71 Hoarseness & Dysphonia Flashcards

1
Q

Describe the function of the larynx.

A

Describe the function of the larynx.

The larynx plays a role in aspiration prevention, respiration, Valsalva, and phonation. The larynx is a complex three-dimensional structure shaped as a triangle anteriorly and transitioning to a circular appearance posteriorly. It consists of numerous cartilages that support both extrinsic and intrinsic muscles as described below and is divided into the supraglottis, glottis, and subglottis (Figure 71-1).

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2
Q

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

A

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

There are three phases to phonation: (1) pulmonary, (2) laryngeal, and (3) supraglottic/oral. Dysfunction in any of these levels can lead to voice changes, which may be interpreted as hoarseness by the patient.

The pulmonary phase is akin to the motor that drives the voice and creates this via inhalation and exhalation of air. This activity provides the larynx with a column of air for the laryngeal phase.

In the laryngeal phase, the vocal folds approximate either voluntarily or involuntarily and then vibrate at certain frequencies as the air rushes past to create a sound that is then modified in the supraglottic/oral phase. Bernoulli’s effect is responsible for the passive vibration of the actively approximated vocal folds. When the column of air stops, vibration ceases. Changes in vocal fold length and changes in the tension of the thyroarytenoid (TA) muscle affect pitch.

The supraglottis, pharynx and sinonasal cavity resonate the sound produced to create a unique individual voice. Articulation of words is formed by the action of the palate, tongue, lips, and teeth.

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3
Q

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

A

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

Hoarseness is a nonspecific term for change in voice quality, typically associated with a rough or harsh sound. Hoarseness is regarded as a symptom of an underlying pathology, and is not a diagnosis. Dysphonia, also a symptom, is an all encompassing term to describe any problem with voice production including the quality of the sound produced, an increase in vocal effort or fatigue, or pain or discomfort with speaking or singing, among others. Aphonia is the inability to produce a voice. Patients with aphonia often speak in a whisper or just move their lips without sound.

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4
Q

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

A

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

Clinical history and physical exam including a complete head and neck exam are all part of the initial workup to evaluate a dysphonic patient. In addition, a 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, a rigid endoscope or a flexible endoscope in the clinic setting. With the exception of a gross mass on the vocal folds, a mirror is typically inadequate to evaluate the larynx in a dysphonic patient.

Laryngovideostroboscopy (LVS) is required in the dysphonic patient to rule in or out various pathologies and can be performed with either a rigid or flexible laryngoscope. LVS uniquely allows for analysis of vocal fold vibration including phase closure pattern, amplitude of vibration, symmetry of vibration, periodicity of vibration, and other mucosal wave abnormalities if present. The LVS exam should be recorded and saved for future comparisons.

When the cause of dysphonia is not obvious during a static white light endoscopy, LVS should be performed because structure may be seen but function is not completely evaluated. Rigid LVS allows for high-resolution visualization of the larynx. However, phonation is limited to sustained vowels due to anterior displacement of the tongue, and the ability to assess vocal fold motion is often suboptimal. Flexible LVS allows dynamic visualization of the larynx in its normal position during all forms of speech and singing. With the recent addition of chip-tip camera technology, flexible LVS is becoming the preferred modality to complete all portions of the laryngeal exam: structural, neurologic, and videostroboscopic.

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5
Q

What are pertinent questions in the clinical history of a dysphonic patient?

(Include associated laryngeal complaints such as breathing and dysphagia.)

