Unilateral Vocal Fold Paralysis

Jeffrey Singh; Robert Wang; Ryan Winters; Gary Kwartowitz

Unilateral Vocal Fold Paralysis

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Continuing Education Activity

Unilateral vocal fold paralysis is characterized by abnormal movement of the true vocal folds, with reduced mobility (paretic) or complete cessation of movement (paralytic). The vocal folds are essential for producing speech and singing sounds by abducting, adducting, and vibrating. The inability of one or both vocal folds to move properly gives rise to vocal fold immobility. The most common causes of this condition include nerve damage, infections, trauma, tumors, and autoimmune disorders.

This activity discusses various etiologies, clinical manifestations, and diagnostic methodologies. The course facilitates the differentiation between paretic and paralytic conditions, thorough assessment of associated symptoms, and exploration of neurologic examinations. Evidence-based treatments, ranging from speech therapy to surgical interventions, and the complexities of injectable vocal-fold-augmenting materials are explored. Long-term management necessitates an interprofessional approach, involving otolaryngologists, speech therapists, and surgical nurses. Referral for laryngoscopic evaluation is crucial, emphasizing the need for comprehensive care in unilateral vocal fold paralysis cases.

Objectives:

Identify the signs and symptoms indicative of unilateral vocal fold paralysis.
Develop a clinically guided diagnostic plan for a patient with suspected unilateral vocal fold paralysis.
Implement evidence-based tailored management plans for patients with unilateral vocal fold paralysis.
Coordinate with an interprofessional team in formulating short- and long-term care plans for patients with unilateral vocal fold paralysis.

Introduction

Vocal fold immobility is a broad term referring to the abnormal movement of the true vocal folds. The abnormal movement can arise from reduced mobility (paretic) or complete cessation of any vocal fold movement (paralytic). The condition can be unilateral or bilateral. Unilateral vocal fold paralysis (UVFP) is more common than the bilateral type.

Vocal Fold Anatomy

The vagus nerve innervates the larynx and its associated muscles. Vagal nerve fibers arise from the nucleus ambiguus in the brainstem medulla. Upper-motor corticobulbar neurons descend from the cerebral cortex to the nucleus ambiguus, stimulating these vagal nerve fibers. The fibers coalesce and exit the brainstem via the jugular foramen as the 10th cranial nerve.

The vagus nerve then descends inferior to the skull base, passes into the neck, and gives off 3 main branches: the pharyngeal branch, superior laryngeal nerve (SLN), and recurrent laryngeal nerve (RLN). The SLN is responsible for laryngeal sensation in the superior glottic aspect and cricothyroid muscle motion.

The RLN classically descends further into the neck and thorax, loops around the subclavian artery on the right and aortic arch on the left, and ascends back into the neck in the tracheoesophageal groove. The RLN then enters the larynx posteriorly, near the cricothyroid joint. However, a small proportion of the population has a "nonrecurrent laryngeal nerve" that directly innervates the larynx without passing the thorax.[1]

The RLN provides sensation to the glottis and subglottis and motor innervation to all remaining intrinsic laryngeal muscles, including the posterior cricoarytenoid, interarytenoid, lateral cricoarytenoid, and thyroarytenoid muscles.[2][3][4][5] The cause of unilateral vocal fold paralysis can arise in the larynx and anywhere along the RLN pathway. The role of SLN injury in UVFP pathophysiology is insignificant.[73]

Etiology

UVFP etiology varies with geography and time. Data obtained from 1985 through 1995 in a large North American case series showed cancer to be the most common cause of UVFP.[6] However, increasing head and neck surgery also increased the prevalence of UVFP arising from iatrogenic surgical injury (37%) from 1996 through 2005. Nonthyroid procedures (66%) surpassed thyroidectomy (33%) as the most common mode of injury. By contrast, a large Italian study showed that thyroidectomy (41.3%), idiopathic paralysis (25.3%), and thoracic surgery (12.1%) were the chief UVFP causative factors.[7]

