The anatomy of the larynx (Figures 15–7 and 15–8) is best understood in the context of its function. The primary function of the larynx is to protect the airway from aspiration during swallowing. The epiglottis and aryepiglottic folds help direct food and liquids laterally into the pyriform sinuses and away from the midline laryngeal inlet. The paired arytenoid cartilages act as attachment points for most of the intrinsic muscles of the larynx, serving to move the vocal folds together (adduction) and apart (abduction). The false vocal folds and true vocal folds adduct to prevent entry of food or liquids into the airway.
Internal anatomy of the larynx as seen on endoscopy.
Cartilaginous and bony laryngeal framework.
The larynx also functions in respiration. Owing to reflex pathways in the brainstem, the glottis opens just prior to inspiration. Other laryngeal reflexes respond to subglottic pressure and hypercapnea. Additionally, initiation of swallowing causes a reflex period of involuntary apnea.
Phonation is the most uniquely human of the three functions of the larynx. At its most basic description, the glottic larynx produces a fundamental tone by the vibration of the free edge of the true vocal folds. This vibration is due to passive vibration of the vocal folds from air moving past the opposed free edges. Changing the tension within the vocal fold changes the pitch at which the vocal fold vibrates.
Several cartilages comprise the framework of the larynx (Figure 15–8). The thyroid cartilage is the largest laryngeal cartilage. This shield-shaped cartilage is responsible for the anterior neck prominence, sometimes called the “Adam’s apple” in lay terminology, and it provides protection to the internal components of the larynx. The cricoid cartilage lies inferior to the thyroid cartilage and serves as the major support for the larynx. It is the only complete cartilaginous ring within the upper airway. Internally, the paired arytenoid cartilages articulate with the cricoid cartilage, and attach to the vocal folds. Movement of the arytenoids results in abduction or adduction of the vocal folds. The epiglottis is a flexible cartilage located above the larynx. It is not involved in structural support of the larynx, but serves to assist in protecting the airway during deglutition (swallowing).
Innervation to the larynx is provided by the vagus nerve (cranial nerve X). The vagus nerve originates from three nuclei located within the medulla—the nucleus ambiguous, the dorsal nucleus, and the solitary tract nucleus. All motor fibers (and thus laryngeal motor innervation) originate from the nucleus ambiguous. The dorsal (parasympathetic) nucleus is the origination for efferents to involuntary muscles of the bronchi, esophagus, heart, stomach, and intestine. Sensory innervation from the pharynx, larynx, and esophagus terminates in the solitary tract nucleus. The vagus nerve exits the skull base through the jugular foramen. It descends in the neck behind the jugular vein and carotid artery and sends pharyngeal branches to the muscles of the pharynx and soft palate. The superior laryngeal nerve arises directly from the vagus, and has an internal and external branch. The internal superior laryngeal nerve enters the larynx through the thyrohyoid membrane and supplies sensation to the larynx above the true vocal cords. The external superior laryngeal nerve innervates the cricothyroid muscle, the only muscle of the larynx not innervated by the recurrent laryngeal nerve. The right recurrent laryngeal nerve arises from the vagus and loops around the subclavian artery. The left recurrent laryngeal nerve arises more distally in the thorax, and loops around the aortic arch. Both recurrent laryngeal nerves then ascend in the tracheo-esophageal grooves, and enter the larynx near the cricothyroid joint. The recurrent laryngeal nerves provide motor innervation to all of the intrinsic muscles of the larynx except the cricothyroid. A summary of the laryngeal muscles is provided in Table 15–4.
