Unilateral vocal fold paralysis (UVFP) occurs from a dysfunction of the recurrent laryngeal or vagus nerve innervating the larynx. It causes a characteristic breathy voice often accompanied by swallowing disabilty, a weak cough, and the sensation of shortness of breath. This is a common cause of neurogenic hoarseness. When this paralysis is properly evaluated and treated, normal speaking voice is typically restored.[1]
Examples of vocal fold paralysis can be seen in the image and video below.
View Image
Preoperatively, the arrow demonstrates the paralyzed vocal fold, which is characteristically foreshortened, lateralized, and flaccid.
View Video
This patient was evaluated for hoarseness. One can appreciate immobility of the left true vocal fold. Stroboscopy in the second portion of the video shows the mucosal wave only with patient effort. Video courtesy of Vijay R Ramakrishnan, MD.
Workup in unilateral vocal fold paralysis
Computed tomography (CT) scanning or magnetic resonance imaging (MRI) of the path of the vagus/recurrent laryngeal nerve should be performed as part of a workup for a UVFP of unknown etiology. The imaging should include the entire path of the vagus/recurrent laryngeal nerve involved.
Other tests in the workup of UVFP include the following:
Voice evaluation - Voice recording provides documentation of the baseline voice quality and ability
Laryngeal electromyography (LEMG) - LEMG findings can be diagnostic and prognostic and can therefore be a useful tool to guide therapy
Management of unilateral vocal fold paralysis
Voice therapy can play a role in the treatment of UVFP. It can be used as sole treatment or as part of combined treatment with surgical medialization of the paralyzed vocal fold. Voice therapy is the primary treatment in patients who have a favorable (ie, median) position of their vocal fold paralysis and fairly equal tonicity between vocal folds, as well as in persons who are unwilling or unable to undergo surgery because of psychological or medical limitations.
Multiple surgeries are available for the treatment of UVFP, and they can be broadly categorized into temporary and permanent procedures. Temporary treatment involves endoscopic injection of a resorbable material into the affected vocal fold, lateral to the thyroarytenoid muscle in the paraglottic space.
Permanent vocal fold surgical treatment can be divided into vocal fold injection and laryngeal framework surgery.
Unilateral vocal fold paralysis (UVFP) most commonly occurs following a surgical iatrogenic injury to the vagus or recurrent laryngeal nerve. Thus, a history of head and neck, skull base, brainstem or chest surgery should be obtained. Specifically, thyroidectomy, carotid endarterectomy, anterior cervical spine surgery, thoracic, or mediastinal surgery most often result in a presentation of UVFP. In a study of 100 children, the incidence of vocal fold immobility after cardiothoracic surgery was 8%. These 8 patients were younger and weighed less than patients with normal vocal fold movement.[2]
The differential diagnosis for an acute UVFP should always include recent upper respiratory tract or viral infection and recent intubation for any surgical procedure. Procedures aimed at restoring glottic competence include permanent and temporary vocal fold injections, as well as laryngeal framework surgery, including medialization laryngoplasty (type 1 thyroplasty) and arytenoid adduction or arytenopexy.
Normal vocal fold function is reliant on vocal fold glottal closure that results from bilateral adduction of the vocal folds. Normally, this vocal fold adduction behavior, in combination with subglottic airflow, induces vocal fold vibration. Unilateral vocal fold paralysis (UVFP) results in glottal incompetence, either partial or complete, resulting in a weak or absent vocal fold vibration that leads to dysphonia. Significant muscle tension is often seen in the larynx as a compensatory mechanism for the glottal gap. Patients with UVFP often describe pain in the throat or neck after voice use, which is likely due to the excessive muscle tension.
Surgical iatrogenic injuries resulting in vocal fold paralysis include thyroid surgery, anterior cervical disc surgery, carotid surgery, or chest surgery.
Malignant invasion of either the vagus or recurrent laryngeal nerve can occur with skull base tumors, thyroid cancer, lung cancer, esophageal cancer, and metastases to the mediastinum (often observed with lung cancer primaries).
Blunt trauma to the neck or chest.
