Bilateral Vocal Cord Paralysis

Etiology

Bilateral vocal cord paresis may represent an early manifestation of a disease that progresses to complete bilateral vocal cord paralysis or may remain a stable, nonprogressive condition, depending on the underlying etiology.[3]

Etiology and Risk Factors

Causes of bilateral vocal cord paralysis include:

• Scarring: Progressive glottic scarring following radiation therapy, prolonged intubation, inhalational burns, caustic ingestion, or inflammatory disorders (eg, scleroderma and relapsing polychondritis) may result in vocal cord fixation, bilateral vocal cord paralysis, or glottic stenosis.

• Iatrogenic causes: Postsurgical injury to the recurrent laryngeal nerves remains the most common cause of bilateral vocal cord paralysis. Although classically associated with thyroidectomy, bilateral paralysis may also occur following tracheal resection, esophagectomy, cervical trauma exploration, carotid surgery, and congenital cardiac or aortic procedures.[4]

• Malignancy: Advanced laryngeal malignancy can destroy the vocal cords or their neuromuscular controls, leading to paralysis. Additionally, subglottic, tracheal, esophageal, and thyroid malignancies can extend and involve the recurrent laryngeal nerves, leading to bilateral vocal cord paralysis.

• Central nervous pathology: Stroke, CNS tumor, and multiple sclerosis can all affect the nuclei of the vagus nerve and potentially lead to bilateral vocal cord paralysis. While multiple sclerosis can have a relapsing or remitting course, most CNS causes of this condition carry a very poor chance of recovery of function.[4]

• Systemic disease: ALS, Miller-Fisher, and other systemic syndromes may include bilateral vocal cord paralysis as a component of a systemic condition. A variant of Guillain-Barré can present with isolated bilateral vocal cord paralysis even in the absence of the classic ascending paralysis.

• Idiopathic: This accounts for a significant minority of adult cases of bilateral vocal cord paralysis, though idiopathic bilateral vocal cord paralysis is far rarer in children.[4]

Benninger et al estimated that bilateral vocal cord paralysis is attributed to surgical trauma in 44% of cases, malignancies in 17%, secondary to endotracheal intubation in 15% of cases, due to neurologic disease in 12% of patients, and idiopathic causes in 12% of cases.[5] Following thyroid or other surgery, bilateral vocal cord paralysis may present with acute respiratory distress necessitating urgent airway intervention. Injury to the recurrent laryngeal nerve denervates both the abductor and adductor muscles of the larynx. Because the adductor muscle fibers outnumber the abductor fibers by approximately 4:1, the vocal cords typically assume a static paramedian position following recurrent laryngeal nerve injury.[6] Endotracheal intubation may also result in bilateral vocal cord paralysis through direct mucosal trauma, cuff-related pressure neuropraxia, nerve compression, postoperative edema, or, rarely, direct injury to the recurrent laryngeal nerve.[7]

In infants and children presenting with stridor due to bilateral vocal cord paralysis, Arnold–Chiari malformation type II associated with hydrocephalus and myelomeningocele is the most common neurologic cause. The diagnosis is typically established by magnetic resonance imaging (MRI), which demonstrates cerebellar ectopia below the foramen magnum.[8] Herniation of the cerebellar tonsils, brainstem, and medulla through the foramen magnum into the spinal canal may compress the vagus nerve, resulting in bilateral vocal cord dysfunction.[9] Birth-related trauma due to vertex or breech delivery and the use of forceps can also cause recurrent laryngeal nerve injury, although bilateral involvement is uncommon.[10] In infants, cardiovascular surgery, including patent ductus arteriosus ligation and repair of a tracheoesophageal fistula, is another important cause of bilateral vocal cord paralysis.[11]

A palsy of the superior laryngeal nerve causes alterations in vocal pitch due to paralysis of the cricothyroid muscle, resulting in reduced pitch range, vocal fatigue, and hoarseness. Bilateral superior laryngeal nerve palsy further compromises laryngeal function and may increase the risk of aspiration because of impaired protective laryngeal reflexes.[12] Although uncommon, vocal cord palsy may occur after stroke involving the cerebral cortex, brainstem, or vagal motor pathways. Laryngeal dysfunction may result from injury to the nucleus ambiguus, with associated sensory impairment when the nucleus solitarius is involved. Tumor-related compression or invasion of the vagus or recurrent laryngeal nerve may also cause recurrent laryngeal nerve palsy; when bilateral, this can leave the vocal cords in a paramedian position.

