Acute management of vocal emergencies can be a difficult and stressful element in otolaryngology. A thoughtful history coupled with appropriate diagnostic instrumentation is the cornerstone of evaluating a patient with a vocal emergency. This article explores the differential diagnosis, evaluation, and treatment of vocal emergencies in the performer. Understanding the various causes of acute dysphonia in the performing artist as well as awareness of the additional pressures placed upon performing artists empowers the otolaryngologist to help patients in this interesting and unusual niche of the specialty.
“The laryngologist should unquestionably have a thorough understanding of the various vocal disorders which he is in a position to observe in singers, orators, and what one might call professional voice-users. He should also know the therapeutic methods suitable to apply them. We are far beyond the time when hoarseness and other manifestations observed in this category of professional voice-users were attributed to “granular” pharyngitis or laryngitis.” E.J. Moure, 1929
The evaluation and management of voice disorders has evolved into a specialized, multidisciplinary, and highly technological practice since the early part of the twentieth century. Nonetheless, a good portion of voice care delivery for professional voice users is performed by general otolaryngologists who do not have an experienced speech pathologist or videostroboscopic equipment available. Even in this modern era, many situations arise where vocal performers are being assessed by dim light reflected off a dental mirror, often outside the office setting—the means by which Czermak performed indirect laryngoscopy in 1860 . Fortunately, the improved quality, portability, and better affordability of endoscopic technology has allowed for better visual assessment of the larynx in the office and the field. In addition, an increased focus on vocal awareness and education in modern otolaryngology training programs has begun to close the experience gap between general otolaryngologists and laryngology subspecialists.
Ultimately, the optimal care of a professional voice user with a vocal emergency occurs within a setting where a full clinical voice evaluation and laryngeal examination, including videostroboscopy, can be performed. This article is designed to be a reference guide for the treatment of vocal performers in the acute scenario, with the hopes of facilitating optimal treatment for these vocal athletes in any setting.
Essentials of the history
“Unquestionably the greatest of all causes of laryngeal disease is the excessive use of one of its normal functions, phonation. This is not surprising in view of the fact that phonation was not the primary function of the larynx; phylogenetically it is very late. The patient with chronic laryngeal disease is almost always a person who either talks constantly or uses his voice professionally, or often, both. There is little use asking the patient if he talks much. For some curious reason a patient who talks all the time he is awake will insist he talks little. It is not only the singer, the lecturer, and the huckster who suffer from occupational abuse of the larynx. Teachers are especially frequent sufferers and persons who talk in noisy places such as factories where machinery is running often develop chronic hoarseness. The noise incidental to our modern life is a large factor in the great and increasing incidence of hoarseness and laryngeal disease.” Chevalier L. Jackson, 1942
A recent review of performers with acute illness before performance found that nearly 75% of complaints center around vocal difficulty, with sinus complaints, pharyngeal irritation, and cough being the next most common primary symptoms . As with any chief complaint, a thorough history is imperative when managing a vocal emergency. Detailed questionnaires have been published previously . Unfortunately, patients typically are vague and occasionally may withhold information when describing their vocal problems . The term “hoarseness” is nonspecific, and the exact symptoms need to be elucidated further with the patient. Challenging the patient to describe one’s voice problem without using general terms, such as “hoarseness” or “laryngitis,” is one way of extracting more information. Asking “What is your voice doing that it should not do?” and “What is your voice not doing that it should do?” are two useful questions to prompt the patient further.
Patients should be questioned regarding the details surrounding the onset of the vocal disorder. Any vocal change with a sudden onset (particularly an acute change that occurs during phonation) is a red flag for a vocal fold hemorrhage or mucosal tear. This finding must be investigated further with laryngeal imaging. Ask specific questions about loss of range or loss of vocal control. Loss of high range during soft singing is a sensitive indicator of vocal fold swelling. Increased effort in singing and delay in vocal onset are other manifestations of vocal fold mucosal edema or lesions. Changes in vocal quality, effort, endurance, and fatigue; the ability to sing or speak loudly or softly at various frequencies; or limitations in dynamic range often give clues that vocal fold pathology is present or developing. The symptoms of throat clearing, rhinorrhea, or coughing may represent associated conditions requiring medical attention, such as laryngopharyngeal reflux (LPR), allergic rhinitis, acute or chronic rhinosinusitis, or an acute upper respiratory tract infection.