Table 15–4.Major muscles of the larynx. ||Download (.pdf) Table 15–4. Major muscles of the larynx.
|Muscle ||Function ||Innervation ||Key Point |
|Posterior cricoarytenoid ||Abducts vocal folds, tenses vocal folds ||Recurrent laryngeal nerve ||ONLY abductor of vocal folds |
|Lateral cricoarytenoid ||Adducts true vocal folds ||Recurrent laryngeal nerve || |
|Interarytenoid ||Adducts posterior glottis ||Recurrent laryngeal nerve ||ONLY laryngeal muscle receiving bilateral innervation |
|Oblique arytenoids ||Closes laryngeal inlet during swallowing ||Recurrent laryngeal nerve || |
|Thyroarytenoid ||Adducts, tenses vocal fold ||Recurrent laryngeal nerve || |
|Cricothyroid ||Increase vocal fold tension, especially at higher pitches ||External branch of superior laryngeal nerve ||ONLY muscle not innervated by recurrent laryngeal nerve |
Urgencies and Emergencies
A. Pediatric Airway Obstruction
The rapid and accurate evaluation of a child in respiratory distress is one of the most critical skills an otolaryngologist must master. Noisy breathing and respiratory distress have multiple etiologies, and differentiation between acute emergencies and chronic conditions is essential. An important point to learn early on is that not all noisy breathing is stridor.
True stridor may represent an impending airway failure, and thus must be distinguished from other upper airway noises that are sometimes mistakenly referred to as “stridor.” Airway obstruction at the level of the nasopharynx produces snoring sounds, or stertor. Tracheobronchitis can produce a wheezy, barking cough characteristic of croup. Asthma, tracheobronchial foreign bodies, and bronchomalacia can produce wheezing. “Stridor” specifically refers to the noise that is produced by air movement through a partially obstructed airway. Inspiratory stridor usually signifies an obstruction above the level of the vocal cords, while expiratory stridor most often occurs with subglottic obstruction. Biphasic stridor usually signifies an obstruction at the level of the vocal cords or subglottis.
The immediate concern in evaluating a child with stridor is verifying or establishing a stable airway. The initial evaluation should consist of non-invasive examination to avoid exacerbating a potentially unstable airway. If the child is in acute respiratory distress, evaluations such as flexible fiberoptic laryngoscopy should not routinely be performed.
A careful history should be obtained, including the duration of the stridor and relationship to feedings. Parents should be questioned about any change in symptoms with position changes. Presence of any birth or intrauterine complications, history of intubation, as well as congenital anomalies should be determined.
If the child is not in acute distress, flexible fiberoptic laryngoscopy may provide valuable diagnostic information. This can be done with the child awake and restrained, or under general anesthesia with spontaneous ventilations. This allows determination of nasopharyngeal and supraglottic anatomy, as well as vocal cord motion. If available, the examination should be recorded to allow playback and review, as real-time examination can be problematic in an often-uncooperative child.
Other investigations should be based on the presence of suggestive symptoms. Swallowing function is often impaired in children with stridor, and should be evaluated. Vascular rings may produce extrinsic compression of the esophagus and trachea leading to stridor, feeding difficulties and failure to thrive. An altered, weak, or absent cry from birth can suggest neurologic impairment. Recurrent pneumonia or excessive cough with feeding may be present with vocal cord impairment, severe reflux, or tracheoesophageal fistula.
One of the most common causes of pediatric stridor is laryngotracheobronchitis, or croup. This is an acute viral illness, most commonly caused by the parainfluenza virus. The typical patient is an infant or young child with low-grade fever, seal-like barking cough, and occasionally biphasic stridor. The classic radiographic finding is a “steeple” sign visible on AP views, indicative of the characteristic narrowed subglottic airway from edema. The typical course for most patients is resolution over several days and few patients require hospitalization. Signs of respiratory distress including tachypnea, retractions, and cyanosis may necessitate closer observation such as hospitalization. For these more severe cases, treatment with humidified air, nebulized racemic epinephrine, and systemic steroids may be indicated. Manipulation of the airway may exacerbate the clinical situation, and should be avoided unless clearly indicated.
Epiglottitis is fortunately becoming vanishingly rare in most industrialized countries, owing to nearly universal vaccination of children against H influenzae type B. If recognized and managed appropriately (with aggressive airway control) outcomes are usually excellent. If managed conservatively, epiglottitis is associated with up to 6%-10% mortality. Patients present with high fever, drooling, and odynophagia and are usually toxic in appearance. Of note, epiglottitis tends to progress quite rapidly; patients can decompensate clinically in a matter of hours. The characteristic position naturally assumed by patients with epiglottitis is the leaning forward position, to maximize their marginal airway opening. Even oral cavity examination with a tongue blade can precipitate an airway crisis; therefore evaluation and treatment ideally consists of immediate control of the airway in the operating room under general inhalational anesthesia. A cherry-red epiglottis will be visible on endoscopic examination. Pharyngeal and blood cultures should be obtained, and the child started on broad spectrum IV antibiotics such as ceftriaxone. Once definitive identification of the culprit organism is made antibiotic selection can be narrowed appropriately. Children are left intubated until air leak around the endotracheal tube is evident.