Another extremely rare cause of bilateral recurrent laryngeal nerve paralysis is Guillain-Barré syndrome, the most common acquired demyelinating neuropathy. Although it classically presents with areflexia and ascending muscle weakness, cranial nerve involvement may also occur, resulting in bilateral recurrent laryngeal nerve paralysis. Severe disease can progress to respiratory failure requiring mechanical ventilation and may be accompanied by cardiac arrhythmias and hemodynamic instability.[13]

Epidemiology

Postsurgical nerve injury is the leading cause of bilateral vocal cord paralysis, with most cases occurring in adults who have undergone thyroid surgery or other bilateral neck procedures. Idiopathic cases may demonstrate a slight female predominance; however, high-quality epidemiologic data supporting this association remain limited.[14]

Although uncommon, vocal cord paralysis remains a recognized cause of neonatal stridor, with most congenital cases presenting as unilateral involvement. Murty et al estimated the incidence of bilateral vocal cord paralysis at 0.75 cases per million births annually.[15] Neonatal bilateral vocal cord paralysis rarely occurs in isolation, frequently coexisting with prematurity, bronchopulmonary dysplasia, and neurologic abnormalities, all of which contribute to poorer clinical outcomes in affected infants.

Congenital vocal cord paralysis should remain an important consideration in the differential diagnosis of neonatal respiratory distress.[16] After laryngomalacia, vocal cord paralysis is the second most common congenital laryngeal abnormality in the pediatric population, although most cases are unilateral. This increasing recognition likely reflects improved survival of premature infants and children and those with complex congenital disorders.[17]

Spontaneous recovery of vocal cord function occurs in approximately 48% to 62% of children with bilateral vocal cord paralysis across all age groups. Prognosis varies according to the child's overall health, underlying etiology, and associated medical comorbidities, with medically complex infants generally experiencing less favorable outcomes.[18]

Pathophysiology

Intrinsic vocal cord or arytenoid scarring and damage result from the replacement of normally mobile laryngeal tissues with fibrosis and scar formation, producing mechanical tethering that restricts mobility and prevents normal vocal cord movement. Recurrent laryngeal nerve injury represents the most common cause of bilateral vocal cord paralysis and therefore warrants a detailed review of its pathophysiology. Vagal motor efferent fibers originate in the medulla oblongata. The nucleus ambiguus contains cell bodies of motor neurons that innervate the soft palate, pharynx, and larynx, while the dorsal motor nucleus contains visceral efferent fibers that supply the thorax and abdomen. The vagus nerve exits the cranium through the jugular foramen, where the accessory nerve joins its course.[19]

The superior laryngeal nerve branches from the vagus nerve as it descends between the common carotid artery and internal jugular vein, then divides into internal and external branches. The internal branch of the superior laryngeal nerve provides sensory innervation to the mucosa above the true vocal cords, while the external branch innervates the cricothyroid muscle, which plays a key role in the modulation of vocal pitch. The right vagus nerve descends anterior to the subclavian artery into the abdomen, while the right recurrent laryngeal nerve branches from it and loops around the subclavian artery before ascending toward the larynx.

The right recurrent laryngeal nerve supplies sensory innervation to the laryngeal mucosa below the vocal folds and motor innervation to all intrinsic laryngeal muscles except the cricothyroid. The left vagus nerve follows a similar course into the abdomen posterior to the aortic arch near the ductus arteriosus, with the left recurrent laryngeal nerve branching off and looping around the aortic arch before ascending through the tracheoesophageal groove to reach the larynx. The longer intrathoracic course of the left recurrent laryngeal nerve increases susceptibility to injury.

Bilateral vocal cord paralysis may result from vagal injury anywhere along its course from the brainstem to the distal thoracic branches. Due to physiologic redundancy within laryngeal innervation, vocal cord position does not always reliably localize the lesion in bilateral paralysis.[20] Recurrent laryngeal nerve injury remains the most common mechanism, classically producing a paramedian vocal cord position in unilateral cases and a median position in bilateral cases. Superior laryngeal nerve injury reduces vocal pitch and may produce vocal cord bowing due to loss of cricothyroid muscle tone. High vagal injury may result in a nearly fully abducted “cadaveric” vocal cord position.[19]

Histopathology

Histopathologic examination has a limited role in the evaluation of bilateral vocal cord paralysis because the disorder is typically caused by neural dysfunction rather than a primary structural abnormality of the vocal folds. From a practical standpoint, clinicians rarely rely on histologic findings because tissue specimens are not routinely obtained during the diagnostic evaluation. Histologic findings therefore vary according to the underlying etiology and are nonspecific.

