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Chest Conditions: Section Articles

Evaluation and Management of Vocal Cord Dysfunction in the Athlete

Wilson, John J.; Theis, Shannon M.; Wilson, Erin M.

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Current Sports Medicine Reports: March 2009 - Volume 8 - Issue 2 - p 65-70
doi: 10.1249/JSR.0b013e31819def3d
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Abstract

INTRODUCTION

Vocal cord dysfunction (VCD), also commonly known as paradoxical vocal fold motion, occurs when the vocal folds adduct on inspiration (and rarely with exhalation) (12), resulting in airflow obstruction and difficulty breathing. Classic symptoms of VCD include dyspnea, throat tightness, inspiratory stridor, dysphonia, respiratory distress, and/or choking. As detailed later in this article, a significant number ofactive individuals are affected by breathing difficulties during exercise as a result of vocal cord dysfunction. VCD presents a diagnostic challenge and often is mistaken for exercise-induced bronchospasm or asthma. A keen awareness of VCD will enable the sports medicine physician to enlist the assistance of appropriate specialists so that a timely and accurate diagnosis is possible. Delayed diagnosis may result in unnecessary, costly, ineffective, and potentially harmful interventions for the patient (27,39), and may deter or exclude athletic participation altogether (41).

Epidemiology

Estimates of the prevalence of VCD are understood poorly; however, a disproportionate percentage of VCD cases occur in young women (6). In fact, women present with VCD more commonly than men with estimates ranging from twice (24) to nearly 20 times that of men (35). There is a high concomitance between VCD and exercise-induced bronchoconstriction (EIB) (>50%) (27,35). VCD can occur in both recreational and elite athletes; however, VCD tends to be more common in athletes participating in outdoor sports (8.3%) than indoor sports (2.5%) (7). VCD most often occurs in young women between 20 and 40 yr of age (35), but has been reported in men and women across all age ranges, including young infants (15).

ANATOMY AND PHYSIOLOGY

An appreciation of normal laryngeal anatomy and physiology is helpful in understanding vocal cord dysfunction.

Anatomy

The larynx is situated in the anterior neck, just superior to the trachea. It is composed of a cartilaginous skeleton consisting of the thyroid cartilage superiorly, cricoid cartilage inferiorly, and the arytenoid cartilages posteriorly. The epiglottis lies just above the larynx and provides reflexive closure during swallowing to prevent aspiration of food into the airway below. The vocal cords (also known as vocal folds) lie near the midsection of the larynx and are stretched horizontally from the thyroid cartilage anteriorly, to the arytenoids posteriorly. The vocal fold complex commonly is referred to as the glottis. The vocal folds appear as a "V"-shaped aperture, narrowest anteriorly, when viewed from the upper airway. The aryepiglottic folds (false vocal folds) lie superior to the true vocal folds. A complex network of muscles articulatewith the cartilaginous structures of the larynx to adduct (close) and abduct (open) the vocal cords. Vocal cord adduction occurs with contraction of the lateral cricoarytenoid muscle, and abduction primarily is controlled by contraction of the posterior cricoarytenoid muscle. Laryngeal innervation is provided by the vagus nerve, recurrent laryngeal nerve, and the superior laryngeal nerve.

Physiology

The primary function of the larynx in humans is protection of the lower respiratory tract. Airway protection occurs reflexively through a complex series of laryngeal motion pre venting 1) aspiration of food during swallowing and 2) inhalation of noxious substances or foreign matter during respiration. This involuntary protective mechanism is referred to as the glottic closure reflex and is characterized by adduction of the vocal cords, approximation of the aryepiglottic folds, and lid-like closure of the epiglottis over the glottis.

The mucosal lining of the larynx is innervated densely with afferent sensory nerve fibers. Four distinct types of nerve fibers are known to exist, including 1) cold (i.e., thermoreceptors), 2) pressure (i.e., tracheal transmural mechanoreceptors), 3) "drive" receptors (which respond to tracheal movement), and 4) irritant receptors (which are responsive to various mechanical and chemical irritants including cigarette smoke, distilled water, CO2, and acid) (37). It has been proposed that irritant receptors play a vital role in airway protective mechanisms (37).

