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Author: Joel A Ernster, MD, Active Staff, Penrose-St Francis Healthcare System; Active Staff, Memorial Health System; Clinical Instructor, University of Colorado Health Sciences Center

Joel A Ernster is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Head and Neck Society, American Rhinologic Society, Colorado Medical Society, and Triological Society

Coauthor(s): Arturo Avila Chavez, MD, Assistant Professor, Department of Otolaryngology and Head and Neck Surgery, Instituto Nacional De Enfermedades Respiratorias of Mexico City; Douglas Skarada, MD, Consulting Staff, Department of Otolaryngology, Salem Hospital

Editors: Clark A Rosen, MD, Director, University of Pittsburgh Voice Center; Associate Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Robert M Kellman, MD, Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York, Upstate Medical University; Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders; Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Author and Editor Disclosure

Synonyms and related keywords: vocal, vocal fold paralysis, vocal cords, vocal cord, bilateral vocal fold paralysis, bilateral vocal cord paralysis, bilateral vocal cord immobility, vocal cord paralysis, bilateral vocal fold immobility, BVFP, BVFI, recurrent laryngeal nerve, cricoarytenoid joint, bilateral vocal fold



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.

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).

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%).1

In adults, conditions that mimic vocal fold immobility include paradoxical vocal fold motion and functional disorder.

Causes of vocal fold fixation differ in adults and in children. In adults, these include mechanical causes, inflammatory processes (affecting the CA or larynx), malignancy, surgery, neurologic causes, radiation injury, metabolic causes, and toxins.  Mechanical derangement of the posterior glottis may also be referred to as posterior glottic stenosis (PGS). Bogdasarian and Olson classified PGS into the following 4 grades:2

  • 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

Mechanical causes

  • Acute complications of intubation
    • Arytenoid dislocation
    • Injury to the recurrent laryngeal nerve (RLN) because of anterior displacement of thyroid cartilage relative to the cricoid cartilage
    • Hyperextension of the neck that stretches the vagus nerve
    • Laryngeal mask airway
    • Excessive cuff pressure that compresses the RLN as it enters the larynx
  • Chronic complications of intubation
    • Posterior glottic stenosis (PGS) due to prolonged or traumatic intubation
    • Excessive cuff pressure compressing the RLN as it enters the larynx
  • Sofferman nasogastric tube syndrome
  • Stent placement in proximal esophagus3

Inflammatory processes that affect the CA

  • Rheumatoid arthritis
  • Gout
  • Tietze syndrome
  • Ankylosing spondylitis
  • Reiter syndrome
  • Crohn disease
  • Collagen vascular disease
  • Mumps
  • Systemic lupus erythematosus

Inflammatory processes that affect the larynx

Malignancy

Surgery

  • Bilateral injury may be caused by the following:
    • Thyroid surgery
    • Parathyroid surgery
    • Esophageal surgery
    • Tracheal surgery
    • Brainstem surgery
  • Contralateral injury after an earlier unrecognized ipsilateral injury may be caused by the following:
    • Completion thyroid surgery
    • Contralateral carotid endarterectomy
    • Anterior approach to cervical disk, which is becoming an increasingly common phenomenon.4
  • Endolaryngeal surgery with a carbon dioxide laser may injure the posterior glottis.

Neurologic causes

  • Arnold-Chiari malformation
  • Meningomyelocele
  • Diabetes mellitus
  • Amyotrophic lateral sclerosis
  • Myasthenia gravis
  • Möbius syndrome
  • Charcot-Marie-Tooth disease
  • Postpolio syndrome
  • Shy-Drager syndrome
  • Creutzfeldt-Jacob disease
  • Hydrocephalus
  • Synkinesis of the RLN
  • Lyme disease
  • Neoplasms or sarcoidosis involving nodes in the mediastinum that impact the RLNs

Radiation injury

Metabolic causes

  • Hypokalemia
  • Hypocalcemia
  • Diabetes mellitus

Toxins

In children, causes of bilateral vocal fold immobility (BVFI) include central neurologic abnormalities, idiopathic causes, and iatrogenic causes.

Central neurologic abnormalities

Central neurologic abnormalities account for most cases of childhood bilateral vocal fold paralysis (BVFP). Arnold-Chiari deformity with meningomyelocele and hydrocephalus is the most common abnormality. Other CNS insults (eg, infarct, craniotomy, asphyxia) account for some cases, according to the findings in a study by Rosin et al.6

Idiopathic causes

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.7 He also conjectured that, since abductor fibers are phylogenetically younger than adductor fibers, they may be more fragile.

Iatrogenic causes

Iatrogenic causes, including mediastinal procedures, cervical procedures, prolonged intubation, and birthing trauma, account for the remaining cases.

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.

In terms of the pathophysiology of CA fixation, inflammatory or fibrotic changes can paralyze or reduce the mobility of the joint. Various disorders can cause these changes.

Clinical

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
  • 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



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 recurrent laryngeal nerve (RLN) or vagus nerve is injured (neurapraxia) but not severed, permanent surgical treatment should be postponed for at least 9 months after injury to allow spontaneous recovery. 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).8 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 cordectomy or limited arytenoidectomy as the initial procedure of choice. Suture lateralization 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, or posterior cricoidotomy with grafting. The literature is less clear concerning the indications for each of these approaches than those of other procedures.

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 o 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.



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.



