Hoarseness and Dysphonia


Key Points

  • 1.

    Acute laryngitis is often associated with a viral upper respiratory tract infection and resolves within 1 to 2 weeks without antibiotic therapy.

  • 2.

    Laryngopharyngeal reflux (LPR) is an inflammatory condition of the upper aerodigestive tract caused by the backflow of gastroduodenal contents into the larynx and pharynx. Pepsin, bile salts, and other gastroduodenal proteins directly induce mucosal modifications associated with LPR, while vagally mediated changes indirectly influence symptoms.

  • 3.

    Systemic inflammatory disorders associated with the larynx include sarcoidosis (supraglottic), amyloidosis (glottic), and granulomatosis with polyangiitis (subglottic).

Pearls

  • 1.

    During phonation the glottis should be in the closed phase for approximately 45% to 50% or more of each vibratory cycle at the most comfortable pitch and loudness. Glottic insufficiency (GI) exists if the closed phase is less than 45% to 50% and the causes of GI should be considered.

  • 2.

    Vocal nodules, often overdiagnosed, are by definition bilateral and symmetric and occur at the junction of the anterior and middle thirds of the true vocal folds. More likely, when bilateral lesions are seen, a dominant subepithelial lesion (cyst, polyp, fibrous mass) on one vocal fold opposes a reactive lesion on the other side.

  • 3.

    Recurrent respiratory papillomatosis (RRP) is primarily caused by HPV types 6 and 11.

  • 4.

    Muscle tension dysphonia is typically associated with compensation for underlying GI and is unusual as a stand-alone primary diagnosis.

  • 5.

    If the suspected LPR does not respond to acid suppression, specific testing to rule out nonacid reflux is required to exclude the diagnosis. A barrier treatment such as sodium alginate products or anti-reflux surgery can be offered.

Questions

Describe the function of the larynx.

The larynx plays a role in swallowing, aspiration prevention, respiration, Valsalva maneuver, and phonation. The larynx is a complex three-dimensional structure shaped as a triangle anteriorly and transitioning to a circle posteriorly. It consists of numerous cartilages that support both extrinsic and intrinsic muscles, as described below, and may be divided into the supraglottis, glottis, and subglottis ( Fig. 73.1 ).

Fig. 73.1, Right posterolateral view of cartilages and intrinsic muscles of the larynx with RLN and SLN (internal branch).

What is the mechanism of phonation including the physiology of vocal fold vibration?

There are three phases to phonation: pulmonary, laryngeal, and supraglottic/oral. The pulmonary phase creates a column of air via inhalation and exhalation. In the laryngeal phase the vocal folds approximate and vibrate as the air rushes past to create sound. Vocal fold vibration begins at the point of “mucosal upheaval” on the inferior lip of the mucosa in the posterior aspect of the membranous true vocal fold (TVF). When the column of air stops, vibration ceases. Changes in vocal fold length and tension via the thyroarytenoid (TA) and cricothyroid muscles affect the frequency of vibration or pitch. The supraglottis, pharynx, and sinonasal cavities act as resonators to amplify frequencies, creating a unique individual voice. Dysfunction in any of these levels can lead to voice changes, which may be interpreted as hoarseness by the patient. Finally, articulation of words is formed by the action of the palate, tongue, lips, and teeth (dysfunction of these structures from neurologic causes is called dysarthria).

What is the difference between hoarseness and dysphonia? What is aphonia?

Hoarseness is a nonspecific term for changes in voice quality and is typically associated with a rough or harsh sound. Hoarseness is regarded as a symptom of an underlying pathology and not a diagnosis. Dysphonia, also a symptom, is an all-encompassing term that describes any problem with voice production, including changes in the quality of the sound produced, increases in vocal effort or fatigue, or pain and discomfort with speaking or singing. Aphonia is an inability to produce a voice.

How is the underlying cause of a patient s dysphonia complaint diagnosed?

Clinical history and physical examination, including a complete head and neck examination, are all part of the initial workup to evaluate a dysphonic patient. In addition, voice evaluation by a speech-language pathologist (SLP) including acoustic and aerodynamic measures, laryngeal function studies, and stimulability testing (to determine if a patient is a candidate for voice therapy) is routinely performed in most voice centers before or after visualization of the larynx.

