Bilateral Vocal Fold Paralysis 

Updated: Oct 20, 2020
Author: Joel A Ernster, MD; Chief Editor: Arlen D Meyers, MD, MBA 

Overview

Practice Essentials

Bilateral vocal fold (vocal cord) immobility (BVFI) is a broad term that refers to all forms of reduced or absent movement of the vocal folds.

Bilateral vocal fold (cord) paralysis (BVFP) refers to the neurologic causes of bilateral vocal fold immobility (BVFI) and specifically refers to the reduced or absent function of the vagus nerve or its distal branch, the recurrent laryngeal nerve (RLN).

Vocal fold immobility may also result from mechanical derangement of the laryngeal structures, such as the cricoarytenoid (CA) joint. This is often termed posterior glottic stenosis (PGS).

Although sometimes difficult to determine, it is important to distinguish which process is present, as evaluation and management differ between the two processes.

Obtention of a thorough history and use of fiberoptic laryngoscopy are the mainstays of clinical assessment. 

Direct laryngoscopic view of the larynx in a patie Direct laryngoscopic view of the larynx in a patient who with bilateral vocal fold immobility (BVFI) is shown. Palpation of the arytenoids revealed cricoarytenoid (CA) joint ankylosis. Close inspection of the interarytenoid space demonstrated interarytenoid scar. This condition is posterior glottic stenosis (PGS).

Although a small number of conditions account for most cases of vocal cord immobility, this article presents a comprehensive differential diagnosis, followed by the clinical presentations, diagnostic workup, and treatment options. The goal of the article is to provide the clinician with a basic understanding of the rare entity of bilateral vocal fold immobility (BVFI).[1]

Workup in bilateral vocal fold immobility

History is essential, as this will reveal any recent surgical procedures that may have resulted in injury to the vagus or recurrent laryngeal nerves. It will also reveal medical or neurologic conditions predisposing the patient to vocal fold paralysis or fixation.

Fiberoptic laryngoscopy is the mainstay of clinical assessment. Direct laryngoscopy under anesthesia allows examination of the posterior glottis and palpation of the arytenoid cartilages. This exam is sometimes an essential step in clarifying the nature of vocal fold immobility.

Computed tomography (CT) scanning along the entire length of the vagus nerve from the skull base to the superior mediastinum may be necessary when no other cause of bilateral vocal fold (cord) immobility (BVFI) is identified. This test will also assess the structure of the larynx and help to determine if intralaryngeal pathology is present.

Features of patient history and clinical findings may suggest that the following studies be performed:

  • Serum K + level
  • Serum Ca + level
  • Blood glucose
  • Antineutrophil cytoplasmic antibody (ANCA)
  • Venereal disease research laboratory (VDRL) test
  • Lyme disease titer
  • Tuberculosis (TB) skin test
  • Uric acid level
  • Rheumatoid factor (RF)
  • Antinuclear antibody (ANA)
  • Sedimentation rate (ESR)

Management of bilateral vocal fold immobility

Medical management of inflammatory conditions of the cricoarytenoid (CA) joint (eg, gout, rheumatoid arthritis) and the laryngeal mucosa (eg, syphilis, tuberculosis) that result in mechanical fixation may improve the patient's airway. Corticosteroids may be effective in several conditions (eg, Wegener granulomatosis, sarcoidosis, polychondritis).

Depending on the patient's presentation, surgical procedures for bilateral vocal fold (cord) paralysis (BVFP) include the following:

  • Tracheostomy
  • Permanent procedures such as posterior vocal fold cordotomy, or partial or complete arytenoidectomy, cordopexy lateralization, and arytenoid abduction lateropexy
  • Less frequent and experimental procedures include reinnervation techniques (experimental) [2] and electrical pacing (experimental){ref3​}

Surgical procedures for bilateral vocal fold (cord) immobility (BVFI) or posterior glottic stenosis (PGS) due to interarytenoid (IA) scarring, with or without cricoarytenoid (CA) ankylosis, include the following:

  • Tracheostomy
  • Permanent procedures such as cordotomy or arytenoidectomy but that also include microflap removal of the interarytenoid scar, laryngofissure with arytenoidectomy, posterior cricoidotomy with stent and/or graft placement, and endoscopic lateralization techniques; there are also innovative techniques such as placement of a self-retaining interarytenoid spring and cricoarytenoid release