A

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, a trauma, a 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.) A rough voice may indicate pathology affecting the vocal fold edge while a breathy voice may suggest hypoadduction of the vocal folds due to vocal cord paresis or paralysis. Tightness or pain in the tongue or strap muscles may point to muscle tension dysphonia (MTD) that is primary or, more likely, as a compensation for an underlying pathology (secondary MTD).
  • 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 laryngopharyngeal reflux (LPR), asthma, allergy, infection or postviral vagal neuropathy. Cancer of the lung 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 (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, other professional voice users, sports fanatics (shouting), and people who eat a diet contributing to LPR are more likely to suffer from benign causes of dysphonia. Smoking and LPR are risk factors for developing laryngeal and esophageal cancer.
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6
Q

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

A

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

Flexible laryngoscopy allows for visualization of the larynx in its physiologic position and when compared to indirect laryngoscopy can provide a more comprehensive dynamic voice evaluation in the office setting. Patients are asked to sit in the sniffing position with the neck flexed and head extended. This position minimizes unnecessary touching and gagging and brings the larynx into ideal position for visualization. Topical decongestants and anesthetics are applied to the nasal cavity prior to the exam to minimize discomfort. The flexible laryngoscope is advanced through the nasal cavity and in addition to the nasal cavity, the nasopharynx, oropharynx, and hypopharynx are evaluated prior to the larynx. 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 low pitch. SLN palsies present themselves as abnormalities with vocal fold lengthening maneuvers. The patient then alternates between “EE” and a sniff through the nose. These portions of the exam allow better evaluation of vocal fold paralysis. To complete the laryngeal exam, stroboscopy is then performed to evaluate vocal fold motion.

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7
Q

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

A

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. Historically, stroboscopy was thought to rely on the phenomenon termed Talbot’s Law, which states that images linger on the retina for 0.2 seconds and only five distinct images can be viewed per second. However, it is now accepted that the phenomenon of flicker-free perception of light intensity, in which the perception of apparent motion is obtained from sampled images along the glottic cycle, provides the image seen in LVS.

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8
Q

Can you confidently diagnose the etiology of dysphonia without laryngovideostroboscopy?

A

Can you confidently diagnose the etiology of dysphonia without laryngovideostroboscopy?

Not really, except in cases of gross abnormality. Even in the case of gross abnormality there are often additional findings that are missed without LVS such as subtle motion abnormalities or reactive subepithelial lesions of the opposite vocal fold. It is often difficult to reliably assess anything less than gross motion abnormalities of the vocal folds, such as supraglottic hyperfunction, without LVS. LVS improves diagnostic abilities by over 25% when compared to isolated flexible laryngoscopy and can alter treatment regimens based on these findings.

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9
Q

What are common causes of dysphonia?

A

What are common causes of dysphonia?

  • Glottic insufficiency (GI) with secondary, compensatory muscle tension dysphonia (MTD): gross, incomplete, or complete but short phase closure of the true vocal folds during phonation with resultant loss of air during phonation. Causes for GI include:
    • Paresis or paralysis of one or both true vocal folds with resultant secondary MTD
    • Atrophy of the true vocal folds with resultant secondary MTD
    • Scar of the true vocal fold epithelium/vibratory layer leading to secondary MTD. Sulcus vocalis is a type of TVF scar where the epithelium is scarred to the vocal ligament, thus creating a void of vibration in that area from loss of superficial lamina propria.
  • Benign phonotraumatic lesions of the vocal folds: nodules, polyps, cysts, granulomas, and hemorrhage
  • Malignant and premalignant exophytic epithelial lesions: leukoplakia (hyperkeratosis, metaplasia, dysplasia), and squamous cell carcinoma. When comparing leukoplakia to erythroplakia, erythroplakia has a higher probability of showing signs of dysplasia or malignancy because it represents a hypervascular lesion (as malignancies often are).
  • Neurologic disorders: spasmodic dysphonia, essential tremor, Parkinson’s disease
  • Inflammatory conditions: laryngopharyngeal reflux, allergy, irritants, and autoimmune diseases
  • Recurrent respiratory papillomatosis from incomplete closure and/or scarring of the vocal folds after intervention
  • Primary MTD: no underlying glottic insufficiency or other pathology is appreciated on LVS but significant supraglottic hyperfunction is present
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10
Q

What is the difference between acute and chronic laryngitis?

A

What is the difference between acute and chronic laryngitis?