When a clear-cut etiology for the unilateral vocal fold paralysis (UVFP) is not found, it is classified as idiopathic. These cases can be attributed to a viral or inflammatory process, but this is usually a presumptive diagnosis.
The recurrent laryngeal nerve is responsible for both abduction and adduction of the vocal fold. The recurrent laryngeal nerve originates from the vagus nerve, which originates from the brainstem (nucleus ambiguous in the medulla) and travels along the carotid sheath (with the jugular vein and internal carotid artery). The left vagus nerve gives rise to the left recurrent laryngeal nerve as the vagus crosses the arch of the aorta. The left recurrent laryngeal nerve then loops under the ligamentum arteriosum and travels cephalad in the tracheoesophageal groove until it penetrates the larynx to innervate the intrinsic muscles of the larynx. The right vagus nerve delivers the recurrent laryngeal nerve branch at the level of the subclavian artery. The right recurrent laryngeal nerve loops around the subclavian artery and proceeds cephalad to the larynx.
The recurrent laryngeal nerve, just prior to its entrance into the larynx, runs deep to the inferior cornu of the thyroid cartilage. For a short section, the nerve is in a space between the cricoid and thyroid cartilage. This is thought to be the space where the nerve is vulnerable to compression from the cuff on an endotracheal tube that is either overinflated or positioned too far cephalad. Because of the circuitous nature of the recurrent laryngeal nerve, multiple disease processes and operative procedures put these important nerves at risk, often resulting in vocal fold paralysis.
Patients with unilateral vocal fold paralysis (UVFP) typically present with a fairly sudden onset of breathy, weak, low-pitched dysphonia. In some cases, however, the dysphonia can be high-pitched because of a compensated lengthening of the vocal folds to achieve better glottic closure. Often, UVFP is associated with dysphagia, specifically with liquids, because the resultant glottal incompetence can lead to aspiration. This is especially true if the UVFP is due to a high vagal lesion that results in both a recurrent laryngeal nerve and superior laryngeal nerve palsy. The latter results in significant anesthesia of the pharynx, contributing to the patient's dysphagia and increased risk for aspiration.
Patients with UVFP often report shortness of breath or a feeling of running out of air. Very little negative physiological impact upon pulmonary function actually occurs in patients with UVFP; however, because of the glottal incompetence, they experience significant air wasting and, thus, experience the sensation of shortness of breath and running out of air during speech. In addition, glottal closure is required for individuals to create positive end expiratory pressure (PEEP). Thus, some patients with an immediate postoperative UVFP can experience decreased pulmonary function because of loss of the natural PEEP that occurs with glottal closure. The glottic closure that allows a forceful cough is also compromised and thus a weak, unsuccessful cough is often reported by patients.
The indications for treatment of unilateral vocal fold paralysis (UVFP) are usually the resultant dysphonia or an ineffective cough in a patient at risk for aspiration or pulmonary compromise. If patients experience dysphagia, then they are at risk for aspiration pneumonia and treatment should be implemented as soon as possible. Improving glottic closure in the setting of UVFP and dysphagia often strengthens the voice and cough; however, it does not always correct the swallowing issue. Other sensory branches affecting the laryngopharynx may also be affected by the injury that caused the UVFP in the first place. Thus, patients should not be guaranteed improvement in their swallowing after augmentation of their vocal fold.
For dysphonia related to UVFP, treatment should be determined based on the patient's functional needs and demands, as well as on a new body of evidence that suggests early augmentation of an immobile vocal fold leads to better long-term voice outcomes (with or without return of physiologic function).[3]
Some patients do not notice any significant functional limitation related to their UVFP. This minimal functional limitation results because of the person's minimal voice demands or comorbidities that occur during postoperative recovery. A temporary injection is often given to allow for an immediate return of glottic competence while the nerve potentially recovers.
Electromyelography (EMG) can be used to determine the prognosis of RLN recovery, even if a temporary injection has occurred. If motion does not return and serial laryngeal electromyography shows no chance for meaningful recovery of vocal fold motion, then a permanent injection of fat, a semipermanent injection of calcium hydroxylapatite, or a medialization laryngoplasty can be offered.
