deepness of his voice. He had not sought treatment during the intervening 51 years. However, he was considering to become a teacher and felt he would be unable to do so with his current voice condition.
FIGURE 3. A. Stroboscopic view of larynx showing that the right vocal fold was higher than the left; the vocal process of the right arytenoid cartilage was bulging medially within the vocal fold. B. Vocal process of the right arytenoid cartilage displaced anteriorly during phonation.
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FIGURE 4. Stroboscopic view of larynx shows the right vocal process bulging anteriorly. It overlaps and is higher than the left vocal process. On physical examination, his voice was somewhat pressed. Strobovideolaryngoscopy revealed right true vocal fold bowing, the right true vocal fold at a higher level than the left, and right incomplete vocal process avulsion (Figure 4). There was also sluggish right adduction and abduction, and increased waveform. Posterior to the vocal process but anterior to the arytenoid cartilage the vocal fold vibration was hypodynamic. Signs of LPR were present. Reflux treatment and voice therapy were prescribed. On follow-up examination approximately 6 weeks later, he reported an improvement of his symptoms through voice therapy. Because of the stability (51 years) and baseline functionality of his voice, and the risks of anesthesia and surgery, the patient opted not to undergo surgical correction and has remained satisfied with his voice. Case 4 A 46-year-old female secretary presented with a 1-year history of dysphonia. She reported that her vocal difficulties began approximately 2 weeks after undergoing septoplasty. She denied vocal difficulties before the surgery and had no dysphonia during the first 2 weeks after septoplasty. She denied any awareness of difficulties regarding her intubation and she denied any previous history of laryngeal trauma. Her dysphonia had been worsening gradually. She complained of hoarseness, vocal fatigue, voice breaks, weak voice, decreased projection, decreased ability to produce a loud volume, postnasal drip, throat clearing, and occasional odynophonia. Six months after her septoplasty, she discussed her vocal difficulties with her otolaryngologist. He referred her to a gastroenterologist who performed upper endoscopy that reportedly revealed signs of gastritis but no Barrett’s metaplasia. She was treated with Carafate. She had also been started on Nexium 40 mg once daily. Strobovideolaryngoscopy revealed a gravely and deep voice, left vocal fold avulsion, left vocal fold paresis, LPR, and muscle tension dysphonia. The left vocal process appeared more anterior than the right, and there was laxity in the left vocal
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FIGURE 5. Strobovideolaryngoscopy shows that the left vocal process appears more anterior than the right. There is also left vocal fold laxity, shortening, and thickening. fold with vocal fold shortening and thickening (Figure 5). Her reflux finding score was 11. LEMG revealed a left RLN paresis with 40–50% reduced recruitment response and left SLN paresis with 30% reduced recruitment response; the right side was normal. Two weeks preoperatively, she was given 3.75 mouse units of Botox into the left thyroarytenoid muscle. She underwent microdirect laryngoscopy with open reduction and internal fixation of her left vocal process avulsion. At the time of surgery, palpation confirmed separation between the vocal process and the body of the left arytenoid. The vocal process was found anteriorly displaced approximately 3 mm (Figure 6). Suture (4-0 chromic) was passed through the body of the arytenoid and the vocal process in a figure-of-eight to restore longitudinal tension and approximate the vocal process and body of the arytenoid cartilage. PREVIOUSLY PUBLISHED CASES Of the four cases previously published by the senior author (R.T.S.),4,5 three had satisfactory voice improvement at least 6 months after surgery. These patients came from long distances and were lost to follow up thereafter. One patient was followed-up for approximately 4 years but has since died of unrelated causes. Case 5 A 69-year-old white male retired teacher presented with a several year history of dysphonia, which worsened after intubation for cervical spine fusion 4 years earlier. He complained of hoarseness, vocal fatigue, decreased ability to project, a choking sensation when speaking, and the inability to maintain pitch. His voice was worse in the morning and after extensive voice use. We observed moderate-to-severe hoarseness and a pressed voice quality with moderate supraglottic hyperfunction. The vocal process of the left arytenoid cartilage jutted medially at a 45 angle toward the midline, and it moved into alignment with the rest of the vocal fold with pressure from the opposite vocal fold. Additionally, the left vocal fold was high, short,
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FIGURE 7. Stroboscopic view of larynx. The left vocal process overlaps the right vocal process and is angled toward midline.
FIGURE 6. A. Intraoperative photograph of Case 4. Suture needle passed through the body of the left arytenoid. The needle is resting over the white, avulsed vocal process. B. The other needle of this double-ended suture is being passed through the avulsed vocal process in preparation for tying the suture in a figure-of-eight, to bring the vocal process in approximation with the body of the arytenoid cartilage. C. The suture has been tied, and the vocal process has been reattached to the arytenoid. Longitudinal tension along the vocal fold edge has been restored.
and bowed; and there was a pattern of ‘‘scissoring’’ with left vocal fold overlapping the right side on phonation (Figure 7). LEMG revealed 30% reduced recruitment in the distribution of the right SLN.