Acute laryngitis is classically associated with a viral upper respiratory tract infection (URTI) and is one of the most common causes of hoarseness. It is self-limiting and resolves with the URTI symptoms within 1 to 2 weeks. Patients typically do not require antibiotics and improve with hydration and voice rest. Chronic laryngitis is general inflammation of the larynx lasting longer than 4 weeks and is often caused by smoking, voice abuse, fungal infections, or laryngopharyngeal reflux (reflux that causes irritation to the larynx, pharynx, and pulmonary system). The voice usually improves if the irritating factors are removed or treated. This may involve smoking cessation, medical or surgical reflux management, antifungal medications, and voice rest.

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11
Q

What is glottic insufficiency?

A

What is glottic insufficiency?

Glottic insufficiency (GI) is the inappropriate escape of air during phonation that leads to incomplete or a complete but short phase closure pattern (approximately 40% to 45% or less of each vibratory cycle in the closed position) as seen on LVS. GI may be gross or subtle and secondary to vocal fold scar, atrophy, paresis or paralysis. Therapeutic goals seek to augment the affected vocal fold(s) to allow for complete, long phase closure during phonation (approximately 45% to 50% or more of the vibratory cycle in closed phase). The presence of benign lesions of the vocal folds often leads to GI.

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12
Q

What are the different treatments for glottic insufficiency?

A

What are the different treatments for glottic insufficiency?

  • Voice therapy (often tried first for many causes of dysphonia)
  • Injection augmentation: Office-based injections versus OR injections. Different substances may be injected into the vocal folds including autologous fat, human acellular dermis, hyaluronic acid gel, carboxymethylcellulose gel, and calcium hydroxyapatite gel.
  • Medialization laryngoplasty with insertion of an implant lateral to the vocal fold comprised of a synthetic material such as silastic or Gore-Tex®
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13
Q

What is muscle tension dysphonia (MTD)?

A

What is muscle tension dysphonia (MTD)?

Muscle tension dysphonia (MTD) is a pathologic condition whereby excessive tension in the extrinsic laryngeal muscles (Figure 71-2) results in an abnormality with physiology/function of the phonatory mechanism involving the intrinsic laryngeal muscles and/or vocal fold mucosa. The supraglottic laryngeal tissues are often observed to be hyperfunctional in cases of MTD. MTD is divided into primary and secondary types.

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14
Q

What is the difference between primary and secondary MTD?

A

What is the difference between primary and secondary MTD?

Primary MTD is dysphonia in the absence of organic vocal fold pathology and is associated with excessive supraglottic hyperfunction often in the setting of atypical or abnormal TVF movements during phonation. Secondary MTD occurs in the setting of and as compensation for underlying glottic insufficiency.

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15
Q

What is spasmodic dysphonia (SD)?

A

What is spasmodic dysphonia (SD)?

SD is a focal dystonia affecting the laryngeal muscles during speech. There are two types of SD: adductor SD (voice breaks during voiced vowels), where the patient describes a strangled quality to the voice; and abductor SD (voice breaks during voiceless consonants such as P and F) where the patient describes an unintentional breathy quality. Symptoms of SD typically improve with singing and when making a “cartoon” voice (ask patient to speak like Mickey Mouse). The treatment of choice for SD is periodic percutaneous botulinum toxin injection into the affected muscle groups under laryngeal electromyographic guidance. In adductor SD the TA/LCA muscle complex is injected, and in abductor SD the PCA is injected.

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16
Q

What are systemic diseases associated with hoarseness?

A

What are systemic diseases associated with hoarseness?

  • Neurologic:
    • Hypofunctional disorders: characterized by weak voice, hoarseness, and dysphagia. Examples include Parkinson’s disease, motor neuron diseases (amyotrophic lateral sclerosis or ALS, primary lateral sclerosis, postpolio syndrome), neuromuscular junction disorders (myasthenia gravis, Eaton-Lambert disease), and multiple sclerosis
    • Hyperfunctional disorders: commonly have irregular loudness or pitch and straining of the voice, examples include dystonia, essential tremor, and pseudobulbar palsy.
  • Inflammatory:
    • Rheumatoid arthritis: cricoarytenoid joint involvement with ankylosis and submucosal vocal fold nodules
    • Sarcoidosis: supraglottic (epiglottis most commonly affected) nodular and “turban-like” thickening
    • Amyloidosis: laryngeal amyloid deposition most commonly near the glottic level in the true and false vocal folds
    • Wegener granulomatosis: classically manifests as subglottic stenosis but may also have glottic changes
17
Q

What benign vocal fold lesions may cause hoarseness?