Along with airway protection, the larynx and vocal cords also are active during voice production and respiration. The production of voice is very complex; briefly, the vocal cords approximate and air pressure from the lungs forces the cords to oscillate at varying frequencies, resulting in the production of voice. During respiration, the vocal cords abduct with inspiration and become narrower, but remain open during exhalation.

VCD ETIOLOGY

The precise etiology of vocal cord dysfunction (VCD) is not understood entirely and likely is multifactorial in nature. Several classifications have been implicated in the cause of VCD and are discussed here.

Laryngeal Hyperresponsiveness

As detailed previously, the larynx and vocal cords are innervated densely by sensory receptors (2,37), which can be stimulated by a variety of environmental, infectious, and intrinsic (e.g., post-nasal drainage or acid reflux) irritants. Morrison and colleagues describe "irritable larynx syndrome," a condition in which the larynx is hyperresponsive to sensory stimulus input, including emotional distress, and irritants (26). Cukier-Blaj and colleagues report a high prevalence of reflux symptoms in patients with VCD and propose that a protective laryngeal motor adaptation occurs in which reflexive vocal cord adduction occurs at pathologically low thresholds (7). One possibility is that VCD represents a hyperfunctional glottic closure reflex induced by repetitive irritant exposure.

Laryngeal Irritants

Gastroesophageal reflux disease (GERD) and laryngopharyngeal reflux (LPR) commonly result in laryngeal irritation and account for up to 10% of visits to an otolaryngologist's office (21). In contrast to esophageal epithelium, the laryngopharynx is highly sensitive to gastric acid irritation, yet LPR often exists without overt patient symptoms (20). As such, many patients with irritant-induced VCD will not report classic symptoms of acid reflux or heartburn but may report hoarseness, globus sensation (lump in the throat), halitosis, and/or throat irritation. Laryngeal abnormalities consistent with acid reflux irritation often are present in patients with VCD. In fact, 95% of juveniles with confirmed VCD exhibited laryngeal findings consistent with GERD (32), and Patel and colleagues report that nearly two thirds of patients with VCD were found to have laryngoscopic evidence of laryngeal inflammation (28). The abnormal laryngoscopic findings often seen in these patients may have important implications in the pathophysiology of VCD. More specifically, a number of studies have implicated reflux disease as a cause of VCD (28,40). In fact, using a reflux symptom index (RSI) scoring tool, 84% of VCD patients exhibit abnormal RSI scores (7).

Respiratory irritants (i.e., environmental, occupational, and infectious) also can have a detrimental impact upon the normal function of the larynx and vocal cords. For many individuals, post-nasal drainage serves as a vocal cord irritant and may lead to laryngeal hyperresponsiveness (4). Several other inhaled irritants, such as methacholine, strong odors, perfumes, ammonia, and inhaled particulate matter, have been documented as causative agents in cases of vocal cord dysfunction (8,30,31). For example, chlorine inhalation has been described by several authors and deserves special consideration in swimmers and divers with VCD (1,5). Furthermore, environmental exposure to inhaled irritants and allergens may account for reported rates of VCD being greater in outdoor athletes (8.3%) compared with indoor athletes (2.5%) (35). Acute viral infections also are known to result in increased airway mucus secretion, wall thickening, and hyperresponsiveness, which may elicit vocal cord dysfunction (14).

Psychogenic Disorders

VCD often is attributed to underlying psychogenic conditions (26). Many early reports of VCD point to a psychogenic cause exclusively, which is reflected in the nomenclature used to describe this condition. As early as the mid-1800s, the condition had been described as "hysteric croup" (11) and has since been labeled with various other psychogenic labels such as "Munchausen's stridor" (29), "poor performance stridor" (6), "factitious asthma" (10), and "psychogenic stridor" (22). Some patients with VCD have even been suspected of malingering. While patients may be able to voluntarily reproduce the stridor associated with VCD episodes, this scenario is unlikely. The tendency of many to consider this condition a predominantly psychological disorder may partly be caused by the inability of clinicians to readily observe organic pathology without the assistance of laryngoscopy.