Chronic pediatric stridor is most often due to laryngomalacia. Parents will usually report onset of symptoms shortly after birth. It often worsens initially, but in the vast majority of cases resolves without the need for intervention, usually by 12-18 months. A variety of factors have been hypothesized to contribute to laryngomalacia including neurologic, muscular, and reflux-induced inflammation. The stridor is worsened while crying or in an excited state, and is usually relieved by placement in the prone position. Flexible fiberoptic laryngoscopy reveals collapse of floppy supraglottic structures such as the epiglottis and aryepiglottic folds. There is a strong association of laryngomalacia with reflux, and presumptive treatment with an acid blocking medication (such as ranitidine) may be beneficial. Surgical treatment of the supraglottis is reserved for severe cases such as patients with cyanosis or failure to thrive. The most common procedure is aryepiglottiplasty, where cold knife or carbon dioxide laser is used to excise redundant mucosa over the arytenoid cartilages. Rarely, tracheostomy may be necessary.
Subglottic stenosis is the second most common cause of chronic pediatric stridor. Causes include both congenital stenosis, and acquired (most often from prolonged intubation). Typically, patients have recurrent “croup” and biphasic stridor. If present in older children, the patient may only become symptomatic periodically, in association with upper respiratory tract infections. Diagnosis requires endoscopic evaluation, and can be defined as a subglottic airway diameter of less than 4 mm in full-term infants and less than 3 mm in premature infants. Pediatric subglottic stenosis is traditionally graded according to the Cotton scale (Table 15–5). Tracheotomy may be required in moderate to severe cases. Treatment of subglottic stenosis can consist of tracheal dilatation (either by rigid serial dilation or controlled radial expansion balloon), debridement by microdebrider or carbon dioxide laser, cricoid split, or laryngotracheoplasty.
Table 15–5.Summary of the Cotton grading system for subglottic stenosis. ||Download (.pdf) Table 15–5. Summary of the Cotton grading system for subglottic stenosis.
|Grades ||Degree of Subglottic Obstruction |
|Grade 1 ||Less than 50% obstruction |
|Grade 2 ||50%-70% obstruction |
|Grade 3 ||71%-99% obstruction |
|Grade 4 ||100% obstruction |
B. Foreign Body Aspiration
Airway foreign body typically involves children between 1 and 4 years of age, but can occur in any age group. Children in this age range tend to place objects in their mouths and lack molars for grinding of food. Objects can range from peanuts (most common) to coins, marbles, and toy products. Adult foreign body aspiration is usually associated with food, typically meat. Foreign body aspiration is potentially life threatening and it is recognized as the fifth most common cause of unintentional-injury related mortality in the United States. Pharyngeal foreign body (most commonly in the vallecula) represents a potential impending airway foreign body, and should be treated as such.
The clinical presentation of patients with airway foreign body depends on the anatomic location. Patients with pharyngeal or hypopharyngeal foreign bodies typically present with dysphagia, odynophagia, and occasionally drooling from inability to tolerate secretions. If large objects become lodged in the larynx, patients may present with pain, dysphonia, inspiratory stridor, and dyspnea. Tracheal foreign bodies produce both inspiratory and expiratory stridor. Distally located foreign bodies (Figure 15–9) often lodge in the right bronchus (especially in adults). This is due to the angles at which the left and right mainstem bronchi branch off the trachea, with the right being a less acute angle. Distal foreign bodies typically produce unilateral wheezing and decreased breath sounds. A history of acute choking episode is very common and is 76%-92% sensitive in diagnosing foreign body aspiration.