In addition to patient history regarding functional aspects of voice use and voice demands, a standardized voice-related outcome measure can be used to assess the patient's vocal limitations and disability. The voice handicap index has been shown to be a reliable and useful patient-based survey instrument, quantifying the patient's voice handicap due to their voice disorder.
Nonsurgical treatment can be offered to patients with UVFP, especially those who are unwilling or unable to proceed with surgical treatment. However, with more evidence demonstrating better long-term voice outcomes when early temporary augmentation is given, it may be best to offer this to all patients with a vocal fold immobility less than 6 months in duration.[3]
The anatomy of the vagus/recurrent laryngeal nerve has been outlined above (see Pathophysiology), and its understanding is crucial to the evaluation of the potential etiology for patients who present with unilateral vocal fold paralysis (UVFP).
An understanding of both the internal and external laryngeal anatomy is important for the surgical treatment of UVFP. For patients who receive a vocal fold injection, an appreciation and thorough understanding of the anatomy of the membranous vocal fold, vocal process of the arytenoid cartilage, and paraglottic space is crucial for successful treatment.
Laryngeal framework surgery for the treatment of UVFP requires an understanding of the relationship and anatomy of the thyroid cartilage and cricoid cartilage. This is especially true regarding the relationship of the membranous vocal fold and paraglottic space to the external landmarks of the thyroid cartilage. For the more advanced laryngeal framework surgery techniques (eg, arytenoid adduction, cricothyroid subluxation), thorough knowledge of the anatomy of the cricothyroid joint and cricoarytenoid joint are required to be successful.
No contraindications exist for the nonsurgical treatment of unilateral vocal fold paralysis (UVFP) other than the patient not indicating or realizing the need for treatment. Contraindications for the surgical treatment of UVFP can include medical problems, such as severe cardiac or pulmonary limitations, or anticoagulation therapy. Although it carries a higher risk of non–life-threatening bleeding, injection of an anticoagulated patient has been routinely performed successfully in the author’s practice. Performing injections on a patient via a transoral or transcutaneous route under local or MAC anesthesia can also be done routinely in the riskier patient.[4]
A careful and detailed medical history and evaluation are required prior to deciding on surgical treatment for UVFP. Often, the most complete history is obtained in conjunction with an internal medicine physician and an anesthesiologist. A poorly abducting contralateral vocal fold is a relative contraindication for surgical treatment of UVFP because of the airway reduction that occurs with surgical medialization of the paralyzed vocal fold.
Although rarely obtained today for the workup of unilateral vocal fold paralysis (UVFP), chest radiography is sometimes the first screening evaluation for a patient with UVFP of unknown etiology, ordered by a physician for other comorbid chest symptoms. This may reveal a chest malignancy as the cause of the UVFP. A Pancoast tumor, a mediastinal mass, or even massive cardiomegaly may be found. The latter has been shown to be a cause of UVFP, albeit rarely, when enlargement of the left atrium results in a stretch injury to the left recurrent laryngeal nerve (Ortner syndrome).
CT scanning or MRI of the path of the vagus/recurrent laryngeal nerve should be performed as part of a workup for a UVFP of unknown etiology. The imaging should include the entire path of the vagus/recurrent laryngeal nerve involved. A left UVFP involves imaging from the base of skull to the mid chest (through the arch of the aorta). The right UVFP evaluation should extend from the base of the skull through the clavicle. Although CT is usually the test of choice, the decision between CT scanning and MRI is personal and can be decided by the otolaryngologist and radiologist.
However, indirect or direct flexible laryngoscopy remains the gold standard for the diagnosis of UVFP, with evidence existing that CT imaging should not be considered a reliable means for diagnosing this condition.