History of the Procedure

The history of the procedures used to treat vocal cord immobility begins in 1855 with Garcia's work on mirror laryngoscopy. In the 1860s, Turk and Knight first described vocal cord paralysis. In 1922, Chevalier Jackson performed the first surgical procedure for bilateral vocal fold immobility (BVFP) when he endoscopically resected a vocal cord. He provided an airway at the expense of voice and airway protection. This dilemma continues to plague present surgeons. Since 1922, pioneers in laryngology have described arytenoidectomy, described vocal cord lateralization, and introduced the use of laser.

Etiology

According to Benninger's findings in a series of 117 cases, BVFI can be attributed to the following causes: surgical trauma (44%), malignancies (17%), endotracheal intubation (15%), neurologic disease (12%), and idiopathic causes (12%).[3]  In adults, conditions that mimic vocal fold immobility include paradoxical vocal fold motion and functional disorder.

Therefore, in most clinical practices, BVFI results from paralysis or fixation of vocal folds from an iatrogenic cause. This is often evident when a satisfactory history is obtained. Realizing this, a focused workup and treatment plan can be undertaken in the vast majority of patients.

When the etiology or treatment plan is uncertain, a more thorough review of causes and treatment alternatives is worth considering.

Causes of bilateral vocal fold paralysis

Iatrogenic

These include the following:

  • Open cervical procedures such as bilateral thyroid or parathyroid surgery, esophageal or tracheal procedures, carotid artery endarterectomy and cervical disc procedures (particularly when surgery on the contralateral side was performed previously), and endolaryngeal surgery affecting the cricoarytenoid joint
  • Intracranial procedures, particularly when brainstem surgery is performed.
  • Endotracheal intubation resulting in trauma to the recurrent laryngeal (RL) nerves as they enter the larynx, usually from compression
  • Nasogastric tube compression of RL nerves
  • Esophageal stent compression of RL nerves

Neurologic

These include the following:

  • Arnold-Chiari malformation
  • Meningomyelocele
  • Diabetic neuropathy
  • Amyotrophic lateral sclerosis
  • Bulbar palsy
  • Myasthenia gravis
  • Mobius syndrome
  • Charcot-Marie-Tooth disease
  • Postpolio syndrome
  • Shy-Drager syndrome
  • Creutzfeldt-Jacob disease
  • Hydrocephalus
  • Lyme disease
  • Cerebrovascular accident
  • Parkinsonisms
  • Neoplasms or sarcoidosis involving the mediastinum, resulting in RL nerve compression
  • In children - Arnold-Chiari deformity with hydrocephalus is a recognized cause, but nonspecific central nervous system (CNS) insults such as craniotomy and hypoxia can result in BVFP 

Metabolic

These include the following:

  • Hypokalemia
  • Hypocalcemia
  • Renal insufficiency with Alport syndrome [4]

Toxins

These include the following:

  • Vincristine
  • Paclitaxel
  • Organophosphates [5]

Idiopathic

In adults, this category is confounding but accounts for a relatively small number of cases

Idiopathic causes are the second most common causes of childhood bilateral vocal fold paralysis (BVFP). Some researchers postulate that the etiology in some children with bilateral vocal fold paralysis (BVFI) is an imbalance between the adductors and abductors of the larynx that results in adducted vocal folds. With time, a balance is restored and symptoms abate as children mature. Although conjectural, this explanation fits with the clinical course of most children with bilateral vocal fold paralysis (BVFI) who spontaneously improve with time. Gacek hypothesized that fewer abductor fibers exist; therefore, injury to the nerve is more likely to cause abductor dysfunction.[6]

Causes of bilateral vocal fold fixation

Vocal fold fixation or mechanical derangement of the posterior glottis may also be referred to as posterior glottic stenosis (PGS). Bogdasarian and Olson classified PGS into the following four grades[7] :

  • Grade I - Interarytenoid scarring with normal posterior commissure

  • Grade 2 - Interarytenoid and posterior commissure scarring

  • Grade 3 - Posterior commissure scarring involving one cricoarytenoid joint

  • Grade 4 - Posterior glottic scarring involving both cricoarytenoid joints

Iatrogenic

Causes include the following:

  • Prolonged intubation
  • Arytenoid dislocation with traumatic intubation

Inflammatory processes

These include the following:

  • Rheumatoid arthritis
  • Gout
  • Tietze syndrome
  • Ankylosing spondylosis
  • Reiter syndrome
  • Crohn's disease
  • Collagen vascular diseases
  • Systemic lupus erythematosus
  • Granulomatosis with polyangiitis (Wegener granulomatosis)
  • Cicatricial pemphigoid
  • Gastroesophageal reflux
  • Relapsing polychondritis

Infiltrative processes

These include the following:

  • Amyloidosis
  • Sarcoidosis

Infectious processes

These include the following:

  • Tuberculosis
  • Syphilis
  • Coccidiomycosis

Malignancy

Laryngeal neoplasms that can result in bilateral vocal fold fixation include squamous cell carcinoma and occasionally chondromas, chondrosarcomas, solitary fibrous tumors, and schwannomas.

Radiation injuries

These include the following:

  • Post-irradiation fibrosis
  • Chondronecrosis

Pathophysiology

Although a comprehensive discussion of each of the causes is beyond the scope of this article, some principles should be emphasized. With the first episode of bilateral vocal fold paralysis (BVFP), patients may have dysphonia because the vocal cords are too far apart. Over time, however, the vocal cords can move to a medial position, and the patient may have a good voice and cough despite stridor and bilateral vocal fold paralysis (BVFP). As the vocal cords migrate toward the midline, the voice (and cough) improves, while the airway worsens. Clinicians should not mistake a good voice and cough as signs of a functioning larynx, especially in a patient with stridor. Aspiration and dysphagia may or may not be present in patients with vocal cord paralysis.

 

Presentation

History

The importance of a complete history cannot be overstated. The history should include the following:

  • Chief symptom, as related to airway, voice, or swallowing[8]

  • Onset of symptoms (acute, subacute, chronic)

  • Changes in the voice and airway over time

  • Related events such as intubation, surgery, or other medical conditions that can affect vocal cord mobility

  • Tobacco use

In children, obtaining a history of birth trauma, central nervous system abnormality, intubations, or surgeries is important.

Physical examination

The physical examination should include listening to the voice and airway as the patient relays his or her history.

  • The voice can be breathy or normal.

  • Airway findings can range from biphasic stridor to normal.

  • Unless patients describe gross aspiration with swallowing, their swallowing function can be challenged by having them sip a small amount of water.

The standard head and neck examination should include careful evaluation of the larynx. Evaluate the following:

  • Mucosal color and condition

  • Stenosis or scarring of the posterior glottis

  • Mobility of the arytenoids

  • Muscle mass and tone of each vocal cord

  • Length of each vocal cord

  • Asymmetry of the vocal cords

Indications

Adults

Only the patients with severe bilateral vocal fold (cord) immobility (BVFI) require surgical intervention. Patients with medical conditions (eg, rheumatoid arthritis, Wegener granulomatosis, gout) or neurologic conditions (eg, amyotrophic lateral sclerosis [ALS], Parkinsonism, stroke) rarely require surgical intervention because treatment of the underlying condition often improves airway compromise.

For patients with bilateral vocal fold paralysis (BVFP) due to iatrogenic injury in which the RL nerve or vagus nerve is damaged (neurapraxia) but not severed, permanent surgical treatment should be postponed for at least 6 months after injury to allow spontaneous recovery. In some centers, laryngeal electromyographic (EMG) monitoring can be helpful in obtaining an index of potential recovery. Obtaining a baseline EMG 30-40 days after injury and second EMG 1 month later can help in evaluating the recovery status of the vocal cords (Munin).[9] On the basis of the surgeon's clinical judgment, tracheostomy for patients with quickly deteriorating airways should be initiated quickly.

For adult patients with bilateral vocal fold (cord) paralysis (BVFP), the literature supports use of an endoscopic approach, with either posterior cordotomy or limited arytenoidectomy as the initial procedure of choice. Suture lateralization (such as the Lichtenberger needle lateralization technique) may play an adjunctive role. All of these are static permanent procedures; therefore, they should be undertaken only after spontaneous improvement has failed to occur or if EMG findings suggest permanent injury.