Although cases have been reported in which no conceivable psychogenic cause can be attributed to the condition (15), a large number of individuals diagnosed with VCD do have coexisting psychiatric conditions (9). Depression, anxiety, perceived stress, and posttraumatic stress disorder have been implicated in VCD, both as triggers and exacerbating factors (33). A study of military personnel with VCD found nearly 94% of subjects to have an underlying psychiatric disorder (30). Dietrich and colleagues documented that nearly half of all patients with VCD had elevated stress, anxiety, and depression (9). Husein and colleagues report ahigh prevalence of somatoform and conversion disorders among adults with VCD, although there was a subset of VCD subjects with no identifiable psychopathology (17). Psychopathology may affect individuals with VCD and may often co-occur with other potential triggers (as detailed previously). Care should be taken to consider all potential causes of VCD to ensure optimal treatment outcomes.

Neurogenic

Neurogenic causes rarely are responsible for VCD but must be considered in the differential diagnosis to avoid neglecting a more serious condition. Maschka (1997) proposed a classification scheme for VCD that details a variety of neurogenic causes, including brainstem compression and neuronal injury (23).

EVALUATION AND MANAGEMENT

The behavioral similarities between VCD and EIB make VCD a challenging diagnosis for the sports medicine physician. Patient history is helpful in distinguishing between the two entities. It is important to conduct a careful physical exam, realizing that findings are usually normal in the absence of acute symptoms. However, during an acute episode of VCD, many patients will have overt stridor or turbulent airflow evident during auscultation of the larynx, whereas patients with EIB will demonstrate expiratory wheezing and a prolonged expiratory phase during lung auscultation. Inhaled bronchodilators are often helpful in aborting an episode of bronchospasm, but usually are of little help in cases of isolated VCD. The often multifactorial nature of vocal cord dysfunction lends itself to a multidisciplinary management approach (Table).

TABLE
TABLE:
Management of vocal cord dysfunction in athletes.

Pulmonary

Athletes suspected of having VCD should be evaluated with pulmonary function testing (PFT) to refute or confirm the presence of EIB or asthma. Spirometry measurements obtained before and after a bronchial provocation challenge with either histamine or methacholine may be helpful. An exercise challenge PFT may be useful when respiratory symptoms are exertional and may be more likely to detect a VCD event than other provocative testing. Negative PFTs or failure to respond to β2-adrenergic agonists following a challenge supports a diagnosis of VCD in a patient with exercise-associated dyspnea. Methacholine challenge PFT testing has been reported to trigger VCD events in susceptible individuals (30). Spirometry flow-volume loops are suggestive of VCD when there is a truncated inspiratory limb consistent with extrathoracic airway obstruction. The presence of normal PFT testing does not reliably exclude the presence of VCD because this test is neither sensitive (25) nor specific for the condition. Chest radiographs are usually normal in the setting of a VCD event but may demonstrate lung hyperinflation and diaphragm flattening in the setting of an EIB attack. Pulse-oximetry and arterial blood gases are normal during acute VCD events, but may be abnormal in the setting of EIB. Pulmonologists also have expertise in performing laryngoscopy to visualize the larynx as detailed later in this article.

Otolaryngology

Consultation with an otolaryngologist is recommended for athletes suspected of having VCD to exclude other pathology of the upper airway and for visualization of the larynx using laryngoscopy. Visualization of the vocal folds via laryngoscopy, which also can be performed by a pulmonologist, is considered the gold standard for VCD diagnosis (33). Exercise laryngoscopy may be used as a tool for diagnosing VCD (16), but it can be difficult to reproduce the intense physical and emotional setting of athletics in an artificial environment (13). Laryngoscopy also will provide important clues about laryngeal irritation or anomalies (e.g., LPR or post-nasal drainage) (28). Some experts recommend empiric treatment with a proton pump inhibitor (PPI) or histamine-2 blocker (7,32,41) because of the high prevalence of LPR inpatients with VCD. Daily proton pump inhibitor therapyiswarranted in those with confirmed laryngopharyngeal inflammation upon laryngoscopic exam. A typical regimen includes once or twice daily dosing of a PPI. Maintenance therapy should be continued at the lowest PPI dose required to control symptoms. A trial off medications may be attempted under medical supervision, ensuring that signs and symptoms of laryngeal inflammation do not return. Therapy also should include recommendations for lifestyle modifications to reduce the likelihood of GERD, such as avoidance of alcohol, caffeine, fatty meals, and carbonated drinks, as well as adopting behaviors such as weight loss, smoking cessation, elevating the head of the bed, and avoiding meals before bedtime (19).