Acute recurrent laryngeal nerve injury may demonstrate axonal degeneration and inflammatory changes, whereas chronic denervation results in neurogenic atrophy of the intrinsic laryngeal muscles with replacement by fibrous and fatty connective tissue. When bilateral vocal cord immobility is caused by mechanical fixation rather than paralysis, histopathologic examination may reveal fibrosis, scar formation, or cricoarytenoid joint ankylosis. Tissue biopsy is generally reserved for cases in which malignancy, granulomatous disease, amyloidosis, or other infiltrative disorders are suspected.

History and Physical

Adults Bilateral Vocal Cord Paralysis

The primary presenting complaints of an adult patient with bilateral vocal cord paralysis are either voice changes (eg, hoarseness, pitch changes, vocal fatigue) or, more commonly, breathing difficulties (eg, stridor, increased work of breathing, aspiration/pneumonia).[21] A history of symptom onset and duration should be obtained, as well as whether symptoms are progressing or stable. Furthermore, any antecedent events should be documented, including prior upper respiratory infection, neck surgery, cervical or thoracic trauma, malignancy, radiation therapy, and a thorough past medical history should be obtained. Of particular interest are any systemic rheumatologic or connective tissue disorders, neurologic disorders, and states of immunosuppression.

Additionally, a thorough physical examination is required, with an emphasis on the head and neck and pulmonary examination. Breathing and the patient's voice at rest and with effort should be noted. After a patient has been speaking for a few minutes, the inspiratory stridor may become evident or worsen. Diagnosis is made clinically based on flexible fiberoptic laryngoscopy, in which the vocal cords are observed to be immobile, and their position is noted. If the diagnosis remains uncertain, video stroboscopy and bronchoscopy can provide additional information about the fluid wave of vocal cord vibration and help rule out subglottic and tracheal pathology (eg, subglottic stenosis or tracheomalacia).

Pediatric Bilateral Vocal Cord Paralysis

In pediatric patients, a detailed family and birth history, including prolonged or difficult delivery, use of assistive devices during delivery, concurrent congenital medical problems, and the duration of any NICU stay, should be obtained. The remaining pertinent points of history are similar to those of adult patients. Bilateral vocal cord paralysis in pediatric patients often presents with stridor and feeding difficulties, and children with congenital bilateral vocal cord paralysis are more likely to exhibit severe manifestations, including cyanosis and apnea. Notably, children with bilateral vocal cord paralysis often present with a normal voice because the vocal cords remain in the paramedian position with abductor paralysis, yet they may have marked inspiratory stridor and accessory muscle use during inspiration.

Diagnosis is usually made via awake fiberoptic laryngoscopy, which is possible even in very small children, though more challenging than in adults. This examination also helps exclude laryngomalacia, which is far more common than bilateral vocal cord paralysis but can present with similar symptoms. If the diagnosis is still uncertain, direct laryngoscopy and bronchoscopy under anesthesia may be required. Direct laryngoscopy and bronchoscopy are performed with the patient breathing spontaneously, allowing assessment of vocal cord motion intraoperatively. This modality also allows for lower airway examination to rule out concurrent or alternative pathology, such as subglottic stenosis, tracheomalacia, or bronchomalacia.[19]

Evaluation

Diagnostic Studies

Diagnostic studies that are utilized in the evaluation of bilateral vocal cord paralysis include:

• Flexible fiberoptic laryngoscopy: This study is an essential part of the initial evaluation of patients presenting with features of vocal cord paralysis. Flexible fiberoptic laryngoscopy is performed with the patient awake in the office to assess spontaneous and volitional vocal cord movement and to document the resting position of the vocal folds.[11]

• Direct laryngoscopy and bronchoscopy: If the status of the vocal cords or of the lower airway is uncertain, examination with direct laryngoscopy and bronchoscopy is indicated. This study also allows palpation of the arytenoid joints to rule out fixation.

• Laryngeal electromyography: This diagnostic modality is performed with the patient awake in the office to assess the innervation status of the laryngeal muscles, which can help determine the duration of paralysis and recovery potential after a neurologic injury. Please see StatPearls' companion resource, "Nerve Conduction Studies and Electromyography," for further information on electromyography interpretation.[22][23]

• Imaging of the recurrent laryngeal nerve: In patients with new-onset, idiopathic bilateral vocal cord paralysis, the entire course of the recurrent laryngeal nerves should be imaged to exclude a tumor or central nervous system lesion. Contrast-enhanced CT of the neck and chest is typically the initial imaging modality, whereas MRI is preferred when brainstem or skull base pathology is suspected. The area evaluated extends from the medulla oblongata (vagal nuclei) to the aortic arch to encompass the entire course of both recurrent laryngeal nerves.

