Botulinum toxin-assisted endoscopic repair of traumatic vocal fold avulsion.
Blunt traumatic laryngeal injury in children often leads to intralaryngeal soft-tissue damage, which can quickly compromise an already small airway. Injuries requiring operative intervention have historically been repaired via open approaches such as thyrotomy and laryngofissure. These approaches carry significant long-term sequelae that can compromise the airway, deglutition, and voice. We describe a safe and effective alternative to open repair that includes the use of a botulinum toxin chemical myotomy to ensure optimal healing. We used this procedure to treat a 13-year-old boy who had experienced a traumatic avulsion of the true vocal folds. Postoperatively, his voice outcome was satisfactory, as evidenced by a marked improvement in his pediatric Voice Handicap Index score. No complication or compromise of the airway or swallowing occurred, and resolution of the botulinum effect was observed by 6 months postoperatively. The endoscopic approach supplemented by botulinum toxin injection avoids scarring and allows for safe postoperative extubation. Compared with open repair, it is associated with a shorter hospital stay and a lower risk of stenosis and fibrosis.
Pediatric laryngeal trauma is uncommon because the larynx is in a cephalad and shielded location. Structural injuries, such as cartilaginous fractures, are rare because the young larynx is noncalcified and pliable. However, its elasticity makes it susceptible to shearing injury, which can manifest as mucosal tears, hematomas, or edema. If left unrepaired, significant soft-tissue injuries can lead to embarrassment of an already small airway and disturbances of deglutition and voice. (1,2)
We present an uncommon case of pediatric laryngeal trauma, and we describe the endoscopic approach we used to repair the damage. We report both the stroboscopic and voice results following this minimally invasive technique, and we describe how botulinum toxin chemical myotomy is a useful adjunct to ensure optimal healing.
A 13-year-old boy sustained a clothesline-type injury when his neck struck a tree branch while he was riding an all-terrain vehicle. He was seen at the Emergency Department, determined to be stable, and referred to our otolaryngology clinic for follow-up.
On presentation to us 3 days later, the patient complained of aphonia following an episode of hemoptysis. Head and neck examination confirmed the aphonia. A small scar was present over the midline neck, but no crepitus was palpable. The patient's responses to the pediatric Voice Handicap Index (pVHI) questionnaire confirmed a severe disability; his score was 92 out of a possible 92. Transnasal videostroboscopy revealed incomplete glottic closure on phonation and a vertical vocal fold height mismatch. The right true vocal fold was irregular with decreased mobility and mucosal wave, and the left true vocal fold was similarly irregular with decreased mobility but no mucosal wave. Based on these findings, the patient was diagnosed with a true vocal fold laceration.
Given his delayed presentation, the patient was treated with oral antibiotics and steroids to reduce the mucosal edema. A continued workup included 1.25-mm computed tomography (CT) through the larynx. CT revealed normal cartilaginous structure and positioning, but a small focus of air was seen within the left glottic soft tissue, which corroborated the finding of a laceration (figure 1).
The patient and his parents were counseled regarding endoscopic true vocal fold resuspension. They were also advised of the possible need for an open repair with laryngofissure and tracheotomy if the endoscopic approach failed to provide satisfactory results, and they provided informed consent.
Surgical technique. Endoscopic access was obtained with a Lindholm laryngoscope suspended with a Lewy bar. A standard operating microscope and microlaryngoscopy instruments were used. A thorough microscopic evaluation of the injury with a blunt ball probe revealed that the arytenoid cartilage was properly positioned within the facets. The vocal processes were fractured bilaterally, and the vocal folds were avulsed and displaced anteroinferiorly (figure 2, A).
A 5-0 Vicryl suture was used to reapproximate the vocal process to the exposed arytenoid cartilage along its medial surface. This stretched the vocal fold posterosuperiorly and back into anatomic alignment (figure 2, B). This process was repeated for the contralateral true vocal fold. Then a 25-gauge butterfly needle was used to endoscopically deliver 2.5 units of botulinum toxin into the belly of the left thyroarytenoid muscle. Hemostasis was achieved with the placement of neurosurgical patties saturated with epinephrine 1:1,000 over the bleeding mucosa. The patient was given 8 mg of intravenous dexamethasone intraoperatively, and he was extubated uneventfully after the procedure. He was discharged on postoperative day 1 on amoxicillin, prednisone, strict voice rest, and a soft diet.
