Vocal fold immobility after finger sweep self-extrusion of impacted food in a choking victim with resolution following laryngeal mask ventilation.
We report a case of unilateral vocal fold immobility in a 57-year-old woman that occurred subsequent to a choking episode, which she resolved by removing impacted food with a finger sweep. Other than the unilateral immobility, no abnormality of the laryngeal mucosa or framework was detected on physical examination, laryngoscopy, and computed tomography. Weeks later, the patient underwent an unrelated surgical procedure necessitating laryngeal mask airway ventilation. When she emerged from the procedure, she noted full resolution of her voice symptoms. Office laryngoscopy confirmed the full return of vocal fold function. We discuss possible explanations for the return of function in the context of this unusual onset and resolution. We also review the literature regarding unilateral vocal fold immobility, including its etiology, presentation, workup, and treatment.
Trauma-induced vocal fold immobility remains difficult to characterize for numerous reasons. Due to the relatively low incidence of blunt trauma to the neck and larynx (< 1%), (1,2) few data are available. Even less literature is available regarding internal blunt force injury to the larynx other than that related to traumatic endotracheal tube insertion or prolonged intubation.
We describe an unusual case of vocal fold immobility that resolved following laryngeal mask airway (LMA) ventilation under general anesthesia associated with an unrelated surgery.
A 57-year-old woman presented to the NYU Voice Center for evaluation of mild hoarseness and dysphagia with thin liquids. She stated that approximately 1 month earlier, she noticed an acute change in her voice after choking on a piece of meat. During the choking episode, she put her finger into her airway and manually removed the bolus. Immediately afterward, she noted hoarseness and dysphagia. She subsequently reported to an emergency department, where computed tomography (CT) demonstrated soft-tissue edema without laryngeal pathology or arytenoid cartilage dislocation.
Over the following weeks, the patient's vocal symptoms improved somewhat. However, she was still experiencing mild hoarseness and occasional choking, primarily on thin liquids.
Upon the patient's presentation to our office for evaluation of these symptoms, a head and neck physical examination revealed only a slightly raspy and weak voice. Videostrobolaryngoscopy identified an immobile right vocal fold in the paramedian position with a positive jostle sign (figure 1). The right arytenoid cartilage appeared to be in an appropriate anatomic position and at the correct vertical level. However, a mild to moderate glottal gap was observed consistently during phonation.
At follow-up 6 weeks later, the patient reported that she had nearly amputated one of her fingers with a kitchen appliance, and she required surgical repair under general anesthesia and LMA ventilation. In an interesting development, when she awoke from anesthesia she noticed her voice had returned to normal. Repeat videostrobolaryngoscopy confirmed full mobility of both vocal folds and complete glottic closure during phonation (figure 2).
Throughout follow-up, the patient remained asymptomatic with regard to both her voice and swallowing issues.
The vocal fold injury sustained by our patient appears to have been related to the finger-sweep trauma. Most often, blunt-force injuries are associated with laryngeal edema, granuloma formation, vocal fold paresis and, in rare cases, vocal fold immobility. The cause of vocal fold immobility can be classified as two different clinical entities: neuropraxia (crush injury) and arytenoid cartilage dislocation.
It is believed that most nonsurgical neuropraxic injuries of the recurrent laryngeal nerve occur as a result of intubation-related trauma, pressure from an inflated endotracheal tube balloon, or prolonged duration of intubation. (3,4) As the recurrent laryngeal nerve enters the larynx at the level of the piriform sinus at the cricothyroid joint, a high endotracheal tube cuff pressure can cause a direct crush injury to the nerve, pinning it against the thyroid cartilage. In addition, a high cuff pressure can induce myopathy of the intrinsic muscles of the larynx.