A blinded study by Bashir et al suggested that CT scanning is not as accurate a tool for predicting vocal fold paralysis as previous studies have implied. CT scans from two groups of individuals, those who had been diagnosed with UVFP and those with normal vocal fold movement, were examined by three radiologists for eight UVFP signs; the evaluators were unaware of which subjects belonged to which group. Based on whether or not the radiologists reached consensus on the presence of absence of a sign, medial displacement of the posterior margin of the ipsilateral vocal fold, dilation of the ipsilateral laryngeal ventricle, and dilation of the ipsilateral pyriform sinus had the highest sensitivities, at 78.8%, 69.2%, and 68.3%, respectively.[5]
The highest specificities were associated with mushroom sign, loss of the subglottic arch, thickening of the ipsilateral aryepiglottic fold, and anteromedial displacement of the ipsilateral arytenoid cartilage, at 97.4%, 97.4%, 94.9%, and 89.7%, respectively; these four signs also had the highest positive predictive values. Medial rotation of the ipsilateral aryepiglottic fold had a sensitivity and specificity of 60.6% and 66.7%, respectively. All eight signs had a low negative predictive value. When all of the CT-scan findings were taken into account, the sensitivity and specificity of the radiologists’ final diagnosis were 68.0% and 64.1%, respectively, with the positive predictive value being 83.3%.[5]
Voice evaluation by a speech-language pathologist is often helpful to determine the degree of maladaptive compensatory behavior present. In addition, voice recording provides documentation of the baseline voice quality and ability. This is important because treatment for the vocal fold paralysis usually begins shortly after evaluation. Often, this voice evaluation includes an objective analysis of the voice quality of the patient, including acoustic and aerodynamic analysis (air flow and laryngeal efficiency) of speech production.
Laryngeal electromyography (LEMG)
LEMG is an electrophysiologic evaluation of the muscles of the larynx. This test is performed using an EMG needle percutaneously under local or no anesthesia. The LEMG most often involves an evaluation of the thyroarytenoid/lateral cricoarytenoid muscle complex, which is reflective of the recurrent laryngeal nerve innervation and the cricothyroid muscle, which is indicative of the superior laryngeal nerve status/function.
LEMG findings can be diagnostic and prognostic and can therefore be a useful tool to guide therapy. LEMG can be used to differentiate between vocal fold immobility caused by cricoarytenoid joint pathology and that caused by vocal fold paralysis. The timing of LEMG is crucial in accurately determining the prognosis of spontaneous recovery of the paralyzed vocal fold. LEMG is most predictive of outcome if performed 6 weeks to 6 months after the onset of symptoms. LEMG can shorten the time until permanent treatment is implemented, subsequently reducing the time of the patient's dysphonia and the number of temporary treatments required.
Studies suggest a robust patient response to nimodipine in acute UVFP, with recovery of nerve function. Although these studies are small, nimodipine appears to be 50% more successful at stimulating nerve recovery than waiting alone. It is important, however, that the patient be able to tolerate any blood pressure issues related to the drug's use; nimodipine, a calcium-channel blocker, can cause hypotension, and patient blood pressure must therefore be monitored.[6]
A retrospective study by Sridharan et al found that in patients with acute VFP, the rate of recovery did not significantly differ between patients whose nimodipine treatment began within 15 days, 15-30 days, or more than 30 days after nerve injury, being 68.4%, 73.9%, and 54.5%, respectively.[7] It is recommended that nimodipine therapy begin any time prior to 4 months after the date of new vocal fold immobility from any cause.
Voice therapy
Voice therapy can play a role in the treatment of unilateral vocal fold paralysis (UVFP). Voice therapy can be used as sole treatment or as part of combined treatment with surgical medialization of the paralyzed vocal fold. Voice therapy is the primary treatment in patients who have a favorable (ie, median) position of their vocal fold paralysis and fairly equal tonicity between vocal folds, as well as in persons who are unwilling or unable to undergo surgery because of psychological or medical limitations.
In the setting of vocal fold paralysis, voice therapy is generally not a long-term treatment modality; substantive results are usually obtained in 2-3 sessions. Postoperative voice therapy used in combination with surgery is often used; however, 1-2 sessions of voice therapy prior to surgical treatment of UVFP can often be efficacious. This type of preoperative voice therapy focuses on vocal hygiene and establishes the principles of voice therapy that will be solidified during the postoperative period.
The most commonly used voice therapy techniques for UVFP include vocal hygiene and modification of voice use and the voice use environment. In addition, direct voice therapy techniques (eg, flow phonation, resonant voice and proper use of the respiratory support for phonation, phrase, and word timing) are often used. Preoperative voice therapy can decrease the secondary muscle tension dysphonia (MTD), while postoperative voice therapy can improve muscle strength, agility, and coordination.