Follow-up. The patient was seen for follow-up I week postoperatively. He had no dysphagia or stridor, and his voice was soft and hoarse. Flexible laryngoscopy revealed mild edema of the posterior commissure and arytenoid mucosa, and the sutures were visible and intact (figure 3). Two weeks postoperatively, the botulinum effect manifested as paresis of the left true vocal fold, but glottic closure was complete. The patient continued to demonstrate excellent healing at his 6-week visit, and by 3 months, his voice had nearly returned to normal. Stroboscopy demonstrated that the edges of the true vocal folds were straight and smooth and that glottic closure remained complete. Voice testing revealed that amplitude, level, and mucosal wave were normal; occasional phase asymmetry was noted, which was attributed to the effects of the botulinum toxin. The 6-month examination revealed continued excellent healing and only a slight left-sided atrophy and phase asymmetry (figure 4). The patient's voice quality was normal, and his pVHI score had improved dramatically to 4.
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Evaluation of every trauma patient begins with the airway. When laryngeal injury is suspected, it should be treated systematically and cautiously. Symptoms of laryngeal trauma include dysphonia, dyspnea, odynophagia, and dysphagia. Physical examination findings of stridor, hemoptysis, subcutaneous emphysema, point tenderness, and visible deformity should raise suspicion of a laryngeal injury. Severe structural compromise may require an urgent tracheotomy because orotracheal intubation could lead to the disastrous complication of cricotracheal separation. In a secure airway, flexible fiberoptic laryngoscopy can be used to directly examine the laryngeal mucosa and assess vocal fold function. Once airway patency is established, a thin-cut CT scan through the larynx should be obtained to diagnose and characterize potential structural compromise. (2,3)
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In adults, soft-tissue injuries limited to small lacerations and minor hematomas can be managed medically. Conservative management involves pulse oximetry monitoring, elevation of the head of the bed, humidification, voice rest, antibiotics, and a soft diet. But in children, these same disturbances can quickly and significantly endanger the small pediatric airway. In both age groups, large disruptions of intralaryngeal soft tissues require urgent intervention. Even in a nonthreatened airway, exposed cartilage can predispose a patient to laryngeal stenosis and webbing, and it should be repaired primarily. Although open exploration arguably provides better visualization and access to the endolarynx, this approach carries significant disadvantages, such as the need for prolonged perioperative intubation or tracheotomy. In addition, open approaches can lead to sequelae of stenosis, fibrosis, and vocal fold height mismatch after closure. (1-3)
Endoscopic repair of laryngeal soft-tissue injuries in properly selected patients has been shown to be an acceptable alternative to open repair. In 1995, Shapshay et al reported the feasibility of endoscopic repair of large mucosal avulsions in live dog larynges. (4) For that experiment, they created 2 x 2.5-cm glottic and subglottic defects and then grafted buccal mucosa to these areas via endosuture and CO/laser welding. In 1996, Wohl reported a case of pediatric vocal fold avulsion that was successfully treated with endoscopic tissue repositioning. (5) The avulsed myomucosal segment was secured via endotracheal tube stenting, and the patient was paralyzed for 72 hours to allow for healing prior to extubation. In a case report by Elmaraghy et al published in 2007, endoscopic repair of a mucosal laceration and hematoma was shown to be a safe and effective approach that did not require intubation or tracheotomy. (6)
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In 1995, Sataloff et al reported a case of misdiagnosed vocal fold avulsion in a patient who had sustained a clothesline-type injury. (7) After multiple procedures by the referring otolaryngologist had been unsuccessful, the patient ultimately underwent successful repair via laryngofissure. A decade later, the same group reported the successful endoscopic repair of vocal process avulsion in 3 patients. (8) It is interesting to note that in 2 of these patients, botulinum toxin was injected into the thyroarytenoid muscle to "diminish forces pulling the vocal process away from the body of the arytenoid cartilage." (8)
Based on the successful management of these previously reported cases, we decided to approach our case of pediatric vocal fold avulsion endoscopically. Understanding how vocal fold avulsion occurs and the proper method of repair requires an understanding of the embryologic development and anatomy of the larynx. Complete arytenoid cartilages arise from two different embryologic origins. The body of the arytenoid cartilage develops from branchial arch mesoderm and is made up of hyaline cartilage, and the vocal process originates in pharyngeal floor mesoderm and is made up of elastic cartilage. (9) The difference in the makeup of the body and the vocal process makes the fusion plane between them especially susceptible to trauma.