For patients with bilateral vocal fold immobility (BVFI) caused by PGS, serial endoscopic approaches with scar lysis or microflap trapdoor reconstruction of the interarytenoid (IA) region can be attempted before the static procedures are used.

Airway obstruction refractory to the above measures is particularly vexing. Treatment options include laryngofissure with arytenoidectomy, IA reconstruction, posterior cricoidotomy with stent placement, posterior cricoidotomy with grafting, and lateralization procedures with endoscopic suturing techniques (eg, arytenoid abduction lateropexy). The literature is less clear concerning the indications for each of these approaches than those for other procedures.

Direct laryngoscopic view of larynx after left pos Direct laryngoscopic view of larynx after left posterior cordotomy
Direct laryngoscopic view of a lateralized left tr Direct laryngoscopic view of a lateralized left true vocal fold (TVF) is shown. Use of a Lichtenberger needle holder facilitates vocal fold lateralization. Posterior cordotomy or submucous resection of the vocal fold precedes suturing.

 

Children

Surgical intervention is indicated when respiratory effects are significant. Cordopexy or arytenoidopexy, along with partial or complete arytenoidectomy, can help solve the airway problem during the ensuing months or years as one waits for possible recovery of the contralateral cord. Children with bilateral vocal fold paralysis (BVFP) require tracheostomy only when the airway fails to improve with other measures. Findings of a literature review suggest that the airway can be managed expectantly, without a tracheostomy. Endoscopic management plays a limited role in children and is useful only for mild fixed stenosis and for revisional procedures in children who have undergone open procedures.

Relevant Anatomy

A review of vagus nerve and RLN anatomy is necessary to understand potential injuries that can cause vocal cord paralysis. The vagus nerve originates in the nucleus ambiguus of the medulla oblongata. At that point, it is composed of cells that receive neural input from the Broca area via decussating corticobulbar tracts; thus it provides input to both the right and left nuclei. Neural input from the cerebellum and extrapyramidal centers, as well as from visceral afferents, provides proprioceptive input that modulates the motor function of the vagus nerve at this site.

The motor fibers or visceral efferents that affect the larynx and pharynx occupy 2 specific sites within the nucleus ambiguus. One site becomes the superior laryngeal nerve (SLN); the other, the RLN. The vagus nerve leaves the medulla and enters the jugular foramen, along with the accessory nerve and jugular vein. Within the jugular foramen, the vagus nerve widens to form the superior ganglion, where the cell bodies of the sensory component of the nerve reside (somatic sensory). They provide sensation to the ear canal skin (Arnold nerve). As the vagus nerve exits the jugular foramen, it widens again to form the nodose ganglion, in which nerve cell bodies containing the sensory or visceral afferents from the larynx and pharynx reside.

Immediately distal to the nodose ganglion, the SLN exits the vagus nerve and courses along the carotid artery to the larynx, where it enters the larynx through the thyrohyoid membrane, dividing into internal and external branches. The internal branch provides sensory function (visceral afferent), and the external branch provides motor function to the cricothyroid muscle (visceral efferent). The vagus nerve then descends in the neck immediately lateral to the carotid artery.

The right RLN fibers exit from the vagus nerve as the nerve crosses anteriorly over the subclavian artery. The RLN loops posteriorly around the subclavian artery to enter the larynx through the Killian-Jamieson area or superior to the fibers of the cricopharyngeal muscle entering the larynx at the cricothyroid space.

The left RLN divides much further in the mediastinum, exiting the vagus nerve as it crosses anterior to the aorta and lateral to the ligamentum arteriosum (ie, remnant of the patent ductus arteriosum between the aorta and the pulmonary vein). It then extends superiorly to enter the larynx opposite the right RLN. The RLN branches into the posterior sensory branch and the motor anterior branch to the posterior cricoarytenoid (PCA), IA, lateral cricoarytenoid (LCA), and thyroarytenoid (TA) muscles. The IA muscle is the only motor branch that receives bilateral innervation, which allows some movement of both vocal folds when one RLN is nonfunctional.