It is interesting that LMAs have been found to similarly affect the recurrent laryngeal nerve if they are improperly positioned and hyperinflated. In extreme cases, they can cause arytenoid cartilage dislocation. With the increasing use of LMAs, surgeons should be aware of these complications. (5)
Arytenoid cartilage dislocation is defined as the disarticulation of the arytenoid cartilage from the cricoid cartilage. Usually quite sturdy, the intrinsic muscles of the larynx and cricoarytenoid ligament maintain the cartilage position within the diarthrodial joint. Patients with an arytenoid cartilage dislocation often present with acute changes in voice quality, decreased vocal intensity, and dysphagia, all of which were present in our patient. (6)
Examination via videostroboscopy can contribute to the diagnosis by showing malposition of the arytenoids, a loss of vocal process height, and shortening of the vocal fold itself. (7) In addition, Rubin et al described the absence of the jostle sign during laryngoscopy as indicative of arytenoid cartilage dislocation. (8) The jostle sign, which is associated with vocal fold paralysis, is described as passive movement of the affected arytenoid cartilage with adduction of the vocal folds.
In cases where there is a high degree of suspicion for laryngeal trauma, high-resolution CT can be obtained. If arytenoid cartilage dislocation is present, imaging will often reveal malpositioning of the cartilage. A careful review of radiologic interpretations is warranted because signs can be subtle or confused with vocal fold paralysis alone. (9)
The gold standard for the diagnosis of arytenoid cartilage dislocation is a prompt evaluation of the joint via direct laryngoscopy. Microlaryngoscopy instrumentation can be both diagnostic and therapeutic when palpation of the immobile arytenoid cartilage is followed by closed reduction of the joint. Speech therapy also has been used as an effective therapy in the treatment of arytenoid cartilage dislocation, although results are based only on isolated case reports. (10)
On rare occasions, spontaneous recovery occurs; this recovery has been theoretically attributed to forceful coughing or retching. If our patient had indeed presented with an arytenoid cartilage dislocation, postextubation coughing secondary to laryngeal irritation might have been a key factor in her recovery. Alternately, LMA placed in direct contact with a dislocated arytenoid cartilage and then inflated could lead to closed reduction of the joint.
Findings on laryngeal electromyography (EMG) can be useful in distinguishing between neural and mechanical causes of vocal fold immobility, although we have only level IV evidence to support its use. (11) Fibrillation potentials or a lack of electrical response is more consistent with an injury to the recurrent laryngeal nerve or to the external branch of the superior laryngeal nerve. (12) Although injury to the latter can result in abnormal cricothyroid function, frank vocal fold immobility is unlikely, as seen in our case. (13) Recurrent laryngeal nerve injury must be ruled out in these cases. If normal recruitment is demonstrated on EMG, the etiology is more likely a mechanical mechanism.
Wide variability (33 to 100%) exists regarding the ability of laryngeal EMG to accurately predict vocal fold paresis and recovery of vocal fold function. (14) In our patient, laryngeal EMG was considered, but since her complaints were relatively minimal, she decided to forgo this test.
Idiopathic vocal fold paralysis should be considered in any patient with an unclear mechanism of vocal fold dysfunction. By definition, idiopathic paralysis is a diagnosis of exclusion, so all other causes of vocal fold paralysis must be ruled out. Rates of idiopathic vocal fold paralysis have decreased with improved imaging and more thorough workups, but the reported incidence of this diagnosis at the initial presentation ranges from 2 to 41%. (15) Recovery in these patients, as noted in a review by Sulica, is quite variable. (16) In view of the immediate change in vocal quality after trauma in our case, idiopathic immobility was unlikely.
In summary, we present an interesting case of acute-onset vocal fold immobility apparently associated with manual trauma to the larynx during a bolus removal maneuver. Although this onset is unusual, the resolution is equally perplexing because the patient emerged from general anesthesia via an LMA with a complete resolution of symptoms, which was confirmed by a finding of normal physiology on laryngeal examination.
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Shaum Sridharan, MD; Milan R. Amin, MD; Ryan C. Branski, PhD
From the NYU Voice Center, Department of Otolaryngology-Head and Neck Surgery, New York University, New York City.
Corresponding author: Ryan C. Branski, PhD, NYU Voice Center, 345 E. 37th St., Suite 306, New York, NY 10016. Email: firstname.lastname@example.org
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|Title Annotation:||ORIGINAL ARTICLE|
|Author:||Sridharan, Shaum; Amin, Milan R.; Branski, Ryan C.|
|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Case study|
|Date:||Jan 1, 2016|
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