A

What benign vocal fold lesions may cause hoarseness?

  • Polyps: usually unilateral, broad based or pedunculated; found at junction of the anterior and middle thirds of the membranous TVFs with an opposing reactive lesion (fibrous callous on the opposite TVF). They can be hemorrhagic due to acute trauma (Figure 71-3A).
  • Nodules: always bilateral, symmetric; found at the junction of the anterior and middle thirds of the membranous TVFs (Figure 71-3B).
  • Cysts: fluid-filled (mucus retention cysts) or cellular (epidermoid cysts); found within the superficial lamina propria with an opposing reactive lesion.
  • Fibrous masses: Often firm, unilateral, broad based lesions; found at junction of the anterior and middle thirds of the membranous TVF with an opposing reactive lesion
  • Varices and ectasias: abnormal enlarged or tortuous blood vessels; found primarily on the superior aspect of the middle of the membranous TVFs. The common pathology to identify in singers with intermittent acute dysphonia.
  • Granulomas: Fleshy masses due to either trauma such as intubation or persistent contact pressure from glottis insufficiency and secondary MTD in the setting of LPR; classically found on the vocal process of the arytenoids, but may appear on the membranous TVF.
  • Polypoid corditis/Reinke’s edema: swelling of the superficial lamina propria, associated with smokers and hypothyroidism
  • Recurrent respiratory papillomatosis: exophytic epithelial lesions caused by HPV (typically types 6 and 11); located anywhere in the larynx, favoring the TVF. Malignant transformation is seen in 1% to 2%.
18
Q

How are nodules different from other benign vocal fold lesions and how are they differentiated?

A

How are nodules different from other benign vocal fold lesions and how are they differentiated?

Nodules are small and discrete lesions located in the membranous portion of the vocal fold, one third the distance from the anterior commissure. Vocal nodules are easily identified because they are paired and symmetric. Seeing bilateral lesions of the vocal folds should not lead to the diagnosis of nodules. Vigilance should be employed during LVS to identify a unilateral dominant phonotraumatic lesion (polyp, cyst or fibrous mass) with an opposing reactive lesion rather than assuming the diagnosis of nodules as the treatment may warrant surgical intervention. Polyps are exophytic, asymmetric, and appear soft and smooth, often coexisting with a reactive lesion of the opposite vocal fold. Vocal fold cysts are mucous retention or epidermoid cysts located in the superficial layer of the lamina propria, usually at the middle third of the vocal fold in the medial and superior aspect and are also found in coordination with a reactive lesion of the opposing vocal fold. Fibrous masses are often firm and broad, significantly limiting the mucosal wave and are seen in the presence of a reactive lesion of the opposing TVF. Vocal process granulomas (VPG) are not actually found on the membranous vocal fold as compared to the other benign lesions presented; VPGs form on the high-pressure contact area of the vocal processes of the arytenoid cartilage. They have a pathognomonic appearance and typically do not require removal/biopsy, but rather regress and become asymptomatic with voice therapy and acid reflux suppressive medications.

19
Q

How do you treat benign vocal fold lesions?

A

How do you treat benign vocal fold lesions?

For benign, overuse/phonotraumatic lesions such as nodules, polyps, and cysts, the patient typically undergoes a course of voice therapy and rests the voice when possible. If voice therapy is not successful, or the lesion is too large to have any potential for success, surgical excision of the lesion followed by voice therapy is offered (see below for technique). For RRP, KTP laser excision has emerged as an effective method to preserve voice and avoid injury to the vibratory layer. KTP ablation is typically offered in the OR or in the office depending on the disease burden. Other methods to remove RRP include cold knife excision, CO2 laser excision, and microdebrider excision. KTP laser is also used successfully in the treatment of TVF ectasias and Reinke’s edema. Reinke’s edema, when excessive, often requires surgical excision.