The physician should gather information regarding the patient’s level of training and vocal awareness. Details of vocal warm-up routines, length and frequency of performances, and vocal obligations between events should be noted. This information will help the clinician to understand the degree of vocal demand and what can and cannot be modified to minimize phonotrauma.
Once the parameters of the chief complaint have been established, it is important for the physician to understand the performance environment and schedule. Not infrequently, these patients are seen on site, allowing for a first-hand assessment of the performance venue. Evaluation of the acoustics, the amplification system, competing sound sources, temperature, cleanliness, air filtration system, and allergen exposures aid in understanding the patient’s relative risk for exacerbating a voice disorder. Often, simple discussion with the stage manager/director/sound technician yields a solution for short- and long-term issues. The primary goal is to minimize laryngeal irritants and maximize the acoustic environment (eg, quality vocal monitors) for the performer.
The event schedule and importance of upcoming events should be closely reviewed with the patient and their manager, if available. There are significant differences in management options if the patient is being evaluated during intermission, hours before a show, or days before a show. How upcoming events relate to the patient’s short, medium and long-term career goals is a vital perspective to gain for the purposes of making management decisions. The financial implications of missing an event or events should also be taken into consideration.
Differential diagnosis of vocal emergencies in the performing artist
A wide variety of pathology can lead to acute dysphonia in performers and result in vocal emergency . Box 1 lists the most common presenting diagnoses.
Vocal fold hemorrhage
Vocal fold mucosal tear
Acute laryngitis
Viral
Bacterial
Fungal
Phonotraumatic edema
Acute edema on chronic fibrovascular (subepithelial) change/preexisting lesions
Asthma exacerbation
Upper respiratory tract infection
Pharyngitis, viral/bacterial
Rhinosinusitis, viral/bacterial
Bronchitis, viral/bacterial
Allergic rhinitis
LPR exacerbation
Hormonal/endocrine changes
Vocal fold hemorrhage
Vocal fold hemorrhages are the result of acute phonotrauma and can be considered a “vocal accident” ( Fig. 1 ). The shearing forces within the superficial lamina propria layer tear the microvasculature, allowing blood to spread within Reinke’s space. The amount of blood and extent of spread depend on the size of the vessel, the fluid pressure within the vessel, and the contents of Reinke’s space (eg, scar tissue may prevent spread of extravasating blood). Patients commonly note sudden voice change that occurred while performing a strenuous vocal task. Anticoagulation (eg, aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], warfarin sodium) and hormonal changes (eg, perimenstrual) put singers at risk for the development of a hemorrhage . Women should avoid the use of NSAIDs and aspirin in the premenstrual and menstrual periods. Identification of a vocal fold hemorrhage in the acutely dysphonic performer is extremely important and is the primary reason why laryngoscopy needs to be performed during the assessment. Vocal fold hemorrhage is treated with absolute voice rest, with or without corticosteroids, until resolution has occurred (ie, resorption or migration of blood away from the vibratory margin). This usually includes cancellation of scheduled performances; thus, the otolaryngologist must be prepared to support the patient in interactions with management. Patients need to be advised of the serious risk for scar or lesion development if they are to perform through a vocal fold hemorrhage.
Vocal fold mucosal tear
Mucosal tears usually result from an episode of harmful singing, yelling, or severe coughing/retching. The overwhelming shearing forces exerted upon the epithelium and superficial lamina propria cause the tissue to literally separate ( Fig. 2 ) . The acute symptoms include immediate hoarseness, loss of range, and discomfort. A mucosal tear may appear as a visible break in the mucosa on stroboscopy, presenting as a jagged edge in the epithelium. Initial findings on examination also can include vocal fold hemorrhage, edema, erythema, and stiffness on videostrobolaryngoscopy. Often, a tear can be difficult to diagnose in the acute setting, and one should have a low threshold to place a patient with these symptoms on absolute voice rest with close serial evaluation. If complete voice rest is followed, healing usually occurs without sequelae. If phonation or coughing persists in the setting of a tear, the epithelium may heal to the ligament, creating a sulcus, or curl up on itself, resulting in an epithelial band. Both of these sequelae can result in an adynamic segment on the phonatory surface of the true vocal fold.