Airway foreign body in a 4 year old. The patient in question had a history of brief choking while eating dinner three nights earlier, followed by intermittent nonproductive cough. He had a normal chest x-ray and slight wheezing heard on one side only. On rigid bronchoscopy, a soft green bean was found in a right distal bronchus.
Acute management of airway foreign body is dictated by patient condition. In a conscious patient who is able to exchange air and cough, an attempt at foreign body removal should not be made immediately. Unconscious patients, or victims unable to cough or move air require immediate intervention. If the means for performing a cricothyrotomy or tracheotomy are not available, the Heimlich maneuver can be performed as three manual abdominal thrusts to compress the lungs and potentially produce enough airway pressure to dislodge the foreign body. For patients without impending loss of airway, anteroposterior and lateral radiographs of the airway including larynx and chest can be helpful. While only radio-opaque foreign bodies can be visualized, radiographs may demonstrate obstructive emphysema, atelectasis, or consolidation. Additionally, they can provide a baseline study for future comparison.
Definitive removal of an airway foreign body requires general anesthesia, and direct laryngoscopy. Distally located foreign bodies are best addressed with rigid bronchoscopy for removal. A clear history consistent with aspiration often should prompt operative evaluation, even if specific symptoms (stridor, unilateral wheezing, decreased breath sounds) are lacking, as these may be absent in up to 40% of cases. Suspected nut aspiration (common in children) should be treated aggressively. Local tissue reactions to the nut oils and proteins are common, and can be robust. Post removal, patients with peanut aspiration may require intensive care unit observation and ventilatory support while the inflammatory reaction resolves.
Laryngeal trauma is rare, representing 1 out of every 14,000-42,000 emergency room visits. Quick recognition of laryngeal trauma is essential as it can rapidly lead to death. Up to one-third of laryngeal trauma victims die prior to arrival to a hospital setting.
Laryngeal trauma can be classified as blunt or penetrating. Blunt laryngeal trauma results from crushing of the laryngeal framework against the cervical spine, and usually results from motor vehicle accidents. Other common etiologies include strangulation type injuries, and clothesline injuries. Penetrating laryngeal trauma usually results from projectile injury, such as a gunshot, or knife wounds to the neck.
Every patient with trauma to the neck should be evaluated for potential laryngeal trauma. Patients may report dyspnea, hoarseness, or aphonia. Other less common symptoms include dysphagia, anterior neck pain, and odynophagia. Evaluation should begin with the ABCs of trauma–airway, breathing, circulation. Severe laryngeal trauma (particularly clothesline-type injuries) can result in loss of airway and necessitate the need for immediate tracheotomy. Physical findings common in patients with laryngeal trauma include stridor, subcutaneous crepitance (emphysema), bruising or edema to the anterior neck, loss of palpable landmarks, and hemoptysis. As outlined above (stridor and airway obstruction) the type of stridor can often give an indication of the site of airflow obstruction.
Further evaluation of laryngeal trauma is dictated by the patient’s condition. If an adult patient’s airway is unstable, most experts would advocate awake tracheostomy or cricothyrotomy under local anesthesia, as endotracheal intubation in the setting of laryngeal trauma can be problematic. For unstable pediatric laryngeal trauma, inhalational anesthetic followed by rigid endoscopic intubation is recommended by many experts. Once a stable airway has been determined or secured, evaluation can proceed.
Flexible fiberoptic laryngoscopy is advocated for awake, stable patients. The airway should be evaluated for vocal cord mobility, edema, laryngeal lacerations, and hematomas. Because the underlying mechanism of injury often results in damage to other adjacent structures, laryngeal trauma patients should undergo complete cervical spine radiography, and evaluation for esophageal or vascular injury should be considered. Some authors recommend fine-cut CT imaging of the larynx to help guide treatment planning. It should be emphasized that CT scanning rarely provides useful information regarding the immediate airway management for patients suspected of having laryngeal trauma, but often provide helpful information regarding surgical planning for repair.
Management of the patient with laryngeal trauma depends on the severity of injury. Patients with small laryngeal hematomas, small lacerations not involving the vocal fold edge or anterior commissure, and nondisplaced stable thyroid cartilage fractures can often be managed without tracheostomy. Most such patients should be hospitalized for 24 hours of airway observation and placed on systemic steroids, humidified air, and proton pump inhibitor (PPI) therapy. If mucosal disruption is present antibiotics should be initiated.