The patient’s reflux medications were optimized, which improved his reflux findings substantially. Voice therapy resulted in partial, improvement in his symptoms. Under microdirect laryngoscopy, the diagnosis of vocal process avulsion was confirmed by palpation. Autologous fat was injected into the left vocal fold in an attempt to secure placement of the avulsed segment yielding better contact with the arytenoid cartilage. The fast was positioned to try to reduce the vocal process and hold it in place against the arytenoid. Fat was also injected laterally to medialize the vocal fold, but overinjection was avoided to prevent distraction (displacement of the vocal process). One month postoperatively, the patient’s voice was improved, and strobovideolaryngoscopy demonstrated substantial improvement in glottic closure. He underwent repeat lipoinjection for medialization several months later because of excessive resorption, but the vocal process position remained better after the first procedure. Postoperatively, he continued to demonstrate improved glottic closure, although his voice was still somewhat hoarse. He therefore underwent a third injection medialization, this time bilaterally with Radiesse. This intervention resulted in a poorer voice quality. Strobovideolaryngoscopy with magnification revealed persistent scissoring of the vocal processes with left over right, but the level mismatch was improved, as was glottic closure. There was also mucosal stiffness after Radiesse injection. Over time, despite voice therapy, his voice continued to worsen. His laryngeal examination demonstrated increasing flaccidity and atrophy in right true vocal fold, and diplophonia. Case 6 A 28-year-old male with no prior voice complaints presented with dysphonia after intubation for removal of a benign stomach mass. He also noted dysphagia, later confirmed as including aspiration on barium swallow. An arytenoid dislocation was diagnosed at another facility, and the patient presented after an attempt at operative reduction. Strobovideolaryngoscopy demonstrated normal arytenoid motion on the right and decreased (but not absent) vocal fold motion on the left. Glottic closure was incomplete. The right
642 vocal process was slightly higher than the left. It was also displaced anteriorly, turned slightly medially, and obviously separated from the body of the arytenoid cartilage (Figure 8). LEMG revealed 50% reduced recruitment in the left RLN, 30–40% reduced recruitment in the right RLN, and 10–20% reduced recruitment in the right SLN. The right vocal process avulsion was confirmed by intraoperative palpation. Autologous lipoinjection was performed on the left to ameliorate aspiration symptoms. Palpation of the right vocal process suggested fibrous union with the body of the arytenoid cartilage. It was suspected that adequate reduction would occur without distracting forces; therefore, botulinum toxin was injected into the vocalis muscle but suture was not placed. Two weeks postoperatively, the patient’s voice was stronger despite the Botulinum toxin. Examination showed expected right true vocal fold sluggishness and flaccidity. Left vocal fold movement was normal. The right vocal process was persistently higher than the left. Three months postopertively, his voice was still slightly hoarse but improved; a result that persisted for 7 months. However, at 13 months, his voice worsened and laryngeal examination demonstrated glottic insufficiency despite improvement in vocal process height and position. Bilateral thyroplasty was performed. This resulted in improved glottic closure, essentially equal vocal process height, and voice improvement. No further treatment was required. Case 7 A 24-year-old male with no prior voice complaints suffered a blow to the neck from an elbow while wrestling, resulting in dysphonia. Strobovideolaryngoscopy revealed decreased abduction and adduction of the right vocal fold, angulation of the right vocal process medially, and separation of the vocal process from the body of the arytenoid cartilage by 3–4 mm. Laryngeal electromyogram showed 40% reduced recruitment in the distribution of the right RLN. Cricoarytenoid joint CT showed a fracture in the posterolateral aspect of the cricoid cartilage and elevation of the right cricoarytenoid joint, but it
FIGURE 8. Stroboscopic view of larynx. The right vocal process is slightly higher than the left, displaced anteriorly and separated from the body of the arytenoid cartilage, and turned slightly medially.