• Laboratory testing: No single laboratory study establishes the diagnosis of bilateral vocal cord paralysis, and the investigations to consider are guided by each patient's history and overall medical picture. Potassium, calcium, glucose, antineutrophil cytoplasmic antibody (ANCA), thyroid function tests, Lyme disease serology, tuberculosis testing, uric acid levels, rheumatoid factor, antinuclear antibody (ANA), and erythrocyte sedimentation rate (ESR) may be considered when clinically indicated.

Current recommendations from otolaryngology societies emphasize flexible laryngoscopy as the initial diagnostic study for suspected bilateral vocal cord paralysis. Laryngeal electromyography is recommended when the diagnosis, prognosis, or distinction between neurologic paralysis and mechanical fixation remains uncertain. Cross-sectional imaging of the vagus and recurrent laryngeal nerves is recommended for patients with idiopathic paralysis or when no clear surgical or traumatic cause is identified. Additional laboratory investigations should be directed by the patient's clinical history and suspected underlying etiology.

Treatment / Management

Treatment Principles

Management of bilateral vocal cord paralysis is guided by the severity of airway compromise, the underlying etiology, and the likelihood of spontaneous neurologic recovery. The primary treatment objective is maintenance of a safe airway while preserving voice quality and swallowing function whenever possible. Reversible interventions are generally preferred when recovery is anticipated, whereas definitive airway-enlarging procedures are reserved for patients with permanent paralysis or persistent airway compromise despite conservative management.

Medical Management

Although surgical intervention is commonly indicated in patients with bilateral vocal cord paralysis, medical management of inflammatory and infectious conditions, eg, syphilis, tuberculosis, gout, and relapsing polychondritis, is essential. Corticosteroids are effective in conditions, eg, sarcoidosis, polychondritis, and granulomatosis with polyangiitis (formerly Wegener granulomatosis). Optimization of glycemic control may improve diabetic neuropathy. Management of reflux is often recommended during the recovery period to minimize untoward irritation of the larynx.

Prognosis and Likelihood of Recovery (Adults Versus Children)

More than 50% of children will experience spontaneous symptom resolution during the first year of life. However, the prognosis is much more guarded for bilateral vocal cord paralysis when compared to unilateral.[24] This fact must be taken into consideration before any invasive intervention that can impact a patient’s ability to phonate or swallow. In adults, however, the prognosis depends largely on the etiology, and additional studies (eg, electromyography) can have predictive value in postoperative cases to assess the likelihood of recovery. If the patient is experiencing increased work of breathing or significant stridor, some form of surgical intervention to improve the airway will be required, even if spontaneous recovery is expected. If the prognosis for recovery is favorable, a reversible procedure, eg, a botulinum toxin injection or a tracheostomy, should be performed. If minimal or no recovery is expected, laryngeal surgery can be considered to attempt decannulation.[25](B2)

Conservative Management

Patients with an adequate airway and an anticipated potential for spontaneous neurologic recovery may be managed conservatively with close observation. Serial flexible fiberoptic laryngoscopy and, when appropriate, laryngeal electromyography can help monitor recovery of vocal cord motion and estimate the likelihood of functional improvement. During the observation period, voice therapy, swallowing rehabilitation, aspiration precautions, and treatment of the underlying etiology should be optimized. Progressive stridor, worsening respiratory distress, recurrent aspiration, or deterioration in airway patency should prompt reevaluation for surgical intervention.

Tracheostomy

In the past, tracheostomy was the most common procedure performed in patients with bilateral vocal cords to establish a secure airway. Tracheostomy provides the most reliable airway while preserving laryngeal anatomy, making it potentially reversible without long-term sequelae. Although tracheostomy remains the standard in settings of glottic obstruction, this intervention is associated with significant chronic care burden, cost, psychosocial impairment, and increased mortality. Studies have noted that patients experienced a reduced quality of life and must undergo continuous management of their tracheostomies, which can be particularly undesirable in children.[26] (A1)