The arytenoid cartilage serves as the primary fulcrum in vocal fold movement, and it articulates with the cricoid ring via the synovial cricoarytenoid joints. Each arytenoid cartilage has a muscular and a vocal process. The muscular process is the insertion point of the posterior and lateral cricoarytenoid muscles. The posterior cricoarytenoid muscle is the single abductor t of the vocal fold, and the lateral cricoarytenoid muscle s contributes to adduction in concert with the action of the thyroarytenoid muscle. This band of muscle reaches from the inner surface of the thyroid cartilage to insert into the vocal process. In our patient, the blunt external force transferred across a contracting and tense thyroarytenoid muscle, which led to shearing and avulsion at a vulnerable embryologic plane. After suture realignment, botulinum toxin chemical myotomy can arrest the tensile pull of a contracting thyroarytenoid muscle during phonation and provide a tension-free environment for healing. Botulinum toxin is ideal because its duration of action is limited and its interactions are known to be safe.
In 1986, Blitzer et al were the first to report the injection of botulinum toxin into the larynx as a treatment for spasmodic dysphonia. (10) Since then, it has been used for a variety of laryngeal dystonias and tremulous disorders. (11,12) Its applications in the treatment of vocal fold granulomas served as our therapeutic model. (13-16) Nasri et al hypothesized that limiting forceful arytenoid closure during phonation and coughing minimizes traumatic inflammation of the perichondrium--the implicated pathophysiology in granuloma formation. (13) As has been shown in glycogen depletion studies, diffusion of botulinum toxin from an injected thyroarytenoid muscle into the adjacent lateral cricoarytenoid muscle may also contribute to the arrest of adduction. (17) Localized injections of small doses theoretically exert the bulk of their effect onto the thyroarytenoid muscle, thereby disabling its major function, which is isolinear contraction. Without the traumatic pull of the thyroarytenoid muscle fibers on their insertion into the vocal process, favorable conditions exist for healing. We encountered no airway or swallowing complications with our use of the described approach. Small doses of 2.5 to 5.0 units of botulinum toxin can create the desired thyroarytenoid muscle arrest without causing complete paralysis or airway compromise. In our patient, botulinum toxin injection did lead to subclinical changes noticed on stroboscopic examination beginning 2 weeks postoperatively in the form of vocal fold paresis. By 3 months, there was evidence of phase asymmetry, but at the 6-month visit, this was noted only occasionally. Slight left-sided muscle atrophy began to manifest at 6 months, a finding that we attributed to chemical denervation of the muscle. The atrophy was insignificant and did not appear to affect the progression toward normal voice. In older patients and in those with vocal comorbidities, subtle findings may manifest as clinical voice disturbances or even aspiration. In most cases, muscle atrophy is amenable to speech therapy because the effects of botulinum toxin are short-lived.
We conclude that endoscopic repair of true vocal fold avulsion is safe in carefully selected patients who have no existing airway compromise. It avoids scarring and allows for safe postoperative extubation. Compared with open repair, it is associated with a shorter hospital stay and a lower risk of stenosis and fibrosis. Simultaneous botulinum toxin injection optimizes healing conditions by minimizing the tensile pull from a contracting thyroarytenoid muscle.
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Rima F. Abraham, MD; Stanley Shapshay, MD; Lisa Galati, MD
From the Division of Otolaryngology, Department of Surgery, Albany Medical College, Albany, N.Y.
Corresponding author: Lisa Galati, MD, University ENT of Northeastern NY, LLP, 35 Hackett Blvd., Albany, NY 12208. E-mail: galatil@mail. amc.edu
Previous presentation: The information in this article has been updated from its original presentation at the Laryngology Update meeting of the New England Otolaryngological Society; April 4, 2008; Boston.
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|Title Annotation:||ORIGINAL ARTICLE|
|Author:||Abraham, Rima F.; Shapshay, Stanley; Galati, Lisa|
|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Case study|
|Date:||Sep 1, 2010|
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