Acute laryngitis
As with many upper respiratory tract infections, the cause of infectious laryngitis can be viral, bacterial, or fungal. Fungal laryngitis should be suspected in immunocompromised patients and in those on inhaled or systemic steroids. Regardless of the pathogen, the effect is essentially identical in the acute setting: Reinke’s space (the superficial lamina propria layer) engorges with inflammatory cells, resulting in increased mass ( Fig. 3 ). This prevents the vocal fold from vibrating periodically. The addition of vocal fold mass and irregular vibration creates a lower or raspy tone. In singers, this also translates into a difficulty, or an inability, in attaining higher frequencies because the vocal folds need to oscillate more quickly at these pitches . Intermittent voice breaks and changes in register transition are additional symptoms. Phonotraumatic edema has the same effect, but it is more easily treatable with conservative measures.
Relative or absolute voice rest is the mainstay of treatment, depending on the severity of the edema. Mild to moderate edema can be treated with relative voice rest and adjunctive measures noted below. Severe edema should be treated with absolute voice rest. Additionally, the patient should be advised against the use of NSAIDs, because there is an increased risk for vocal fold hemorrhage secondary to the fragility of the vocal fold blood vessels in the acutely inflamed state. Appropriate antibiotics should be prescribed if clinical suspicion for bacterial infection is present. For mild to moderate vocal fold edema, corticosteroids can be used acutely to treat edema effectively and facilitate performance. Intramuscular steroids, such as dexamethasone and cortisone, can begin to have an effect within 1 hour; oral steroids, such as prednisone and methylprednisolone, typically produce the desired effect within 1 day. Patients should be reexamined before returning to performance. Steroids have limited effect in cases of severe edema. In general, steroids should be used with caution, counseling patients regarding the risk for vocal fold hemorrhage, mood swings, agitation, appetite change, sleep disturbance, acid reflux exacerbation, and more serious but rare risks, such as osteopenia, precipitation or worsening of diabetes, gastric or duodenal ulcers, and avascular necrosis of the hip. Steroids should not be used in isolation without modified voice rest, defined as essential voice use only, and supportive measures. Vocal fold tear, hemorrhage, scarring, or permanent hoarseness are risks that need to be discussed with the patient when performing while taking steroids. Often, the voice sounds normal, despite the acutely fragile state of the vocal folds. The otolaryngologist also needs to be aware of performers living “shot to shot,” using steroids as a crutch for voice overuse or misuse. Taking a careful history about steroid use and effect can give clues to this problem. Vocal rehabilitation with voice therapy helps to free these patients from their chronic steroid use by instilling fundamental changes in how they use their voice and maximizing vocal efficiency.
Acute edema on chronic fibrovascular change
Phonotrauma in a setting of chronic fibrovascular change often results in acute edema, which results as a consequence of the increased vocal effort necessary to overcome the decreased pliability of the scarred regions. The combination of these changes results in convexities of the midmusculomembranous true vocal folds. During phonation, these areas contact prematurely—resulting in an “hourglass configuration”—and air escapes anterior and posterior to the lesions. In addition, the affected areas are stiffer than the surrounding superficial lamina propria, resulting in a differential pliability between the two vocal folds and within each true vocal fold. Diagnosis is difficult without videostroboscopy, and short-term management is similar to acute laryngitis.