More severe laryngeal traumas often require tracheotomy and direct laryngoscopy or even open laryngeal exploration and repair. This should ideally be performed within 24 hours of the initial injury. Open laryngeal exploration is performed via a midline thyrotomy approach. A horizontal skin incision is made at the level of the cricothyroid membrane. Subplatysmal flaps are elevated, and the strap muscles divided at the midline. The airway is then entered in the midline of the cricothyroid membrane, and a vertical incision through the midline thyroid cartilage extended superiorly. Care must be taken to avoid injury to the underlying endolaryngeal mucosa. Following this, the mucosa is incised allowing inspection of the endolarynx. Once the endolarynx is exposed, all mucosal lacerations should be repaired to cover all exposed cartilage. If the anterior commissure is disrupted, a laryngeal stent may need to be placed, although placement of a stent itself leads to some degree of laryngeal injury. If placed, stents should be removed as soon as possible, usually around 2 weeks.
Outcomes for laryngeal trauma patients are fairly good once initial control of the airway is obtained. Most patients usually achieve a stable airway and undergo decannulation, which may take from 1 to 6 months or longer depending on the extent of injury. Overall, up to 90% of patients can recover a satisfactory vocal quality if managed appropriately.
Hoarseness or dysphonia is defined as an alteration in the quality or character of phonation. Patients may describe their voice as breathy, harsh, or rough. Common etiologies of hoarseness include viral illness, vocal fold paralysis, laryngopharyngeal reflux (LPR), laryngeal polyps, allergy, vocal abuse, dysplasia, and cancer.
Patients should be questioned about onset, frequency, and nature of the hoarseness. As previously discussed, the larynx is an essential part of swallowing, and any history of coughing or choking after eating should be elicited. Likewise the patient should be questioned about recurrent episodes of pneumonia. Any history of intubation, head and neck trauma, or previous head and neck surgery should be sought. Patients should be questioned about smoking and alcohol use.
Physical examination begins with a full head and neck examination. It is important to visualize the larynx. Methods of visualization include indirect mirror examination, rigid endoscopy, or transnasal flexible fiberoptic laryngoscopy. Videostroboscopy offers invaluable information about vocal fold motion and can identify adynamic segments and altered areas of mucosal wave propagation.
One common benign cause of hoarseness is vocal polyps. These are due to local tissue inflammation. Vocal nodules are distinct from polyps, and always occur bilaterally. They are most often a result of vocal abuse/misuse and usually respond dramatically to voice therapy. Vocal fold granulomas are usually due to extra-esophageal acid reflux damage.
Hoarseness can also be the presenting symptom for cancer, most often for cancer of the true vocal folds. The vast majority of laryngeal cancer is squamous cell cancer, and smoking is the biggest risk factor for its development. Laryngeal cancer is discussed further in the section Head and Neck Cancer. While early stage laryngeal cancer is highly curable, advanced stage carries a dramatically reduced prognosis. Thus, any patient with hoarseness lasting longer than 2 weeks should be evaluated and undergo visualization of their larynx.
B. Laryngopharyngeal Reflux
LPR impacts hundreds of thousands of patients annually, with some studies estimating as many as 30% of Americans may suffer from some degree of LPR. It is increasingly clear that LPR is a disease separate and distinct from classic gastroesophageal reflux disease (GERD). Patients with LPR typically present with frequent throat clearing, globus sensation, cough and hoarseness (as opposed to postprandial heartburn with GERD).
Physical examination of patients suspected of LPR should include an examination of the larynx, most commonly by flexible transnasal fiberoptic laryngoscopy. Hoarseness is not pathognomonic for LPR, and can also be present in more serious disorders. Several laryngeal findings are common in patients with LPR. Presence of vocal cord granuloma or pseudosulcus vocalis, although uncommon, is highly suggestive of LPR. Other common laryngoscopic findings consistent with LPR include posterior laryngeal hypertrophy, laryngeal edema and erythema, cobblestoning, or posterior commissure bar.