20
Q

What is voice therapy and what is the role of voice therapy in the treatment of dysphonia?

A

What is voice therapy and what is the role of voice therapy in the treatment of dysphonia?

Voice therapy consists of vocal and breathing techniques that retrain the patient to produce the best sound with the least injury. It is designed to relieve or “unload” the larynx of hyperfunctional behaviors and instills new muscle memory techniques (akin to a baseball pitcher recovering from an arm injury). It is performed over 4 to 6 weeks by a speech-language pathologist, or voice pathologist, who specializes in voice therapy. It is offered as first-line therapy for anyone with benign laryngeal pathology who is deemed a candidate for voice therapy by a voice pathologist.

21
Q

What are the surgical treatments for benign phonotraumatic vocal fold lesions?

A

What are the surgical treatments for benign phonotraumatic vocal fold lesions?

  • Microsuspension laryngoscopy (MSL, or suspension microlaryngoscopy) with excision of the offending lesion via medial microflap technique. The incision for the microflap can be made with cold steel or with the CO2 laser. Dissection then ensues with microinstruments. In some instances the lesion is densely adherent to the overlying epithelium (typical with fibrous mass) or is pedunculated (some polyps) and a microflap cannot be separated from the benign lesion. In these cases the epithelium is removed with the lesion (Figure: MSL view pre/post microflap excision of right TVF polyp and left reactive lesion with three different telescopic views.).
  • Office-based or operative steroid injections for scar, nodules or fibrous masses
  • Office-based or operative KTP laser photoangiolysis for vascular lesions (ectasias or hemorrhagic polyps) or deep fibrous masses that are adherent to the epithelium and would result in a significant TVF defect if excised.
22
Q

What is laryngopharyngeal reflux disease?

A

What is laryngopharyngeal reflux disease?

Laryngopharyngeal reflux (LPR) is the backflow of stomach contents including acid and pepsin into the laryngopharynx. This causes vocal fold and laryngeal inflammation and, in some cases, voice change due to exposure of the glottic mucosa to gastric contents. It differs from GERD because it affects a different target end organ, the laryngopharynx as opposed to the esophagus, and presents and is treated differently. LPR is often “silent” because patients don’t have typical GERD symptoms like heartburn or feelings of regurgitation. Acid is likely the cofactor that activates pepsin, and therefore LPR should not be considered an acid-only issue.

23
Q

How do you diagnose and treat laryngopharyngeal reflux?

A

How do you diagnose and treat laryngopharyngeal reflux?

Patients with LPR-induced laryngitis present with symptoms of chronic hoarseness, chronic cough, throat irritation, frequent throat clearing, a mucus sensation in the throat, and globus sensation (a feeling of a lump in the throat and often increased effort with swallowing). All of these symptoms are attributed to LPR, but they overlap dramatically with other laryngeal pathologies that lead to glottic insufficiency and secondary MTD. History alone without an LVS exam is usually insufficient to rule out another etiology for the dysphonia. LPR is often diagnosed too quickly when LVS is not available and studies have shown the high likelihood of an alternative or concurrent diagnosis for the dysphonia that requires intervention. If no other pathology is identified on LVS, a presumed diagnosis is made and empiric PPI trials remain the mainstay of therapy. Most patients respond to diet and lifestyle changes along with acid suppression in the form of high-dose, twice-daily proton pump inhibitors because this removes the acid cofactor. Because the nonacid components of reflux, primarily pepsin, have been demonstrated active even at neutral pH, not all patients will respond to acid suppressive medications. Without dietary changes to avoid acidic foods, dietary acids likely reactivate pepsin that remains in the throat despite medical acid suppression. As with GERD, LPR patients may benefit from sleeping with the head of the bed elevated, avoiding tomato based, spicy or fatty fried foods, and waiting 3 to 4 hours after eating before going to bed.