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was unremarkable at the site of the avulsion. Avulsion of the vocal process was confirmed by microdirect laryngoscopy. Right cordotomy allowed by reapproximation with 4-0 chromic figure-of-eight suture placement through the body of the arytenoid cartilage and the avulsed vocal process. Botulinum toxin was injected into right thyroarytenoid muscle. Dramatic voice improvement was appreciated postoperatively.5 He was lost to follow up after 6 months. Case 8 This 26-year-old male had no voice complaints before motor vehicle collision 5 years before evaluation. During the accident, he struck his neck on the steering wheel. Nasotracheal intubation was performed in the emergency room. He was diagnosed with laryngeal fracture and ‘‘degloving injury of the left arytenoid.’’ An otolaryngologist sutured the mucosa through a laryngofissure and subsequently performed a laryngoplasty. The patient underwent voice therapy, but he remained hoarse. Four months later, he had a vocal fold Teflon injection with some voice improvement, but it remained soft, hoarse, and fatigued easily. Repeat Teflon injection at 6 months did not result in significant change. His voice was stable for the next 3.5 years until he was referred to our practice. Strobovideolaryngoscopy revealed a Teflon granuloma laterally in the ventricle. The left true vocal fold was erythematous, and the vocal process was 3–4 mm below the right vocal process, allowing the right vocal fold to overlap the left on adduction. Both arytenoids were mobile, but movement was diminished on the left. He had suffered avulsion of the left vocal process, and the thyroarytenoid muscle had contracted anteriorly. Much of the Teflon was removed, and the vocal process was sutured to the arytenoid at an appropriate height. His voice improved somewhat. However, as expected, it was not restored to normal because of the Teflon granuloma and muscle atrophy. He did not return for recommended postoperative care. DISCUSSION Vocal process avulsion is a traumatic separation of the vocal process from the body of the arytenoid cartilage. Although few cases have been reported in the literature (Table 1), this injury requires specialized management for satisfactory voice outcome. The junction of the vocal process of the arytenoid and the arytenoid cartilage may be vulnerable because of the separate embryological origins of its components and the fragility of the structures.3 Vocal fold instability after vocal process avulsion leads to hoarseness and breathiness. It is possible that the junction between the vocal process and body of the arytenoid cartilage may be more vulnerable in younger people. If this is so, it might be because of immaturity of the cartilaginous framework; but there are no data to shed light on this question. It is interesting to note that of the cases we compiled, combined with the cases in the literature we reviewed, seven out of the 11 cases reported were 30 years old or younger.4,6–9 This unusual condition may be confused easily with arytenoid cartilage dislocation. The most common mechanisms of
Age (y)
Mode of Injury
Abraham et al, 20096
_
13
Clothes line injury from a tree branch
Knapp et al, 20007
_
15
Anterior neck trauma from slip and fall onto a log
Wohl, 19968
_
Newborn Intubation
Diagnostic Process
Treatment
Outcome
(Continued )
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Return to normal Oral antibiotics and steroids Aphonia and hemoptysis / voice quality with pre-/postoperatively. Direct Transnasal videostroboscopy— slight left-sided atrophy visualization under operating Incomplete glottis closure, and phase asymmetry microscope with bilateral vertical fold mismatch. Right true at 6 mo suture reapproximation. vocal fold—irregularity with Botulinum toxin injection into decreased mobility and mucosal left thyroarytenoid muscle wave. Left true vocal fold— irregularity with decreased mobility, no mucosal wave / CT—Small focus of air in left glottis soft tissue at the site of suspected laceration / Direct laryngoscopy—Bilateral vocal process fractures Decannulated post-op Tracheostomy, DL, bronchoscopy, Hoarseness and small amount day 5, good glottic and esophagoscopy and laryngeal of hemoptysis. supraglottic airway fracture repair. DL revealed No airway distress. CT scan avulsion of right arytenoid revealed small thyroid cartilage cartilage with laceration overlying fracture and disruption of the mucosa, repositioned and mucosa of the right supraglottic repaired. Avulsion and mucosal airway. laceration with 6-0 chromic gut. Flexible laryngoscopy revealed Repair of laryngeal fracture by right arytenoid edema and false open cervical approach with vocal fold laceration causing simple interrupted closure using inability to visualize the right prolene sutures true vocal fold. The left true vocal fold is intact and mobile. Blunt probe and fine tip Postop granuloma Postextubation biphasic stridor suction catheter alignment, repaired at 4 wk 1 Flexible laryngoscopy—left-sided 8 mo—Normal, followed by sedation and glottic soft-tissue encroachment paralysis for 72 h symmetric vocal fold into the glottic airway / growth and mobility. Direct laryngoscopy—‘‘Gouge Grossly normal voice injury’’ extending the posterior portion of the membranous left vocal fold to the superior arcuate line. Lateral extension through the vocalis muscle and into the medial aspect of the thyroarytenoid muscle. A triangular wedge of muscle with attached vocal fold ‘‘flopping’’ into the laryngeal airway
Vocal Process Avulsion
Sex
Author
Scott S. Harris, et al
TABLE 1. Review of Literature
644
Outcome
Decannulated, adequate airway, no aspiration/ dysphagia, weak voice with R TVF paralysis
Diagnostic Process
Treatment
MVA 14 _ Wootten et al, 20099
Mode of Injury Age (y) Sex Author
TABLE 1 (Continued )