The diagnosis of LPR relies on a combination of symptoms and physical findings rather than one isolated factor being pathognomonic. Several studies have demonstrated the presence of many of the above symptoms and laryngeal findings in healthy, normal control patients. Many clinicians advocate the use of a metric scale that combines multiple common symptoms or physical findings. Two such instruments are the reflux finding score (RFS) and the reflux symptom index (RSI). In general, an RFS of greater than 8 is suggestive for LPR, and a score of greater than 13 on the RSI is likewise indicative of LPR.
Treatment for LPR currently consists of PPIs as a first-line therapy with surgery (eg, Nissen fundoplication) for selected treatment failures. It should be pointed out that although multiple uncontrolled studies have demonstrated benefit of PPIs for the treatment of LPR, the majority of randomized controlled trials have failed to confirm this. Possible confounding factors include lack of clear “gold standard” for the diagnosis of LPR, and differing treatment regimens. Our current practice is to place patients with LPR on once-daily PPI therapy for a 3- to 6-month period, after which response to treatment is assessed. The extended length of time is critical, as studies have shown that resolution of laryngeal findings can take up to 6 months to resolve once PPI therapy is initiated. If there is no response to once-daily PPI therapy, the patient can be advanced to twice-daily PPI therapy. Disease severity can prompt initiation of PPI therapy at twice-daily dosing; severe laryngeal edema or presence of subglottic stenosis would be two such indications.
It should also be mentioned that if a patient is diagnosed with LPR, some form of evaluation of the esophagus should be undertaken. There is up to a 20% incidence of unsuspected esophageal abnormalities in patients with LPR. This evaluation can take the form of imaging modalities such as barium swallow, or endoscopic examination such as esophagoscopy.
C. Vocal Cord Immobility/Paralysis
Vocal cord mobility problems represent a wide range of etiologies characterized by diverse patient presentation and prognostic outcomes. The distinction between unilateral and bilateral, and between paretic (hypomobile) versus paralyzed cords is imperative.
Patients with unilateral vocal cord paralysis may be asymptomatic, but often present with a hoarse, breathy voice. Their voice often starts out stronger in the morning and worsens throughout the day as they develop vocal fatigue. Accompanying symptoms can include frequent throat clearing, cough, vague globus sensation, and aspiration. Often patients will report subjective shortness of breath or a feeling of “running out of air” despite normal pulmonary function. This is secondary to glottal incompetence (lack of apposition of the vocal folds) resulting in escaped air during phonation. Thus a patient with unilateral vocal fold paralysis may be able to climb a flight of stairs without difficulty, yet feel short of breath when attempting to carry on a telephone conversation. Patients should be questioned specifically about swallowing, weight loss, recent illnesses or intubations, and surgeries (especially cardiac, cervical spine, and thyroid procedures).
The etiologies of vocal cord paralysis reflect the diverse nature of illnesses and injuries that can result in the final common pathway of vocal cord immobility or paralysis. The vocal cords derive their innervation from the vagus nerve, and any injury along the course of this nerve may result in vocal cord paralysis. Unilateral vocal cord paresis is by far the most common, with bilateral representing less than 20% of all paralysis. Historically, the most common cause of unilateral vocal cord paralysis was malignancy (such as lung cancer or skull base tumors). More recent studies show that iatrogenic surgical injury is now the most common cause. Nonthyroid surgical procedures (including anterior approaches to the cervical spine and carotid endarterectomy) now account for the majority of these iatrogenic injuries. Thyroid surgery remains the most common cause of bilateral vocal cord paralysis. Table 15–6 summarizes the most common causes of vocal fold paralysis. It should be noted that laryngeal manifestations of rheumatoid arthritis can rarely mimic vocal cord paralysis, although the underlying problem in this case is vocal cord immobility secondary to fixation of the arytenoid cartilages.