Malignancy is the most worrisome cause of UVFP and is most commonly seen in primary and metastatic lung and laryngeal carcinoma. Thyroid and central nervous system (CNS) cancers are less frequently seen.[8] A 1991 Stanford University study reported that out of 1,019 UVFP cases from 1970 to 1991, neoplasm (35.5%) was the most common etiology, 54.8% of which had a lung primary.[9]

Iatrogenic injury has traditionally been attributed to thyroid surgery (see Image. Unilateral Vocal Cord Paralysis After a Left Parathyroidectomy). Aberrant recurrent laryngeal nerve anatomy, thyroid malignancy, and revision surgery increase the likelihood of postsurgical UVFP.[10][11][12][13] Intraoperative nerve stimulators are frequently used to avoid injury. The effectiveness of these devices has not been clinically proven, though continuous nerve monitoring has been associated with lower paresis and paralysis rates compared to intermittent nerve stimulation.[14][15][16][15]

Other surgeries with a significant recurrent laryngeal nerve risk include anterior cervical spine surgery, esophagectomy, and cardiothoracic surgery. However, any procedure requiring endotracheal tube (ETT) insertion may cause paralysis, either via pressure from the ETT or mechanical trauma to the arytenoids.[17]

Central causes, such as previous cerebral vascular accidents, brain stem or high skull-base tumors, and peripheral neurologic etiologies, must be entertained in the differential of a new-onset UVFP. A detailed neurologic examination is indicated in patients suspected to have UVFP of neurologic origin. New, isolated, neurologically related UVFP is rare, accounting for less than 5% of cases. One study following idiopathic UVFP over time demonstrated that up to 20% of these patients were subsequently diagnosed with a primary neurologic disorder.[18][19]

Mechanical causes, such as cricoarytenoid joint dislocation, must be considered, especially in the setting of recent laryngeal trauma or intubation. A history of blunt or penetrating neck trauma should strongly suggest this event as the cause. Meanwhile, the UVFP occurrence rate after routine intubation is extremely low, often quoted as 0.1% or less.[20]

Idiopathic UVFP, which some postulate as a postviral syndrome, is a common cause of UVFP but is a diagnosis of exclusion. The entire course of the vagus nerve, or RLN, must be examined to rule out more sinister pathologies before labeling the condition idiopathic. Overall, 29 to 67% of UVFP cases are classified as idiopathic, comprising the 2nd or 3rd largest etiologic category.[21]

Epidemiology

An American study examined the incidence of idiopathic UVFP over 7 years and described an overall prevalence of 1.04 cases per 100,000 persons per year[22]. Meanwhile, another study found that UVFP of a neurologic origin did not significantly differ in age, gender, or duration of symptoms from UVFP of a nonneurologic origin. However, previous cancer or thyroid disease history was significantly more common in the neurogenic group.[23]

Preoperative UVFP incidence in patients undergoing thyroid surgery has been documented as 1.3%. About 76% of individuals with preoperative UVFP were ultimately diagnosed with a thyroid malignancy.[24][25] UVFP is not pathognomonic for thyroid malignancy but is a worrisome sign. The incidence of UVFP after thyroid surgery ranges from 0.5 to 9.5%[26][27][28][27].

UVFP was reported in 1.2% of patients who underwent surgery for a primary lung malignancy, 0% to 59% of patients who underwent surgery for an esophageal malignancy, and 25% of patients undergoing cardiothoracic surgery.[29][30][31] The incidence of UVFP after cervical spine surgery ranges from 2.3% to 24.2%.[32]

UVFP incidence after nonsurgical neck trauma is not well described and remains in the realm of case reports.[33] Neck trauma, particularly blunt neck trauma, is more often associated with bilateral vocal fold paralysis.[34][35]

Pathophysiology

Any lesion, inflammation, or trauma along the RLN's course can cause vocal cord movement alteration and dysphonia. UVFP can also arise from vocal fold or laryngeal injury. Intubation trauma is the most frequent reason for these injuries, though intubation-related UVFP is exceedingly rare, occurring in less than 1% of these procedures.[36] Arytenoid joint dislocation is the most common mechanism, potentially surgically correctable if identified in a timely fashion[37].