 

Workup

Laboratory Studies

Features of the history and clinical findings may suggest performance of the following studies:

  • Determination of serum K+ level

  • Determination of serum Ca+ level

  • Determination of glucose level

  • Antineutrophil cytoplasmic antibody (ANCA) test

  • Venereal disease research laboratory (VDRL) test

  • Determination of Lyme disease titer

  • Tuberculosis skin test

  • Uric acid test

  • Rheumatoid factor test

  • Antinuclear antibody (ANA) test

  • Determination of sedimentation rate

Imaging Studies

Computed tomography (CT) scanning along the entire length of the vagus nerve from the skull base to the superior mediastinum may be necessary when no other cause is identified.

Magnetic resonance imaging (MRI) of the brain is not used as a routine study for bilateral vocal fold (cord) paralysis (BVFP).

Other Tests

See the list below:

  • Pulmonary function tests: Although diagnosis is based on clinical findings, results of pulmonary function tests performed with flow volume loops help support a diagnosis of upper airway obstruction. Also, they are used to provide an indicator of the severity of the obstruction and to monitor change after treatment.

  • Acoustic analysis: Voice quality usually is not significantly altered. Assessing the voice with acoustic analysis as a baseline test can be helpful in evaluating recovery over time.

  • Neurologic tests: In certain patients, a neurologist may perform a more thorough examination to assess central disorders or neuromuscular disorders that may result in bilateral vocal fold (cord) immobility (BVFI).

Diagnostic Procedures

Fiberoptic laryngoscopy

  • This procedure is the mainstay of clinical assessment.

  • Stroboscopic videolaryngoscopy may provide further information about vocal fold motion abnormalities when asymmetric mucosal wave patterns are identified.

  • Malingering or other psychogenic disorders may be identified by asking the patient to sniff or whistle, since these maneuvers work the abductors without the patient's volition.

Direct laryngoscopy

  • Examination of the posterior glottis and palpation of the arytenoid cartilages are essential steps in clarifying the nature of vocal fold immobility.

  • Cricoarytenoid (CA) joint ankylosis or IA scars that limit arytenoid motion are readily ascertained with direct laryngoscopy with the patient under general anesthesia and paralysis.

  • The subglottis, trachea, and main bronchi also may be examined to exclude subglottic stenosis, subtle infiltrative neoplasms, and other lesions along the entire airway.

    Direct laryngoscopic view of the larynx in a patie Direct laryngoscopic view of the larynx in a patient who with bilateral vocal fold immobility (BVFI) is shown. Palpation of the arytenoids revealed cricoarytenoid (CA) joint ankylosis. Close inspection of the interarytenoid space demonstrated interarytenoid scar. This condition is posterior glottic stenosis (PGS).

Laryngeal EMG

  • Ideally, laryngeal EMG is used to assess both the TA and the PCA muscles, and it should be performed with local anesthesia rather than general anesthesia. It has been performed in anesthetized children.

  • The TA muscle is approached through the cricothyroid membrane, while the PCA muscle is approached percutaneously by rotating the larynx.

  • The glottic compromise caused by bilateral vocal fold immobility (BVFI) may render EMG hazardous. Therefore, waiting until after tracheostomy to perform the test may be prudent in some cases.

  • In evaluating a patient with bilateral vocal fold immobility (BVFI), EMG provides the potentially useful information in the following:

    • Differentiating between fixation and paralysis

    • Differentiating between neurapraxia and axonal transection

    • Determining the presence of neuromuscular disorders or peripheral neuropathy

  • In the recording the EMG, correct timing is essential. EMG can be performed as soon as 2 days after injury to aid in differential diagnosis. As a prognostic tool, a baseline EMG should be obtained at least 30 days after injury and a second one should be obtained 30-60 days after injury. After 6 months, laryngeal EMG should be used only to differentiate between fixation and paralysis and not to assess neural regeneration.

  • Laryngeal EMG can predict poor recovery 90% of the time.[10]

 

Treatment

Medical Therapy

Medical management of inflammatory conditions of the cricoarytenoid (CA) joint (eg, gout, rheumatoid arthritis) and the laryngeal mucosa (eg, syphilis, tuberculosis) that result in mechanical fixation may improve the patient's airway. Corticosteroids may be effective in several conditions (eg, Wegener granulomatosis, sarcoidosis, polychondritis). 