Psychopathology

A sports psychologist may be a useful consultant in managing performance-related stress and anxiety in athletes with VCD. When appropriate, patients should be offered pharmacologic treatment and/or mental health counseling. Therapies including hypnosis (3) and biofeedback (6) have been reported in the management of VCD; however, little data exist to support their routine use. Anxiolytic medications have been used with some success in management of acute VCD attacks (34), although their long-term use is discouraged. Along with behavioral therapy, psychotherapy also has been strongly recommended by some practitioners (18).

Allergy and Immunology

Laryngitis may result from chronic post-nasal drainage secondary to rhinosinusitis (4), thereby triggering VCD. Clinical history and physical examination should evaluate the presence of rhinitis signs and symptoms including sneezing, rhinorrhea, congestion, or itching. Allergic rhinitis and vasomotor rhinitis are two of the more common forms of rhinitis affecting athletes. Acareful history should assess for the presence of possible environmental allergen exposures, both in the home and in the athletic setting. Oral antihistamines, decongestants, and nasal steroids are often quite effective in managing allergic rhinitis. Both corticosteroid and ipratropium nasal sprays are often effective in managing athletes with vasomotor rhinitis and post-nasal drainage. Referral to an allergist/immunologist may be beneficial for difficult-to-manage patients or for those who may benefit from identification of environmental allergens or immunotherapy treatment.

Speech Language Pathology

Speech language pathologists play a vital role in the treatment (and often evaluation) of VCD. After a diagnosis has been confirmed, the speech language pathologist introduces specific behavioral strategies that can be used to recognize, thwart, and/or manage a VCD episode. The training involves a "tightening/relaxing exercise" that helps the athlete recognize the sensation and early onset symptoms of an impending attack. The athlete also is trained to use relaxed diaphragmatic breathing rather than chest or clavicular breathing to reduce tension near the larynx before or during an episode. Finally a "breathing recovery" strategy (i.e., deep nasal sniff) is introduced and rehearsed to help the athlete manage an episode (see Sandage and Zelazny, 2004 for a detailed review of these strategies) (36). Briefly, the strategy involves teaching the athlete to sniff in through the nose and slowly exhale through the mouth while making an "sss" or "sh" sound. This strategy reflexively forces the vocal folds to open (sniff) while forcing the athlete to slow the rate of breathing (exhaling through a constriction).

The following are two case studies that highlight the necessary multidisciplinary assessment and medical and behavioral management protocol for VCD.

CASE STUDIES

Case Study #1

A 16-yr-old male wrestler reported sudden onset of difficulty breathing during a tournament wrestling match. Evaluation in the emergency department revealed a normal chest x-ray, electrocardiogram, and basic chemistry labs. He was therefore diagnosed as having exercised-induced bronchospasm (EIB) and was treated with inhaled bronchodilators (i.e., albuterol).

Despite proper use of albuterol before exercise, his breathing difficulties progressively worsened during periods of intense exertion in both practices and matches. The patient's athletic trainer then referred him to a sports medicine physician for evaluation of exercise-associated dyspnea.

During his evaluation the patient described "trouble getting air in" with associated chest pain and tingling in his hands during an episode. The patient denied a history of exercise-induced bronchospasm, asthma, or environmental allergies. The patient did report symptoms of reflux, including globus sensation and throat clearing. Physical examination performed by the sports medicine physician was negative for significant cardiac or pulmonary findings. Pre- and post-bronchodilator exercise spirometry testing was negative for EIB or asthma. A proton pump inhibitor was prescribed for management of suspected acid reflux.

The sports medicine physician then referred the patient to an otolaryngology clinic for assessment of laryngeal anatomy and function. Flexible fiberoptic laryngoscopy was conducted, and the posterior glottis appeared erythematous and edematous, suggestive of laryngopharyngeal reflux. The vocal fold edges were smooth and straight, without evidence of pathology. Vocal cord adduction was observed during phonation, with a return to an abducted position during inhalation, indicating normal vocal fold motion. The patient was able to reproduce the feeling of "trouble getting air in" during which time the vocal folds were noted to adduct during inhalation. This finding was suggestive of VCD.