CNS pathologies such as stroke, tumors, high spinal lesions, and multiple sclerosis can also lead to vocal fold paresis and paralysis. Dysfunction severity and final vocal fold position typically depend on the neurologic lesion's site.[38]

History and Physical

Hoarseness is the most common presenting complaint of UVFP.[39] Symptoms that may also be reported include coughing, choking, aspiration, dyspnea, dysphagia, and globus sensation.

Dysphonia severity may relate to the paralyzed vocal fold's position. Laterally, patients often complain of a breathy voice and a poor or "bovine" cough due to air escaping through an abnormal glottal gap.[40][41] The gap forms as the paralyzed vocal fold cannot completely appose with the contralateral, nonparalyzed, vocal fold. Meanwhile, medial or paramedian lesions usually result in less severe dysphonia, and sensory symptoms may only be observed intermittently.[42]

Dysphagia is another common complaint due to the inability to close the glottis completely, thus impairing swallowing.[43] Severe dysphagia may lead to loss of airway protection, recurrent aspiration, and pneumonia.

Symptom onset, progression signs, accompanying neurologic changes, and antecedent trauma or infections are pertinent. Neoplastic, cardiovascular, or neurologic disease may be elicited in one's personal and family history. Chronic smoking, drinking, and carcinogenic exposures at home or work may be clues to a potentially malignant etiology.

A comprehensive physical exam should include a thorough head and neck examination to identify potential malignant sites. Thoracic pathology may damage the RLN as it descends at the level of the great blood vessels, so a complete inspection of this region is also vital.[44] A detailed neurologic examination may also help localize the lesion.[45] Patchy neurologic deficits may be indicative of multiple sclerosis.[46]

The vocal folds should be visualized either via mirror examination or flexible laryngoscopy. Stroboscopy can be a very useful adjunct. The vocal fold must be examined for residual movement in the paretic or paralytic fold, which can have prognostic and etiologic significance. Incomplete paralysis may suggest an evolving pathology, such as inflammation or infection, or recovery from one.[47] The paralytic fold's relative position—lateral or medial—should be noted to identify the potential pathology site and tailor the remainder of the workup.[48]

Evaluation

Patients presenting with UVFP immediately following thyroid or other neck surgery often do not require further formal workup. However, the operating surgeon must ascertain whether the nerve was physically intact at the end of the surgery. On the other hand, investigations of UVFP of unknown etiology should start with imaging of the RLN throughout its course from the skull base to the neck and chest. Both computed tomography and magnetic resonance imaging can provide adequate information, though the choice should be based on clinical presentation and physician preference. Evidence of cranial nerve involvement, especially if concerning for a high-vagal injury like the presence of palatal weakness, necessitates CNS and skull-base imaging.[49][50][51][52]

Laryngeal electromyography (LEMG) may specifically rule out cricoarytenoid (CA) joint dislocation as a cause of UVFP. CA joint dislocation would present with normal LEMG findings, indicating that neuromuscular function is intact.[53] LEMG is more commonly utilized for monitoring paralytic vocal fold recovery or response to laryngeal reinnervation procedures[54]. This modality is most useful at 1 to 6 months following the injury or onset of paralysis.

LEMG findings may include the following:

Normal motor unit potentials, indicating an intact neuromuscular junction
Fibrillation potentials, indicating denervation injury to the muscle
Polyphasic action potentials, signifying muscle reinnervation

These findings may be useful to help direct treatment options, depending on the clinical scenario.[55]

Treatment / Management

UVFP management should focus on removing the identified cause, preventing aspiration, and improving dysphonia. Treatment decisions must be tailored to each clinical scenario.

Idiopathic UVFP and its prognosis deserve special mention. Although not well-defined in the literature, this condition is believed to be secondary to a postviral or postinfectious insult, as happens in postviral facial paralysis and sensorineural hearing loss.