Selective electrical stimulation
A retrospective study by Kurz et al indicated that in the treatment of early UVFP, selective electrical stimulation (SES) of the larynx produces functional improvement comparable to that obtained through voice therapy. The investigators reported that following as much as 3 months of therapy, vocal fold mobility was restored in 53.8% of the patients who underwent voice therapy and in 40% of those treated with SES, with both vocal folds in these patients demonstrating symmetrical abduction and adduction and no significant difference found with regard to vocal outcome and glottal configuration.[8]
Multiple surgeries are available for the treatment of unilateral vocal fold paralysis (UVFP), and they can be broadly categorized into temporary and permanent procedures. Temporary treatment involves endoscopic injection of a resorbable material into the affected vocal fold, lateral to the thyroarytenoid muscle in the paraglottic space. The resultant medialization of the paralyzed vocal fold improves vocal quality by restoring glottal competence and may improve swallowing function. Temporary vocal fold injection can be used when return of recurrent laryngeal nerve function is expected or when the prognosis for recovery is unknown during the first 6 months after onset of paralysis (especially when a favorable prognosis is found on LEMG).
There is also evidence to suggest that patients who receive a temporary vocal fold injectable for a newly diagnosed vocal fold immobility are statistically significantly less likely to undergo permanent medialization laryngoplasty (thyroplasty) compared with those patients who are treated with conservative management (watch and wait) alone.[3]
Many temporary injection materials are available. Radiesse voice gel is composed of water, glycerin, and sodium carboxymethylcellulose (an organic polymer used as a carrier in other injectable pharmaceutical products and an additive in gelatinous foods). Radiesse voice gel effectively medializes the paralyzed vocal fold for 1-3 months and does not require extra time to harvest, prepare, or reconstitute, which is common with other injectable materials.[9]
Hyaluronic acid (HA) is a polysaccharide ubiquitous in the extracellular matrix of most species and, therefore, is nonimmunogenic. Widely used as a filler by facial plastic surgeons, hyaluronic acid also can be used as a temporary injection material to medialize the paralyzed vocal fold, although it has a limited track record in laryngology.
Gelfoam is a bovine gelatin agent with a long history of safety, efficacy, and predictability, and, therefore, remains the most common injectable material today. Nevertheless, its disadvantages, such as a large (18 gauge) needle requirement and a short duration of effect (4-6 weeks), have prompted a shift toward newer, longer-lasting materials.
A retrospective study by Mattioli et al indicated that UVFP can be safely and effectively treated with endoscopic injection laryngoplasty using the silicone polymer polydimethylsiloxane, with good long-term results. The outcome of the study, of 26 patients, demonstrated significant improvement at long-term follow-up (mean period 73 mo) with regard to objective, perceptive, and subjective parameters. This material is not yet available on the US market.[10]
Permanent vocal fold surgical treatment can be divided into vocal fold injection and laryngeal framework surgery. Injection technique is similar to that with temporary materials: however, more permanent substances such as fat, fascia, or the semipermanent calcium hydroxylapatite (CaHA) are used.
Autologous fat is typically harvested from the patient's abdomen with liposuction technique. Variability in resorption somewhat limits the predictability of long-term voice outcomes and repeat lipoinjection may be necessary to achieve the desired results.
CaHA consists of calcium phosphorus in the form of microspheres in a gel carrier. The gel carrier resorbs, so slight overinjection (10-15%) is necessary; however, the microspheres have shown resorption on average over 18 months in a recent study.[11]
Teflon is acceptable only in patients with UVFP due to a terminal disease because of the significant long-term complication rate of Teflon granuloma formation. The incidence of Teflon granuloma formation is estimated to be over 50% with long-term follow-up, and the treatment of this complication usually requires surgery (often several) and permanent diminution in vocal function. With other options available, Teflon is rarely used today.