In a national series of 885 infants undergoing tracheostomy, the in-hospital mortality was 14%.[27] Endoscopic techniques have been shown to be more cost-effective than tracheostomy in the management of permanent bilateral vocal cord paralysis.[28] Although several alternative procedures have been developed to manage bilateral vocal cord paralysis, they all can produce permanent changes of the larynx that may predispose patients to lifelong aspiration and dysphonia postoperatively.[29](A1)

Botulinum Toxin

Botulinum toxin, produced by Clostridium botulinum, is a neurotoxin that prevents the release of acetylcholine from presynaptic axon terminals, leading to flaccid paralysis of the target muscle. For patients with vocal cord paralysis, toxin injection is utilized to block aberrant reinnervation of adductor muscles by inspiratory motor neurons. This enables abductor inspiratory motor neurons to become more effective, thereby facilitating glottic opening.[30] This technique only affects a transient improvement in symptoms for approximately 3 to 6 months at a time, requiring repeated injections for longer-lasting relief. Botulinum toxin may serve as a temporary treatment option in selected patients with bilateral vocal cord paralysis who are expected to recover but require interim improvement in glottic opening. Because its effects are temporary, repeated injections are required to maintain benefit. Botulinum toxin is also known as a viable option in idiopathic spasmodic vocal cord dysfunction.(B2)

Arytenoidectomy

Arytenoidectomy is an irreversible procedure involving the endoscopic removal of the arytenoid cartilage (sometimes only the prolapsed cuneiform cartilages are removed) to expand the glottic inlet transversely, creating a larger-diameter airway for inspiration.[31][23] Arytenoidectomy is performed either on its own or in combination with vocal fold resection; in the latter case, the procedure is referred to as arytenoid cordectomy. Resection of the mucosa and cuneiform cartilage over the arytenoid leads to a widening of the glottis. This technique has demonstrated positive results in augmenting ventilation in patients with bilateral vocal cord paralysis, particularly in pediatric patients.(A1)

Further refinement of arytenoidectomy techniques occurred with the introduction of the CO₂ laser, which improved procedural precision while enhancing hemostasis and reducing postoperative edema.[32] Despite these advances, some patients experience worsening postoperative dysphonia following arytenoidectomy, and these voice changes may become permanent.[33] The procedure also increases susceptibility to scar formation and granuloma development, both of which may contribute to progressive airway narrowing and necessitate multiple surgical revisions.

Endoscopic laser resection techniques offer the advantage of avoiding tracheostomy placement in many patients undergoing surgical airway enlargement. In one study, utilization of an endoscopic plasma coblator instead of a CO₂ laser resulted in reduced scar formation, likely secondary to decreased thermal injury to adjacent tissues.[34](B3)

Cordotomy

Cordotomy is another endoscopic surgical procedure to enlarge the glottic airway. A cordotomy is accomplished via an incision of the vocal fold, ligament, and the thyroarytenoid muscle posteriorly at the attachment to the arytenoid. Cordotomy, similar to arytenoidectomy, is susceptible to granuloma and scar formation. Revision cordotomy can be required in up to 30% of patients secondary to reduced glottic diameter from scarring or granulation tissue formation.[35] The most common complication associated with cordotomy was altered voice quality due to vocal fold damage.[36] Laser endoscopic cordotomy has become the favored therapeutic intervention for vocal cord paralysis as compared to an arytenoidectomy, as cordotomy is less invasive and reduces the incidence of aspiration. Voice quality can be impaired after resection, but overall voice outcomes are often superior to arytenoidectomy, particularly in adult patients.[35](B2)

Reinnervation

The goal of reinnervation is to restore vocal cord abduction by restoring activity of the posterior cricoarytenoid (PCA) muscle. While this procedure enables the return of spontaneous vocal cord abduction, it does not affect adduction. Anastomosis of the recurrent laryngeal nerve is a complex procedure due to the variability and complexity of its innervation.[2] The phrenic nerve has been used to reinnervate the PCA muscle; in one study, inspiratory vocal fold abduction was achieved in 93% of cases.[37] Functional improvement typically requires several months because axonal regeneration is necessary before reinnervation can occur.(B3)

Although patients had hemidiaphragm paralysis, they had substantial recovery of diaphragmatic motion and respiratory function within 12 months. Marina et al previously showed that only a branch of the phrenic nerve could be used to minimize loss of diaphragmatic function and maintain respiratory parameters.[2] A more modern technique is to use a pedicled neuromuscular flap from the ansa cervicalis, thereby avoiding the diaphragmatic complications of phrenic nerve sacrifice. This procedure is technically very challenging and is most successful when performed by a few surgeons with significant experience with it. All of these laryngeal reinnervation procedures are far more commonly used in unilateral vocal cord paralysis.[38][3](B3)