Table 15–6.Most common causes of vocal cord paralysis. ||Download (.pdf) Table 15–6. Most common causes of vocal cord paralysis.
|Unilateral Vocal Cord Paralysis (%) || |
|Surgical injury ||37 |
| Cardiovascular, anterior cervical spine procedures ||(51) |
| Thyroid surgery ||(33) |
|Idiopathic (viral, inflammatory) ||19 |
|Malignancy ||18 |
|Intubation-related injury ||6 |
|Trauma ||6 |
|Bilateral Vocal Cord Paralysis (%) || |
|Surgical injury ||37 |
| Cardiovascular, anterior cervical spine procedures ||(10) |
| Thyroid/parathyroid surgery ||(90) |
|Malignancy ||14 |
|Intubation ||13 |
|Idiopathic (viral, inflammatory) ||11 |
|Neurologic (Wallenberg syndrome, Parkinson, multiple sclerosis, Guillain-Barre, others) ||11 |
|Trauma ||7 |
It is important to note that vocal cord immobility or paralysis is a sign of pathology and not a diagnosis. Thus the first concern when evaluating a patient with vocal cord paralysis should be investigation of the etiology. Often the cause is not identifiable, and the vocal cord paralysis is deemed idiopathic. A thorough head and neck examination should be performed, including endoscopic evaluation of the larynx. This most often is by flexible fiberoptic laryngoscopy, with most laryngologists recommending videostroboscopy as well. For unilateral recurrent laryngeal nerve injury, the affected immobile cord will usually lie in a paramedian position. This is due to lack of abduction, with some retained adduction (due to the cricothyroid muscle, which is innervated by the superior laryngeal nerve). For more proximal vagal lesions, the affected cord will usually rest in intermediate position, due to loss of both abduction and adduction innervation. There is also loss of sensation to the affected hemilarynx, and aspiration is common.
Diagnostic testing should include a chest radiograph and CT scan following the entire vagus nerve course (ie, neck and chest, from skull base to the mid-chest). More esoteric tests are likely to be low yield and poorly cost-effective, and should be reserved for more selective use. Many laryngologists advocate the use of laryngeal electromyography (EMG). This test is performed percutaneously, and tests the superior laryngeal nerve and recurrent laryngeal nerve by evaluating motor unit electrical activity in the cricothyroid and thyroarytenoid muscles, respectively. Laryngeal EMG can provide useful information regarding the degree and likely site of injury (central vs peripheral), as well as the potential for spontaneous recovery. It is most predictive if performed 6 weeks to 6 months after initial injury.
Initial therapy for unilateral vocal cord paralysis consists of observation and speech therapy. Often the opposing vocal cord can compensate by crossing the midline and closing the glottal gap. This can produce an acceptable vocal quality, usually occurring within a 3-6 months time span. Patients not obtaining a good result using these conservative measures can be treated by a variety of surgical interventions. The goal of surgical treatment for unilateral vocal cord paralysis is medialization of the affected cord. This reduces the glottic gap and allows the opposing, innervated cord to contact the other vocal fold with less effort. Treatment selection for unilateral vocal cord paralysis depends on the potential for recovery. In cases such as iatrogenic surgical injury with little chance of spontaneous recovery, definitive therapy can be initiated early. For idiopathic causes, a more conservative approach is usually advocated. Overall, up to 60% of patients with idiopathic unilateral vocal cord paralysis will recover to a near-normal voice within 8-12 months. Thus, most experts would recommend waiting at least 1 year before proceeding with definitive therapy. Clear indications for earlier intervention include significant dysphagia and aspiration from glottic incompetence.
Definitive surgical procedures for unilateral vocal fold paralysis include laryngeal framework surgery, injection of longer lasting material, and reinnervation techniques. The thyroplasty technique (a laryngeal framework surgical procedure) is performed through an external skin incision. After exposing the thyroid cartilage, a window is cut in the thyroid ala overlying the position of the vocal fold on the affected side. An implant is then placed in a subperichondrial window, thus pushing the vocal fold toward the midline. Implants can include Silastic, autologous cartilage, and Gore-Tex. Most laryngologists perform this procedure with the patient lightly sedated. A flexible fiberoptic laryngoscope can be suspended in position, and the patient is asked to phonate periodically so that the surgical effects can be evaluated in real time and adjusted accordingly.