Diagnostic modalities not described—Vertical thyroid cartilage fracture creating laryngofissure, unequal true vocal fold height, right arytenoid rotation with true vocal fold vulsion from vocal process, cricothyroid membrane tear, cricoid fracture, and pharyngeal tear
Emergent tracheotomy; suture fixation of cricoid fracture, completion of laryngofissure with suturepexy of the right true vocal fold and prolapsed glottic and subglottic mucosa over Aboulker Stent, repair of pharynx and cricothyroid membrane
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injury in both conditions are intubation and external laryngeal trauma.3,7,10 The differential diagnosis must also include vocal fold paresis and paralysis, which are much more common. Similar symptoms of all these conditions dictate that comprehensive evaluation should be performed to establish an accurate diagnosis. Various approaches to diagnosis and treatment have been reported (Table 1). On the basis of these reports and our experience, we rely primarily on strobovideolaryngoscopy supplemented by LEMG. Intraoperative palpation provides the most definitive assessment. CT scan sometimes provides important information about surrounding structures that may have been injured, but it has not provided useful images of vocal process avulsion. Perhaps, technological improvements will eventually remedy this deficiency. Strobovideolaryngoscopy is valuable to confirm the position and hypermobility of the avulsed vocal process and detect functional consequences and related injuries. LEMG can help differentiate vocal fold paresis/paralysis from anatomical and structural defects. A normal or mildly reduced recruitment pattern would imply intact neuromuscular function, making primary paresis or paralysis an unlikely cause of substantial movement impairment or dysphonia.11 If the diagnosis is still unclear, laryngeal CT may be useful primarily to rule out other diagnoses. Laryngeal CT may help diagnose arytenoid cartilage dislocation and identify fractures of the cartilaginous framework, although fractures of un-ossified cartilage in children and young adults may be missed.10,11 CT may be helpful in diagnosis of vocal fold paralysis also, although a CT suggestive of vocal fold paralysis is not definitively diagnostic.12,13 All of our patients undergo objective voice analysis and are advised to undergo pre- and postoperative voice therapy to eliminate compensatory hyperfunction and optimize safe phonation. It is important to recognize that even in newborns, intubation may result in vocal process avulsion. Wohl recommends conservative management with observation, with vocal fold realignment via gentle tissue manipulation to recreate normal anatomical position under laryngoscopic visualization. He advises that this should be followed by 72 hours of tissue immobilization achieved by sedation and paralysis, with the infant remaining intubated with an uncuffed endotracheal tube. In severe cases, or if realignment fails, suture placement or open repair may be considered. Treatment of older children and adults may begin with a trial of voice therapy to eliminate compensatory hyperfunction and optimize safe phonation. When results are unsatisfactory, surgery may be performed. Surgical approaches include closed reduction using fat injection to force the vocal process posteriorly, stabilizing it against the body of the arytenoid; botulinum toxin injection, and endoscopic open reduction and suture of the fracture. A combination of these procedures may also be used. In the author’s (R.T.S.) experience, endoscopic reduction and suture have produced the best and long-lasting results. Botulinum toxin can be injected into the thyroarytenoid muscle, causing temporary paralysis of the muscle that would tend to pull the
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vocal process away from its sutured position. Botulinum toxin can be used intraoperatively or several days preoperatively. This allows reduced tension during healing; occasionally botulinum toxin injection alone may be therapeutic.8
ertheless, the best voice quality and most durable results are achieved with open reduction and suture fixation, which we now consider our primary approach to this challenging problem for most patients.
CONCLUSION Strobovideolaryngoscopy is the mainstay of diagnosis of vocal process avulsion. Findings that support the diagnosis include visualization of the vocal process moving freely in vocal fold, bulging medially within the vocal fold, and occasional correction of vocal process angulation with pressure from the contralateral vocal. The vocal process may also be seen to move freely on phonation. There may be movement abnormalities anterior to the avulsed segment, particularly on abduction, and decreased mucosal wave between the vocal process and body is common. Confirmation is achieved with intraoperative palpation, appreciating the defect between the vocal process and the body of the arytenoid cartilage. Voice therapy alone was insufficient to restore acceptable voice in most of our cases. Endoscopic reduction with suture fixation with or without botulinum toxin injection proved most successful in reestablishing union between the arytenoid body and the vocal process, but currently we prefer preoperative Botulinum toxin injection. If avulsion is incomplete, suture fixation may not always be necessary, and botulinum toxin injection to achieve chemical tenotomy may be sufficient to allow healing. Autologious fat injection also may result in voice improvement, but it has not been as successful as vocal process suture. Assessment of long-term outcomes in our cases was confounded by the co-existence of paresis and other vocal fold abnormalities (as is usually the case). However, improvement in voice and increased function was achieved in all of the reported cases. Nev-
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