In November 2018, the US Food and Drug Administration (FDA) approved silk-HA for the treatment of UVFP. This compound is a mixture of HA cross-linked with purified silk proteins derived from the Bombyx mori silkworm. The material does degrade over time, being projected to last approximately 18 months, but its effects are proving to last longer due to the stimulation of fibroblasts by the silk and to collagen ingrowth to the silk-HA matrix. Silk-HA's permanence is being studied.[12, 13]
Both temporary and long-acting vocal fold injections are performed more frequently in an office-based outpatient setting. Newer injection materials with fine-gauge needles and chip-tip flexible endoscopes have facilitated this transition from the operating room to the office. The patient is seated in the sniffing position and the airway is topically anesthetized. Under endoscopic guidance, the paralyzed vocal fold can be injected via peroral or transcutaneous (thyrohyoid, transthyroid, or cricothyroid) routes. Advantages of office-based injections include patient convenience, cost savings, real-time monitoring of voice quality, and avoidance of general anesthesia.
Despite the increasing popularity and availability of long-acting injection materials, laryngeal framework surgery remains the criterion standard for long-term treatment of UVFP. Isshiki reintroduced laryngeal framework surgery for the treatment of UVFP to the world in 1974 when he described a type I thyroplasty. This was a concept that Payr initially described. The concept of medialization laryngoplasty is to medialize the paralyzed vocal fold from an external approach and work through the thyroid cartilage. A small window is incised and removed from the thyroid cartilage, and an implant is placed through the window to medialize the paralyzed vocal fold. See the images below.
View Image
Preoperatively, the arrow demonstrates the paralyzed vocal fold, which is characteristically foreshortened, lateralized, and flaccid.
View Image
Postoperatively, the image shows the same vocal fold as the image above following laryngeal framework surgery (arytenoids adduction and medialization ....
The most common implant used is a silastic block that is either sized from a variety of prefabricated implants or custom carved to address the 3-dimensional nature of the patient's UVFP. Gore-Tex is another implant option for medialization laryngoplasty and has been long regarded as a safe, well-tolerated implant in other parts of the body. Gore-Tex has dramatically increased in popularity in recent years because of its ability to be finely adjusted easily during surgery.
This operation has recently been widely accepted, and from a conceptual perspective, appears quite simple. A national survey found that complication rates with this procedure are higher in surgeons with inexperience or infrequent use of this operation. This most likely is related to the complex 3-dimensional anatomy of the vocal fold, paraglottic space, and implant design. Note that the implant design using medialization laryngoplasty must simultaneously address the treatment of the paralyzed vocal fold in the medial-lateral, superior-inferior, and anterior-posterior dimensions. Optimal voice results from medialization laryngoplasty involve appropriate consideration and treatment of the paralyzed vocal fold in all 3 of these dimensions with the implanted material.
More advanced and recent techniques for surgical treatment of UVFP using laryngeal framework surgery have involved manipulation of the arytenoid cartilage, namely arytenoid adduction.[14] Isshiki also pioneered arytenoid adduction, an operation that places the arytenoid cartilage in the most favorable position for rehabilitation of the paralyzed vocal fold. Isshiki described placing a suture through the muscular process of the arytenoid cartilage and drawing the suture anteriorly into the larynx (arytenoid adduction). Woodson and Zeitels have proposed modifications to the Isshiki procedure to enhance the arytenoid repositioning. The former suggests the placement of a second suture on the muscular process of the arytenoid and securing it to the lateral-inferior aspect of the cricoid to simulate the pull of the vertical belly of the posterior cricoarytenoid muscle.
Surgical treatment of the arytenoid cartilage for UVFP is important to restore optimal length/tension of the paralyzed vocal fold and to medialize the posterior glottis. The latter has become an indication for patients with severe dysphagia, especially those patients who have been identified to have aspiration pneumonia due to incompetence of the posterior glottis.
These operations are more technically challenging than a medialization laryngoplasty and are not required for every patient with UVFP; however, combined surgical treatment of UVFP with both an adduction procedure involving the arytenoid cartilage and medialization laryngoplasty has been found to yield maximal vocal rehabilitation by many leading surgeons. This is a reasonable conclusion because medialization laryngoplasty addresses the position and bulk of the membranous vocal fold while operations on the arytenoid address tension and length of the paralyzed vocal fold. Addressing all of the distinct and important features of the paralyzed vocal fold yields the best surgical result for this condition.