Sulica reported in 2008 that individuals who develop idiopathic UVFP do not completely recover vocal cord mobility at the same time, though vocal therapy can promote dysphonia resolution before full recovery. Most of these patients should recover fully a year after symptom onset.[56]

If the diagnostic workup does not find aspiration or any ominous pathology, a 12-month observation period and a speech therapy referral are recommended to see if the patient can regain vocal fold motion without aggressive intervention. Speech therapy can help patients recover vocal and swallowing functions and may negate the need for surgery even if complete vocal fold motion recovery does not occur[57].

Surgical interventions include temporary or permanent vocal fold augmentation, formal thyroplasty (medialization laryngoplasty), and arytenoid adduction. Vocal fold augmentation repositions the paralyzed vocal fold closer to the midline. Thus, the contralateral, fully functional true vocal fold can close the glottis during deglutition and phonation, helping prevent aspiration and improve dysphonia.

On the other hand, patients with UVFP and aspiration require a more aggressive approach, such as immediate injection augmentation, to protect the airway and prevent pneumonia. This procedure may still help patients without aspiration but are symptomatically dysphonic, as temporary injection augmentation can improve the voice. Hyaluronic acid is the preferred injectable agent if spontaneous recovery is expected.[58]

Permanent augmentation is indicated for patients with UVFP longer than 12 months. Permanent vocal-fold-augmentation options include formal thyroplasty and serial injections with longer-acting injectable materials, such as autologous fat.[59]

Teflon was a widely used injectable vocal-fold-augmenting agent in the past. However, this material is rarely used today, given the potential for morbidity from Teflon granuloma.[60] Historically, gel foam has also been used, though it lasts only 4 to 6 weeks.[61] By comparison, acellular dermal matrix (AlloDerm, Cymetra) can last 2 to 4 months. However, potential risks include intralaryngeal abscess and, if injected into Rienke's space, micronodule formation.[61] Calcium hydroxyapatite can last 18 months and has comparable safety and efficacy to hyaluronic acid.

Hyaluronic acid is the most widely studied injectable vocal-fold-augmenting material available in various brands. This material's viscosity is similar to that of natural mucosa and thus interferes less with the mucosal wave. Low-viscosity preparations are injected submucosally or into Rienke's space, while high-viscosity preparations can be injected intramuscularly.[62] Reported duration is variable but averages 4 to 12 months, depending on the brand or formulation used.[63]

Potentially permanent injectable materials include autologous fat and fascia. Both are advantageous in that they are completely autologous, living material. The long-term outcomes, however, have been extremely variable in terms of duration and phonatory results. For example, autologous fat has nearly the same viscoelastic properties as the native mucosa. However, fat's survival and duration of benefit are extremely variable. Thus, this option has fallen from favor in many centers.[64] Meanwhile, fascia can last years but is less widely used. Donor site morbidity remains a concern, and fascia has been described as less suitable for correcting wide glottic gaps.[65]

Injection augmentation can be performed under general anesthesia in a hospital setting with direct vocal cord visualization via microsuspension laryngoscopy. Alternatively, the procedure can be done percutaneously via nasolaryngoscopy in an office setting and with the patient awake.

Awake procedures in these cases may be indicated if multiple comorbidities can make general anesthesia risky.[66] Additionally, office-based injection has the benefit of immediate feedback regarding dysphonia resolution. However, one limitation of this approach is that injection might not be as accurately placed or as easy as compared to augmentation in an anesthetized patient.[67]

A more permanent surgical option is laryngeal framework surgery (medialization laryngoplasty or thyroplasty), commonly used in longstanding UVFP. The surgical detail of this procedure is beyond the scope of this article, but in brief, a window is made in the thyroid cartilage, and an implant is placed to medialize the true vocal fold. Various materials have been used, including Gore-Tex, Silastic implants, and Silicone blocks.[68]

Laryngeal reinnervation utilizes functioning nerves in the RLN's vicinity to reestablish laryngeal tone and movement. The ansa cervicalis, phrenic, and hypoglossal nerves have all been used as nerve pedicles with good voice outcomes[69].