In adults, any definitive procedure to address vocal cord paralysis, whether unilateral or bilateral, must not be undertaken while a possibility for recovery exists. Recovery can occur as long as 12 months after injury. Every attempt must be made to determine if function is likely to return. This determination should include video direct laryngoscopy, during which the vocal fold can be palpated to assess mobility and bronchoscopy. In addition, laryngeal EMG can be used to evaluate normal action potentials (normal nerve), the absence of potentials (nonfunctioning nerve), defibrillating potentials (worsening nerve), or polyphasic potentials (regenerating nerve). The 12-month wait for return of function can be shortened by obtaining 2 laryngeal EMGs several months apart and by looking for evidence of improved function or stabilized function.8

As many as 70% of children with bilateral vocal fold (cord) paralysis (BVFP) require a tracheostomy. However, spontaneous recovery occurs in half of the patients, sometimes in those as old as11 years. If the condition spontaneously resolves, it typically does so 24-36 months after diagnosis. Therefore, destructive static procedures should be delayed for approximately 3 years because of this potential for recovery. Delaying surgery in children with bilateral vocal fold (cord) immobility (BVFI) caused by PGS is not beneficial; consequently, bilateral vocal fold immobility (BVFI) must be diagnosed correctly in these children to prevent restriction from surgical repair.



Lab 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

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

Other Tests

  • 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 immobile vocal folds.
    • 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.
  • 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.



Medical therapy

Medical management of the inflammatory conditions of the cricoarytenoid (CA) joint (eg, gout) 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). Glucose management may help neuropathy due to diabetes mellitus. Reflux management may be helpful in patients with bilateral vocal fold (cord) immobility (BVFI) due to laryngopharyngeal reflux.

Surgical therapy

Procedures for bilateral vocal fold immobility (BVFI) due to IA scarring with or without CA ankylosis

  • Tracheostomy
  • Functional procedures
    • Microflap trapdoor techniques
    • Laryngofissure with posterior cricoidotomy with cartilage grafting and stent placement (or only stent placement)
    • Local mucosal flap reconstruction
    • Excision of the scar and mucosal or skin grafting
  • Static procedures
    • Posterior cordotomy (unilateral or bilateral)
    • Arytenoidectomy (endoscopic or external, partial or complete)
    • Suture lateralization

Procedures for bilateral vocal fold (cord) paralysis (BVFP)

  • Tracheostomy
  • Reinnervation techniques (experimental)
  • Electrical pacing (experimental)
  • Permanent procedures
    • Posterior cordotomy (unilateral or bilateral)
    • Arytenoidectomy (endoscopic or external, partial or complete)
    • Cordopexy, lateralization of the vocal cord

Intraoperative details

Procedures for BVFI

This discussion does not specifically address surgical management of glottic fixation other than to warn of the difficulty in differentiating between fixation and paralysis in some patients.

Procedures for BVFP

General algorithm

A general algorithm for the treatment of patients with BVFP 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), and laryngofissure with arytenoidectomy.

Posterior cordotomy or cordectomy

Kashima and Dennis proposed these procedures in 1989.9 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.10 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.

Endoscopic limited or complete arytenoidectomy

Ossoff et al first described complete arytenoidectomy via an endoscopic approach in 1984.11 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.12 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.

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 adults13, 14) provides a superior decannulation rate (84%) compared with that of endoscopic laser arytenoidectomy (56%).15 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.



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.



Spontaneous recovery can be expected in 55% of patients; almost half of patients who recover do so within the first year. Recovery may occur as late as 11 years after initial diagnosis.

All 6 patients treated by Dennis and Kashima with a posterior cordotomy achieved a functional airway without a tracheostomy.9 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.11 Remacle et al had the same result in 40 of 41 patients with endoscopic partial arytenoidectomy.16 Eckel et al compared the results of patients treated with posterior cordotomy with those of a group of patients treated with complete arytenoidectomy.12 Both techniques were equally effective for achieving a functional airway, but patients treated with complete arytenoidectomy had more subclinical aspiration.

The plethora of etiologies in bilateral vocal fold (cord) paralysis (BVFP) and the multiple 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.



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 has recently reported results with a combined procedure in which arytenoid adduction was performed with ansa cervicalis anastomosis to the RLN in a group of patients with UVFP.17 The reinnervation group had no benefit.

A group in the Netherlands selectively reinnervated the feline PCA muscle by using the phrenic nerve.18 Reinnervation was confirmed in 10 of 11 cats, but significant abductor function was restored in only 4 of 11. The authors' explanation was gradual ankylosis of the cricoarytenoid (CA) joint that limited the effects of improved abductor muscle function. This approach might be useful in patients with bilateral vocal fold (cord) paralysis (BVFP) and significant airway obstruction. The role of reinnervation in patients with BVFP remains undefined.

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 prevent widespread adoption of this technology.

Use of the Cummings mechanical device

Cummings has reported the use of an implantable device placed into the larynx through a thyroplasty window. This device engages the soft tissues of the larynx (including the TA muscle) with a screw. The screw then is rotated to pull the tissue laterally. Cummings et al conducted the investigation in sheep, with favorable results. Human studies are pending.



Media file 1:  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).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo

Media file 2:  Direct laryngoscopic view of larynx after left posterior cordotomy
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Media type:  Photo

Media file 3:  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.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo



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Vocal Fold Paralysis, Bilateral excerpt

Article Last Updated: Sep 9, 2008