During flexible fiberoptic laryngoscopy, the patient was taught the breathing recovery strategy, which involves the deep nasal sniff technique. The patient was initially trained to complete this strategy during the laryngoscopic procedure to help the patient associate the obvious vocal fold abduction with improved inhalation. The otolaryngologist and speech language pathologist then provided the patient with extensive education about VCD, including training in identifying the onset of an attack, the relaxed diaphragmatic breathing techniques, and behavioral and dietary modifications to reduce the occurrence of laryngopharyngeal reflux. At follow-up, the patient reported one episode of stridor during practice, although he indicated he was able to prevent afull VCD attack by implementing the deep nasal sniff technique. He had continued to practice daily breathing exercises without subsequent VCD episodes.

Case Study #2

A 15-yr-old female athlete presented with a history of "shortness of breath during exercise" during basketball and swimming practice for several months. Initial evaluation by a pulmonologist confirmed a diagnosis of exercise-induced bronchospasm (EIB). Medical management with inhaled bronchodilators and inhaled corticosteroids were attempted but did not completely resolve her symptoms. She subsequently was referred to the otolaryngology clinic for evaluation of possible co-morbid VCD.

The assessment revealed that the patient was unable to differentiate clearly between difficulties with inhalation versus exhalation during episodes, but stated that her breathing resulted in a feeling of "panic" and "noisy breathing." She indicated that episodes always occurred following strenuous exercise, specifically sprints. She also reported an escalation in the frequency of events over the last year, which she attributed to increased intensity of high school level competition. Other reported diagnoses included anxiety, gastroesophageal reflux, and a history of viral-induced asthma since the age of 2 yr. Medications included a nasal steroid, PPI, and inhaled steroids and bronchodilators for asthma.

Flexible fiberoptic laryngoscopy revealed normal vocal fold motion, with evidence of laryngopharyngeal reflux (vocal cord edema and erythema) (Figure). During reproduction of symptoms, vocal cord adduction was appreciated. The deep nasal sniff recovery technique was taught during the assessment and resulted in a widely patent airway.

Figure
Figure:
A. Abducted larynx during inspiration. Note the vocal cord edema. B. Partially abducted larynx during VCD event.

Despite ongoing therapy with the speech pathologist and attempts with the deep nasal sniff breathing recovery technique, she continued to have difficulty breathing with intense exertion. Flexible fiberoptic laryngoscopy was performed during an exercise treadmill test. Laryngoscopy was performed at two separate times during the session: 1) early asymptomatic treadmill running, and 2) at onset of dyspnea with noisy breathing, which occurred at maximal exertion. Her examination while symptomatic revealed vocal cord adduction, which was consistent with her prior examination when asked to reproduce symptoms. Nasal sniffing during symptoms resulted in abduction of the vocal folds, a patent airway, and cessation of her dyspnea.

Following this evaluation, the role of EIB and LPR were reviewed and the importance of continuing with medical management for these issues was stressed, including the importance of breathing strategies and techniques. Exercise laryngoscopy proved to be an effective bio-feedback tool for the patient, as she was able to recognize and successfully abort subsequent episodes of VCD during sports participation.

CONCLUSION

Vocal cord dysfunction is a condition affecting athletes, occasionally with disabling effects. The sports medicine physician must have a high index of suspicion for VCD when evaluating the athlete who presents with difficulty breathing. Accurate diagnosis can prevent interventions that may be unnecessary or harmful (27,39).

The complexity of this disorder suggests that a multi-disciplinary approach often is the most effective means for evaluation and management. A comprehensive approach to diagnosis and therapy may require several medical specialists, including but not limited to pulmonologists, otolaryngologists, speech pathologists, immunologists, gastroenterologists, psychologists, athletic trainers, and sports medicine physicians. The prevalence of laryngeal abnormalities associated with VCD (28) emphasizes the importance of laryngeal visualization to exclude additional airway pathology. The case studies presented in this article highlight the benefit of collaboration among the various specialists involved in the patient's care. Optimal treatment outcomes may require management of VCD risk-factors (e.g., GERD, LPR, post-nasal drip, and anxiety), including pharmacologic interventions as indicated. Behavioral management techniques taught by speech language pathologists remain a mainstay of therapy for these patients.

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