Gene Therapy

Gene therapy remains in the preclinical phases but holds several promising avenues for future treatment. With this technique, gene delivery to injured or denervated muscles promotes the growth of damaged neurons, aiding the rejuvenation of damaged laryngeal muscles. These genes encode neurotrophic or growth factors that stimulate muscle differentiation and proliferation.[39] Either delivered directly into the laryngeal muscles or into the recurrent laryngeal nerve, they are absorbed by neuronal cell bodies through retrograde axonal transport.[40] Once appropriately transduced into target cells, they produce peptides that promote the growth of the recurrent laryngeal nerve, synaptic formation, and regeneration.[3] At present, gene therapy remains investigational and has not entered routine clinical practice.(B3)

Differential Diagnosis

Differential diagnoses that may also cause  bilateral vocal cord immobility or upper airway obstruction include:

• Unilateral vocal cord paralysis
• Subglottic stenosis
• Laryngomalacia
• Laryngeal neoplasm
• Squamous cell carcinoma
• Chondromas and chondrosarcomas
• Postirradiation fibrosis of the cricoarytenoid joint, vocal folds, or both
• Chondronecrosis

Underlying etiologies of bilateral vocal cord paralysis include:

• Inflammatory, autoimmune, and rheumatologic disorders
  • Rheumatoid arthritis
  • Gout
  • Tietze syndrome
  • Ankylosing spondylitis
  • Reiter syndrome
  • Crohn disease
  • Collagen vascular disease
  • Systemic lupus erythematosus
  • Wegener granulomatosis
  • Amyloidosis
  • Sarcoidosis
  • Cicatricial pemphigoid
  • Relapsing polychondritis

• Infectious disorders
  • Tuberculosis
  • Syphilis
  • Lyme disease
  • Mumps

• Neurologic disorders
  • Arnold-Chiari malformation
  • Meningomyelocele
  • Amyotrophic lateral sclerosis
  • Myasthenia gravis
  • Möbius syndrome
  • Charcot-Marie-Tooth disease
  • Postpolio syndrome
  • Shy-Drager syndrome
  • Creutzfeldt-Jakob disease
  • Hydrocephalus
  • Synkinesis of the recurrent laryngeal nerve

• Metabolic and systemic disorders
  • Diabetes mellitus
  • Hypokalemia
  • Hypocalcemia
  • Renal insufficiency with Alport syndrome
  • Gastroesophageal reflux disease

• Iatrogenic causes
  • Radiation therapy
  • Thyroid surgery
  • Parathyroid surgery
  • Esophageal surgery
  • Tracheal surgery
  • Brainstem surgery
  • Carotid endarterectomy

Prognosis

In adults, recovery from idiopathic vocal cord paralysis (or vocal cord paralysis due to nontransecting nerve injury) can occur within 12 months following injury. Although spontaneous recovery is expected in 55% of patients, full recovery can be very prolonged. The prognosis for complete spontaneous recovery is significantly poorer in bilateral vocal cord paralysis than in unilateral vocal cord paralysis. Recovery of glottic function is otherwise most dependent on the underlying etiology and the overall prognosis of this root cause.[41] Patients with complete recurrent laryngeal nerve transection are unlikely to experience meaningful spontaneous recovery, whereas those with neurapraxia or partial nerve injury have a more favorable prognosis.

Long-term outcomes vary according to the need for airway intervention, the degree of recovery of vocal fold motion, and the presence of associated neurologic or systemic disease. Advances in endoscopic airway procedures, laryngeal reinnervation techniques, and selective use of tracheostomy have substantially improved long-term airway function and quality of life for many patients, although persistent voice and swallowing dysfunction may occur in those with severe or irreversible paralysis.

Complications

Complications associated with bilateral vocal cord paralysis include:

• Airway complications
  • Stridor
  • Dyspnea
  • Airway obstruction
  • Respiratory failure
  • Difficult airway management [42]
  • Tracheostomy dependence

• Voice and swallowing complications
  • Altered voice quality
  • Hoarseness
  • Weak cough
  • Difficulty swallowing
  • Feeding difficulty
  • Aspiration
  • Aspiration pneumonia

• Procedure-related complications
  • Scar formation
  • Granuloma formation
  • Arytenoid chondritis
  • Laser-related airway fire

• Long-term complications: Reduced quality of life associated with tracheostomy [29]