Upper respiratory tract infection
Viral and bacterial upper respiratory tract infections can lead indirectly to acute vocal changes by way of localized edema, secretions, pain, throat clearing, coughing, dehydration, generalized malaise, nasal congestion, or headaches. A careful history of onset, location, and severity of symptoms and physical examination helps make the diagnosis and treatment and should be directed to the site of pathology. Empiric treatment with antibiotics is warranted in cases with suspected bacterial etiology. Symptomatic relief of nasal congestion can be achieved with the short-term use of topical nasal decongestants (eg, oxymetazoline). Topical nasal steroid sprays also can be helpful in the acute setting. Oral decongestants (eg, pseudoephedrine) can be extremely drying and may have secondary deleterious effects. The use of drying agents can lead to increased shearing forces, predisposing patients to vocal fold tears, subepithelial thickening, and fibrosis. Patients should be cautioned regarding the use of topical anesthetics for pharyngitis because numbness can lead to loss of vocal control. Vigorous hydration and modified voice use is encouraged. Performance during an acute upper respiratory tract infection is discouraged.
Allergic rhinitis
The rhinorrhea and nasal mucosal swelling associated with allergic rhinitis can affect the vocal performer significantly, although symptoms rarely are severe enough to warrant show cancellation. Short-term relief can be achieved with oral antihistamines and nasal decongestion, although patients should be warned about the drying side effects and potential sedation seen with antihistamines. Newer antihistamines (eg, loratadine) have less anticholinergic side effects. Long-term treatment of allergic rhinitis with appropriate therapy (eg, nasal steroids, oral or topical antihistamines, leukotriene antagonists, mast-cell stabilizers, immunotherapy) should be recommended as indicated .
Laryngopharyngeal reflux
Performers are particularly at risk for the development of symptoms from LPR . Erratic dietary habits, stress, and abdominal support associated with singing—combined with the sensitive nature of high-level vocal performance—make the vocal performer more susceptible to acute vocal change from LPR. Patients should be queried regarding typical gastroesophageal reflux disease symptoms of heartburn and regurgitation and typical LPR symptoms of throat clearing, globus, cough, and postnasal drip. The threshold for treatment with dietary, behavioral, and medical therapy (proton-pump inhibitors [PPIs] and histamine-2 receptor (H 2 )-blockers) should be low, and the otolaryngologist should be aware that LPR may be an exacerbant to other acute ailments, such as acute laryngitis and phonotrauma. In the acute setting, over-the-counter antacids may be of benefit. Treating reflux acutely and aggressively with twice-daily dosing of PPIs and a nighttime dose of an H 2 -blocker, even in asymptomatic individuals, may hasten recovery from an upper respiratory tract infection.
Acute asthma exacerbation
As with the general population, professional voice users are subject to medical conditions that may affect vocal quality. Asthma can diminish vocal strength, endurance, and quality by weakening the power source to the larynx. It is important to recognize this problem so that proper medical management for an acute asthma exacerbation can be instituted in a timely fashion. Inhaled steroids in conjunction with rescue inhalers are the mainstay of treatment for reactive airway disease. The clinician and the patient need to be aware of the deleterious effects that inhaled steroids can have on vocal fold muscle bulk, the voice, and the predisposition to fungal laryngitis . When possible, the patient should discuss using noninhaled or nebulized preparations to treat asthma acutely and chronically with his/her pulmonologist.
Functional dysphonia
Vocal performers and orators experience a significant amount of stress or anxiety, especially when nearing an event or performance. Poor vocal behaviors, including muscle tension dysphonia, can create speaking and singing difficulties that may require urgent voice therapy intervention before vocal performance. Stage fright is a behavioral problem that is addressed best with behavioral solutions. The anxiety associated with performance leads to a sympathetic “fight or flight” response. The main adverse consequence for the vocal performer is overwhelming anxiety that manifests as excessive laryngeal muscle tension and reduced breath support. The result is impaired vocal performance. Intervention consists of strategies to optimize respiration support and phonatory control, maximizing resonance, and reassurance. Hydration and good health habits are essential adjuncts. Performers should be advised to avoid turning to β-blockers and anxiolytics. These medications blunt mental and physical sharpness as well as the performance edge that results from the natural sympathetic response necessary for optimal performance. Identification of these problems and an established relationship with a trained voice/singing pathologist are essential to address this issue adequately.