Daniel and Cardona reported on the successful use of onabotulinumtoxinA in children with bilateral abductor vocal fold paralysis. The toxin was injected into the cricothyroid muscles of six pediatric patients, five of whom were consequently able to avoid a tracheostomy, with the sixth patient able to undergo decannulation.[11]

Surgical Therapy

It is important to realize that patients with bilateral vocal fold (vocal cord) immobility (BVFI) may present with symptoms ranging from mild inspiratory noise of gradual onset (or no symptoms at all if mild enough) to urgent airway compromise requiring emergent intervention. The wide range in presentation and cause of BVFI makes a discussion of management difficult. Suffice it to say that management of a compromised airway is paramount and takes precedence over other considerations.

Occasionally, patients present with such mild findings and symptoms that watchful monitoring is an effective strategy.

Depending on the patient's presentation, surgical procedures for bilateral vocal fold (cord) paralysis (BVFP) include the following:

  • Tracheostomy
  • Permanent procedures such as posterior vocal fold cordotomy, or partial or complete arytenoidectomy, cordopexy lateralization, and arytenoid abduction lateropexy
  • Less frequent and experimental procedures include reinnervation techniques (experimental) [2]  and electrical pacing (experimental){ref3​}

Surgical procedures for bilateral vocal fold (cord) immobility (BVFI) or posterior glottic stenosis (PGS) due to interarytenoid (IA) scarring, with or without cricoarytenoid (CA) ankylosis, include the following:

  • Tracheostomy
  • Permanent procedures such as cordotomy or arytenoidectomy but that also include microflap removal of the interarytenoid scar, laryngofissure with arytenoidectomy, posterior cricoidotomy with stent and/or graft placement, and endoscopic lateralization techniques; there are also innovative techniques such as placement of a self-retaining interarytenoid spring and cricoarytenoid release

There is some overlap in the choice of these procedures. Recognize, however, that BVFP is a neurologic condition that is potentially reversible and leaves the structure of the larynx intact. Therefore, less destructive procedures are preferable for managing this disorder.

PGS, on the other hand, is caused by structural changes in the larynx; therefore, structurally altering the larynx is often the only way to address the problem.

Intraoperative Details

A general approach for the treatment of patients with BVFI is the following.

If the patient does not require a tracheotomy for a significantly compromised airway, the first procedure can be unilateral posterior cordotomy. The patient is told that this may not provide a sufficient airway, but it has the least adverse effects on his or her voice. The results may need to be revised, or a medial arytenoidectomy may be considered as the next step. Total arytenoidectomy can be performed if necessary.

Suture lateralization is a newer procedure, and its role has yet to be defined. Laryngofissure with arytenoidectomy is reserved for major reconstructive surgery in patients with a severely compromised airway. Decisions of the appropriate surgical procedure must be based on individual clinical parameters. Four techniques are discussed in further detail:

  • Posterior cordotomy or cordectomy
  • Endoscopic limited or complete arytenoidectomy
  • Suture lateralization (Ejnell procedure)
  • Laryngofissure with arytenoidectomy.

Posterior cordotomy or cordectomy

Kashima and Dennis proposed these procedures in 1989.[12] Complications are rare. The procedures are effective and easily repeatable in cases of recurrence. Laccourreye recently reported a 92% decannulation rate with this approach in 25 patients.[13] The procedure is performed as follows:

  • Perform suspension laryngoscopy with any laryngoscope that provides satisfactory glottic exposure and allows use of a carbon dioxide laser with an attached microscope with a 400-mm lens.

  • Ventilate the patient with a laser-resistant tracheotomy tube (ie, jet ventilation) or a small (eg, 6-mm–outside diameter [OD]) laser-resistant endotracheal (ET) tube positioned in the IA region.

  • Use cottonoids soaked in a vasoconstrictor (eg, oxymetazoline) to protect the ET tube and cuff.

  • Set the carbon dioxide laser for continuous delivery at 2-5 W. Use of higher power settings and the superpulse mode also have been described.

  • Make an incision in the posterior true vocal fold (TVF) at the vocal process. This results in a wedge-shaped defect. Extending the incision anteriorly along the ventricle, as some have proposed, is not advised because this leads to deleterious and irreversible effects on the voice.