Arytenoid adduction is specifically used to treat persistent or severe posterior glottic gaps.[54] A suture is suspended from the arytenoid muscular process anterior to the thyroid cartilage. Thus, the muscle can mimic the lateral cricoarytenoid's vocal-fold adducting effect. Although rarely used alone, this procedure may be a useful adjunct in treating UVFP in select cases.

Differential Diagnosis

The differential diagnosis of UVFP includes the conditions listed below. A thorough clinical evaluation and judicious use of diagnostic tests can help differentiate UVFP from these conditions.

Allergy and environmental asthma
Anaphylaxis
Asthma
Bilateral vocal fold paralysis
Epiglottitis
Exercise-induced asthma
Foreign body obstruction
Laryngeal abnormalities
Laryngeal edema from C1 inhibitor deficiency or ACE inhibitor use
Laryngeal spasm
Upper respiratory tract infection
Vocal polyps and nodules

Pertinent Studies and Ongoing Trials

Siu et al's systematic review revealed that injection thyroplasty, type 1 thyroplasty, laryngeal reinnervation, and arytenoid adduction do not exhibit significant differences in voice outcome or quality of life.[70] Type 1 Isshiki thyroplasty is often highly favored due to its greater long-term benefit over injection techniques. However, a growing body of evidence supports long-acting injectable materials' comparable longitudinal outcomes.[71] Thus, surgical intervention for UVFP should be reserved after a lack of response to a trial of conservative management has been demonstrated. The choice of surgical technique must be based on the surgeon's experience and patient preference.

Prognosis

The outlook for most patients with UVFP depends on the underlying pathology. Spontaneous recovery is expected in most individuals with idiopathic UVFP. However, cases with malignant and CNS etiologies have variable outcomes.[72]

Complications

The potential complications of UVFP include the following:

Aspiration pneumonia
Respiratory distress
Dysphagia
Decreased exercise tolerance
Psychosocial effects of vocal changes

Underlying conditions like malignancies, thoracic injuries, and neurologic disease also bring unique sets of complications, such as debility, paraneoplastic syndromes, and death.

Deterrence and Patient Education

Preventing UVFP involves addressing its potential underlying causes and minimizing the risk of RLN damage. Measures that can help patients include taking precautions to avoid neck and throat trauma, treating infections promptly, and going to regular health checkups. Some UVFP risk factors are beyond an individual's control, but maintaining overall health can minimize the risk of complications that might lead to this condition.

For clinicians, head and neck surgical and instrumentation procedures must be performed carefully. Providers should seek to improve competence in performing common procedures like ETT insertion by continuous training and simulation.

Enhancing Healthcare Team Outcomes

In summary, UVFP is a relatively common disorder presenting to otolaryngologists and other medical practitioners. The condition can arise from RLN and laryngeal lesions from sources like malignancy and iatrogenic injuries. Some common symptoms are hoarseness, coughing, choking, aspiration, dyspnea, dysphagia, and globus sensation.

Once identified, imaging from the skull base superiorly to the aortic arch inferiorly is necessary to evaluate the RLN for any lesions. Treatment plans vary depending on the patient and etiology, but options are generally focused on airway protection and improving dysphonia. In idiopathic UVFP, spontaneous recovery can be expected in most patients after a year. Interval speech therapy may improve long-term outcomes. Early injection medialization has also been shown to improve final voice outcomes.

UVFP is best managed with an interprofessional approach. Both primary care providers and specialists in clinical practice encounter this disorder often. Referral to an otolaryngologist is highly recommended for formal laryngoscopic evaluation, emphasizing the need for comprehensive care in UVFP cases. Early referral for speech therapy is beneficial in nearly all patients. The anesthesiologist may be involved if the vocal-fold-augmentation procedure is performed under general anesthesia. Surgical nurses' services are crucial in caring for patients with UVFP admitted for surgical augmentation or respiratory distress.

(Click Image to Enlarge)

<p>Unilateral Vocal Cord Paralysis After a Left Parathyroidectomy

Unilateral Vocal Cord Paralysis After a Left Parathyroidectomy. This image shows right vocal-cord abduction and left vocal-cord palsy.

Contributed by S Bhimji MD

Details

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