Another common surgical intervention is injection medialization. This can be performed as an office-based procedure using only local anesthesia, or in the operating room under general anesthesia. In either case, a variety of injectable materials are placed within the vocal fold lateral to the vocal process, to medialize the cord. In the past, Teflon was commonly used for this purpose, but has now largely fallen out of favor secondary to a high rate of complications. An alternative, long lasting (but not permanent) injectable is calcium hydroxyapetite microspheres in methylcarboxycellulose carrier gel (Radiesse Voice). Temporary injectables include gelfoam paste, hyaluronic acid, micronized cadaveric dermis (Cymetra), cross-linked collagen (Zyderm), and methylcarboxycellulose gel (Radiesse Voice Gel).
Surgical reinnervation for unilateral vocal cord paralysis is gaining popularity. Approaches can include nerve-muscle pedicle (using the omohyoid and ansa hypoglossi nerve) and direct nerve-nerve reinnervation (ansa cervicalis to recurrent laryngeal nerve). Results from these techniques are generally good, but can take 6 months or longer to be realized. For this reason, many surgeons combine reinnervation with injection medialization using a temporary substance.
For bilateral vocal cord paralysis, treatment approaches have a different perspective. Whereas restoration of voice is the primary goal for unilateral paralysis, resolution of potential or actual airway compromise is of tantamount importance in cases of bilateral paralysis. Most patients are initially treated with a tracheotomy to bypass the glottic obstruction. One common surgical procedure is lateralization of the vocal folds by arytenoidectomy. While this usually provides a patent airway and allows decannulation (reversal of the tracheotomy) the patient’s vocal quality usually suffers significantly.
Another surgical approach, partial posterior cordectomy) can often preserve vocal quality to some degree, while providing improved airway. This approach uses a laser through a surgical laryngoscope to remove a c-shaped wedge from the posterior portion of one vocal cord. This preserves a bilateral vibratory margin anteriorly while providing an airway posteriorly. The technique is often best performed as multiple less aggressive procedures to fine-tune vocal quality versus airway, rather than a single definitive procedure.
D. Recurrent Respiratory Papillomatosis
Recurrent respiratory papillomatosis is caused by the human papilloma virus, specifically types 6 and 11. Human papilloma virus is a small nonenveloped virus that infects the nuclei of host cells for replication. Papillomaviruses show a preference for infection of epithelial tissues and are very common in humans. Human papillomavirus (HPV) is responsible for a variety of disease including skin warts, recurrent respiratory papillomatosis, and invasive cancers such as cervical or oropharyngeal carcinoma. Transmission is hypothesized to involve vertical transmission during childbirth; maternal presence of condylomata during the perinatal period confers a 200-fold increase in relative risk for developing respiratory papillomatosis.
Benign, recurrent hyperplastic tissue growth of the upper airway characterizes this disease. It has a bimodal age distribution, with incidence peaks in children (infants to 12 years old), and in adults (30-40 years of age). Patients typically present with dysphonia or aphonia, although advanced disease can cause stridor from impending airway obstruction.
The primary site affected is the larynx, with the glottis being the most common area followed by the supraglottic larynx (Figure 15–10). Respiratory papillomatosis generally remains confined to the larynx but can spread distally to affect the trachea, bronchi, and lungs. Disease recurrence is frequent, and reports of children requiring more than 100 surgical procedures are not uncommon.
Adult recurrent respiratory papillomatosis. The right true vocal fold is involved with respiratory papillomatosis. In this patient, the disease was confined mostly to the single true vocal fold, although some disease was also present in the anterior portion of the contralateral vocal fold.
The primary therapy for respiratory papillomatosis remains surgical debulking, primarily by microdebrider or carbon dioxide laser ablation. Adjuvant medical treatments include cidofovir, indole-3-carbinol, ribavirin, mumps vaccine, and photodynamic therapy. The role for these adjuvant therapies in the treatment of respiratory papillomatosis is still being elucidated. Many otolaryngologists advocate avoidance of tracheotomy if possible, because this has been epidemiologically associated with increased risk of spread of papillomas to the lower respiratory tract. It is possible because patients with inherently more aggressive disease are also those who are more likely to require tracheostomy.