    Direct laryngoscopic view of larynx after left pos Direct laryngoscopic view of larynx after left posterior cordotomy

Endoscopic limited or complete arytenoidectomy

Ossoff et al first described complete arytenoidectomy via an endoscopic approach in 1984.[14] Subsequent findings from both dog models and patient series suggest that a complete arytenoidectomy is unnecessary to achieve a high decannulation rate. Eckel et al, however, compared arytenoidectomy with posterior cordectomy and found no difference in effectiveness, but the chance for subclinical aspiration in patients who underwent complete arytenoidectomy was increased.[15] The procedure is performed as follows:

  • Expose the larynx with a suspension device that provides a satisfactory view of the posterior glottis. Use a microscope with a 400-mm lens and a laser attachment.

  • Vaporize the mucosa overlying the arytenoid and corniculate cartilage.

  • Vaporize the bulk of the arytenoid without the vocal or muscular process. Preserving the posterior portion of the muscular process attached to the IA muscle reduces the likelihood of posterior commissure scarring.

Suture lateralization (Ejnell procedure)

This technique may be performed alone or with posterior cordectomy, limited arytenoidectomy, or submucosal partial cordectomy. The suture may be placed with the needle inserted from the skin into larynx. This technique is a technically demanding and requires appropriate positioning of the needles and passage of the suture through the needles. The Lichtenberger needle greatly facilitates this approach. This technique may be a reasonable for revision in cases in which additional lateralization of the TVF is desired. The procedure is performed as follows:

  • Position the laryngoscope to allow satisfactory visualization of the entire glottis. Use a microscope with a 400-mm lens and laser attachment.

  • Via the laryngoscope, introduce the laryngeal needle holder.

  • Insert a curved needle while holding a 2-0 polypropylene suture in the distal end of the curved shaft with the plunger within the shaft retracted.

  • Place the shaft into the supraglottic larynx in the middle of the false vocal fold (FVF). Direct the shaft laterally and engage the plunger, directing the needle from the shaft through the mucosa, cartilage, and neck skin. At this point, retrieve the needle.

  • Repeat the procedure in the subglottic larynx by using the same suture.

    Direct laryngoscopic view of a lateralized left tr Direct laryngoscopic view of a lateralized left true vocal fold (TVF) is shown. Use of a Lichtenberger needle holder facilitates vocal fold lateralization. Posterior cordotomy or submucous resection of the vocal fold precedes suturing.

A study by Su et al of a simplified endoscopic suture lateralization procedure indicated that the surgery is effective in patients with bilateral vocal fold paralysis (BVFP). The operation, performed in 20 patients, resulted in adequate respiration in the 19 patients who did not have an artificial airway. In addition, 19 patients had acceptable voice quality, with preoperative voice quality maintained in 14 patients. Eighteen patients suffered mild postoperative aspiration, but only for the first few days.[16]

A cadaveric study by Sztano et al indicated that in cases of posterior glottic stenosis, endoscopic arytenoid abduction lateropexy creates a greater amount of space in the posterior glottic area than does classic vocal cord laterofixation, transverse cordotomy, or arytenoidectomy.[17]

Laryngofissure with arytenoidectomy

A surgical procedure is warranted for patients in whom vocal fold paralysis persists for several years and who are tracheostomy dependent. Bower et al showed that an external arytenoidectomy via a laryngofissure (originally described by Helmus and later by Singer et al in adults[18, 19] ) provides a superior decannulation rate (84%) compared with that of endoscopic laser arytenoidectomy (56%).[20] The procedure is performed as follows:

  • Expose the larynx with a previous tracheotomy by making a curvilinear transverse neck incision through skin and platysma.

  • Create a midline thyrotomy through thyroid cartilage and cricoid cartilage.

  • Visualize the posterior larynx, and inject 1% Xylocaine with 1:100,000 epinephrine into the mucosa over the arytenoids.

  • Make a transverse incision through the mucosa to free the arytenoids from the cricoid and muscles.

  • Achieve hemostasis with bipolar cautery, and close the mucosa with a chromic suture.

  • Place polypropylene lateralization sutures around the TVF, exiting the thyroid lamina and overlying skin.

  • Close the thyrotomy in layers. Close the skin and place a drain.

  • Perform laryngoscopy to confirm positioning of the lateralization sutures.

  • Perform endoscopy after 4 weeks to plan decannulation

Postoperative Details

Adults

The use of systemic corticosteroids and systemic antibiotics generally are recommended in each of the described endoscopic procedures. Topical fibrin glue may decrease scarring and hasten improved healing at the surgical site.