The larynx can be visualized with a mirror, rigid endoscope, or flexible endoscope in the clinical setting. The mirror examination allows identification of a gross mass in the larynx as well as vocal fold motility; however, it is typically inadequate for detailed evaluation of surface lesions or vibratory anomalies in a dysphonic patient. Videolaryngoscopy allows for better visualization of the laryngeal anatomy including structural pathologies and subtle mucosal changes.

When the cause of dysphonia is not obvious during static white light endoscopy, laryngovideostroboscopy (LVS) should be performed with either a rigid or flexible laryngoscope. LVS uniquely captures vocal fold vibratory characteristics including phase closure pattern, amplitude of vibration, symmetry of vibration, periodicity of vibration, and other mucosal wave abnormalities if present. With the recent addition of chip-tip camera technology, flexible LVS is becoming a popular modality to complete all portions of the laryngeal examination: structural, neurologic, and videostroboscopic. If possible, the LVS examination should be recorded and saved for future comparisons.

What are pertinent questions in the clinical history of a dysphonic patient? (Include associated laryngeal complaints such as breathing and dysphagia.)

  • When was the onset of symptoms? What is the duration of symptoms, and is there any progression? Such questions determine whether the process is acute or chronic.

  • Were there any associated events such as an upper respiratory infection; trauma; recent surgery of the head, neck, or chest; an intubation; a period of increased demand or overuse of the voice; or an emotional stressor?

  • How has the quality of voice changed? (Raspy, rough, breathy, weak, tightness, change in pitch.)

  • Is there dysphagia or odynophagia? If present, these symptoms may indicate a problem with the pharynx, esophagus, and/or larynx.

  • Is there a cough? Cough may be associated with LPR, asthma, allergy, infection, or postviral vagal neuropathy. Lung cancer with vocal fold paralysis (secondary to recurrent laryngeal nerve involvement) often presents with dysphonia and cough.

  • Is there hemoptysis? This potentially serious symptom may indicate malignancy.

  • Are symptoms of typical allergy (sneezing, itchy or watery eyes, cat sensitivity), LPR (throat clearing, mucus sensation, cough, globus sensation), or gastroesophageal reflux disease (GERD; heartburn, regurgitation/acid brash, dyspepsia) present?

  • What is the timing of the complaint (i.e., am or pm)? Does the voice get better or worse as the day goes on? Does the voice fatigue with use?

  • What other medical problems exist? Hoarseness may be associated with underlying hypothyroidism, an autoimmune disorder, and medications that cause drying of the laryngeal mucosa.

  • What are the occupation and habits of the patient? Singers, teachers, sports coaches, lawyers, or other professional voice users, as well as people who eat a diet contributing to LPR are more likely to suffer from benign causes of dysphonia.

  • How are these symptoms affecting the patient’s quality of life? Voice health has a significant, multidimensional impact on general health and quality of life, independent of other comorbidities.

Which laryngeal functions are evaluated with the flexible laryngoscopy portion of the examination?

Flexible laryngoscopy allows for visualization of the larynx in its physiologic position, and when compared to indirect laryngoscopy it can provide a more comprehensive dynamic voice evaluation in the office setting. Patients are typically decongested and anesthetized with topical medication. The laryngoscope is introduced through a nare and advanced into the oropharynx. The larynx is first observed with the patient breathing quietly, making note of abnormalities in adduction. Next, the patient is asked to produce a sustained “EE” sound and the larynx is evaluated for any lesions, vocal fold abnormality, or atrophy. Continuing the “EE” sound, the patient is asked to slide from low to high pitch and back down. The vocal folds lengthen when moving to a high pitch and shorten when moving to a low pitch. SLN palsies present as abnormalities with vocal fold lengthening maneuvers. The patient then alternates between “EE” and a sniff through the nose. These portions of the examination allow for a better evaluation of vocal fold paralysis. To complete the laryngeal examination, stroboscopy is then performed to evaluate vocal fold motion.

How does stroboscopy generate a slow-motion image of vocal fold vibration?

Stroboscopy requires extraction of the frequency of vocal fold vibration via a flat microphone typically held to the patient’s neck. The strobe light then shines on the larynx and flashes at specific points in the glottic cycle that are slightly out of phase with the vibration to create the appearance of slow-motion imaging of the vocal folds.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here