In 1999, Zeitels described a new laryngeal framework procedure for UVFP called cricothyroid subluxation.[15] This procedure involves anteriorly displacing the ipsilateral inferior cornu of the thyroid cartilage. This is performed by placement of a suture that runs from the inferior cornu of the thyroid cartilage to the midline of the cricoid cartilage. This effectively rotates the thyroid cartilage on the cricoid cartilage, providing additional length to the paralyzed vocal fold.
See the videos below.
View Video
Vocal fold paralysis, presurgery.
View Video
Vocal fold paralysis, postsurgery.
A retrospective study by Sanuki et al suggested that nerve-muscle pedicle (NMP) flap implantation may lead to reinnervation of the laryngeal muscles in patients with UVFP. In the study, 12 patients with the condition underwent a combination of refined NMP flap implantation and arytenoid adduction. Postoperatively, patients demonstrated improved phonatory function, while LEMG showed improved motor unit recruitment.[16]
During both in-office vocal fold injections and laryngeal framework surgery (thyroplasty and arytenoid adduction), voice is monitored. Voice quality is observed both perceptually and with laryngeal examination via flexible fiberoptic nasolaryngoscopy. This allows the surgeon to control or adjust the surgery to optimize the voice quality at the end of the procedure. This is an essential to high-quality phonosurgery and is the reason these procedures in general should not be conducted under general anesthesia. Today, vocal fold injections are commonly performed as office-based outpatient procedures with topical anesthesia.
After lipoinjection, patients are placed on voice rest to enhance the survival of the transplanted fat. This is typically for 5-7 days in duration. One or 2 days of voice rest are usually sufficient for other injectable materials, particularly those that use small (25- or 27-gauge) needles. No rest or minimal voice rest is necessary after laryngeal framework procedures.
A voice evaluation is indicated following surgical treatment of a unilateral vocal fold paralysis (UVFP). This evaluation should include a patient-based assessment of the voice function and head and neck examination, including indirect laryngoscopy and voice evaluation by a speech pathologist. The latter is important to assist in deciding whether the patient would be best served with postoperative voice therapy.
Complications of surgical treatment for unilateral vocal fold paralysis (UVFP) include poor voice outcome, airway difficulties, and migration of the medialization implant. Given that surgical treatment for UVFP involves manipulation of the airway, factors such as swelling or a hematoma from either laryngeal framework surgery or vocal fold injection can cause airway difficulties. Prevention of this complication involves meticulous and precise surgical technique and the use of preoperative and postoperative steroids. A greater risk exists for airway compromise and difficulties when a bilateral procedure is performed, such as bilateral medialization laryngoplasty or bilateral vocal fold injection (for UVFP or contralateral vocal fold atrophy).
Unless the surgery is performed strictly for dysphagia or pulmonary toilet/cough improvement, most surgical procedures for UVFP are elective in nature and are aimed at improving voice quality; if voice quality does not improve, this should be considered a complication of the procedure. Often, poor voice quality or the inability to improve the voice following laryngeal framework surgery can be rectified with revision medialization laryngoplasty, with or without an arytenoid adduction procedure.
The most common reason for poor voice quality following medialization laryngoplasty is improper placement of the thyroplasty implant in a too anterior and/or too superior direction. In addition, the implant size can be either too large or too small. Often, the implant is made too small because of a false sense of adequate medialization that occurs intraoperatively as a result of perioperative edema prior to implant placement of the thyroplasty implant. This can be prevented by the use of preoperative steroids, as well as expedient surgery, to minimize paraglottic edema prior to placement and sizing of the thyroplasty implant.
Thyroplasty implant migration can occur postoperatively, either medially into the airway or laterally into the neck. The former obviously is of great concern but appears to be rare. A single case report exists of complication of medialization laryngoplasty (silastic) caused by a delayed allergic response to the silastic implant.