Children

After a laryngofissure is created with arytenoidectomy, perform periodic endoscopy to determine the need for decannulation or downsizing the tracheostomy tube.

Complications

The goal of all the described procedures is to restore a glottic airway despite compromised abductor and adductor function. Altered vocal quality and loss of airway protection resulting in poor cough and aspiration are possible consequences of each of these static procedures. All voice parameters are negatively affected as the airway is improved. Once the voice is affected, returning it to its previous condition often is impossible.

These complications develop with varying probabilities based on the degree of airway opening achieved with a specific technique, amount of residual abductor and adductor function, and laryngeal sensation.

Specific complications of posterior cordotomy and endoscopic partial or complete arytenoidectomy include granuloma formation, chondritis of arytenoids, carbon dioxide laser–related fire, IA scar formation, possible aspiration, and a breathy voice.

Outcome and Prognosis

All 6 patients treated by Dennis and Kashima with a posterior cordotomy achieved a functional airway without a tracheostomy.[12] In 10 of 11 patients in Ossoff et al, a functional airway without tracheostomy was created after complete arytenoidectomy with an endoscopic carbon dioxide laser.[14] Remacle et al had the same result in 40 of 41 patients with endoscopic partial arytenoidectomy.[21] Eckel et al compared the results of patients treated with posterior cordotomy with those of a group of patients treated with complete arytenoidectomy.[15] Both techniques were equally effective for achieving a functional airway, but patients treated with complete arytenoidectomy had more subclinical aspiration.

A study by Scatolini et al of pediatric patients with bilateral vocal fold (cord) paralysis (BVFP) indicated that those with idiopathic paralysis were more likely to regain vocal fold mobility (62.5%) than were those whose condition was congenital (44%) or acquired (31%).[22]

The plethora of etiologies in BVFP and PGS and the multiple potential interventions do not allow easy comparison of techniques. Most series involving surgical techniques are small, and the findings generally support the authors' biases. Nonetheless, creative surgeons have a number of options that eventually should allow creation of a decannulated and safe airway in most patients.

Future and Controversies

Several techniques and approaches for the restoration of glottic competence in patients with bilateral vocal fold (cord) immobility (BVFI) are experimental but are promising. They include PCA muscle reinnervation, electrical stimulation of the laryngeal muscles, and use of the Cummings mechanical device.

PCA muscle reinnervation

Most efforts at laryngeal reinnervation have been focused on patients with unilateral vocal fold paralysis (UVFP). Chhetri et al reported results from the use of a combined procedure in which arytenoid adduction was performed with ansa cervicalis anastomosis to the RLN in a group of patients with UVFP.[23] The patients obtained no benefit from the surgery. Nonetheless, a literature review by Marina et al reported that several promising surgical procedures exist for laryngeal innervation in bilateral vocal fold paralysis (BVFP).[2] Such techniques, however, remain experimental.

Electrical stimulation of the laryngeal muscles

Electrical muscle stimulation has been studied for more than 20 years. Current technology permits the creation of implanted laryngeal stimulators. Laryngeal stimulators send a stimulus that can be administered as a continuous current, an intermittent current, or a triggered (preferably by respiratory effort) pacing current. MedTronic has manufactured a number of prototype devices for this purpose, and they are still being researched.

In patients with BVFP, laryngeal pacing involves the use of an external apparatus that senses inspiration and reanimates the paralyzed larynx of the patient. Stimuli are delivered through a needle electrode to locate and pace the abductor muscle and through an electrode implanted in the PCA muscle or RLN branch that extends to the PCA muscle. Challenges include imprecise and excessive electrical stimulation, scar formation, bulky power sources, muscle fatigue with continuous stimulation, and difficulty in synchronizing the pacing with the respiratory effort in a convenient way. Researchers express optimism, but technical problems with the electrodes at the muscle site have prevented widespread adoption of this technology.

In a study of nine symptomatic persons with BVFP who underwent unilateral implantation of a laryngeal pacemaker, Mueller et al found that neurostimulation produced an immediate and stable improvement in peak expiratory flow. Moreover, voice quality and glottal closure during phonation were not negatively affected.[2]