Expected voice outcome following the treatment for unilateral vocal fold paralysis (UVFP) is excellent. Most patients resume normal speaking activities and functions and are able to meet all normal voice demands. Singing is a higher demand than speaking and may not be restored to its premorbid condition. The ability to project one's voice over a large area in a loud manner is also often never fully restored despite optimal medical, behavioral, and surgical treatment. Most patients should have a normal or near-normal speaking voice ability with minimal to no functional limitations of their everyday voice use following successful treatment.[17]
A prospective cohort study by Fang et al indicated that in patients with acute UVFP, the postinjury prognosis is poor in those who also suffer from combined involvement of the thyroarytenoid-lateral cricoarytenoid muscle complex and cricothyroid muscle.[18]
Understand that present surgical treatments only provide static improvement to the vocal fold and cannot provide the dynamic activity of the vocal fold to voice production that was present in the premorbid state.
Studies of the drug nimodipine in the setting of acute vocal fold immobility have shown promise in the recovery of actual vocal fold motion. While the use of nimodipine is not mainstream, ongoing research continues to indicate potential benefit from the agent.[19, 7]
Thus, the future goal of laryngology research is to create a method of dynamic rehabilitation of the paralyzed vocal fold. This goal has been present for decades, and much work has been devoted to the concept of reinnervation of the vocal fold. In humans, the optimal result from reinnervation is a static vocal fold but one that has tone. Often, laryngeal reinnervation is performed simultaneously or sequentially with medialization laryngoplasty. The future of laryngeal reinnervation is unknown but serves as a vast area for research and progress.
Thomas L Carroll, MD, Instructor, Department of Otolaryngology, Harvard Medical School; Director, Brigham and Women's Voice Program, Brigham and Women's Hospital
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Pentax Medical, Merck and Co., Bellus Health<br/>Scientific advisory board, stock options for Sofregen Medical ad N-Zyme for: Book Royalties from Plural Publishing.
Coauthor(s)
Clark A Rosen, MD, Director, University of Pittsburgh Voice Center; Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Merz North America Inc<br/>Received consulting fee from Merz North America Inc for consulting; Received consulting fee from Merz North America Inc for speaking and teaching.
Ryan J Soose, MD, Director, Division of Sleep Surgery, Assistant Professor, Department of Otolaryngology, University of Pittsburgh Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Robert M Kellman, MD, Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York Upstate Medical University
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Emeritus Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan; Neosoma; MI10;Invitrocaptal,Medtechsyndicates<br/>Received income in an amount equal to or greater than $250 from: Neosoma; Cyberionix (CYBX);MI10;Invitrocaptal;MTS<br/>Received ownership interest from Cerescan for consulting for: Neosoma, MI10 advisor.
Additional Contributors
John Schweinfurth, MD, Professor, Department of Otolaryngology, University of Mississippi Medical Center
Disclosure: Nothing to disclose.
Acknowledgements
Medscape Reference thanks Vijay R Ramakrishnan, MD, Assistant Professor, Department of Otolaryngology, University of Colorado School of Medicine, for assistance with the video contribution to this article.
Preoperatively, the arrow demonstrates the paralyzed vocal fold, which is characteristically foreshortened, lateralized, and flaccid.
This patient was evaluated for hoarseness. One can appreciate immobility of the left true vocal fold. Stroboscopy in the second portion of the video shows the mucosal wave only with patient effort. Video courtesy of Vijay R Ramakrishnan, MD.
Preoperatively, the arrow demonstrates the paralyzed vocal fold, which is characteristically foreshortened, lateralized, and flaccid.
Postoperatively, the image shows the same vocal fold as the image above following laryngeal framework surgery (arytenoids adduction and medialization laryngoplasty). The left vocal fold is now midline and has improved length.
Vocal fold paralysis, presurgery.
Vocal fold paralysis, postsurgery.
Preoperatively, the arrow demonstrates the paralyzed vocal fold, which is characteristically foreshortened, lateralized, and flaccid.
Postoperatively, the image shows the same vocal fold as the image above following laryngeal framework surgery (arytenoids adduction and medialization laryngoplasty). The left vocal fold is now midline and has improved length.
Vocal fold paralysis, presurgery.
Vocal fold paralysis, postsurgery.
This patient was evaluated for hoarseness. One can appreciate immobility of the left true vocal fold. Stroboscopy in the second portion of the video shows the mucosal wave only with patient effort. Video courtesy of Vijay R Ramakrishnan, MD.
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