INTRODUCTION — "Hoarseness" is a term often used to describe any change in voice quality. This reflects a variety of complaints including vocal tremor, weakness, fatigue, altered pitch, breathiness, or strained voice quality.
The approach to the adult who presents with hoarseness will be reviewed here. The approach to hoarseness in children is discussed separately. (See "Hoarseness in children: Evaluation".)
LARYNGEAL ANATOMY AND PHYSIOLOGY — The main functions of the larynx involve phonation, respiration, swallowing, and performance of Valsalva maneuver:
●Phonation refers to production of a primary vocal tone at the level of the vocal folds. Vocal quality is then modified by resonation through the upper airway and sinonasal tract and articulated into speech.
●Airway patency and protection is important during respiration and swallowing. The normal swallow mechanism includes laryngeal elevation, posterior deflection of the epiglottis, inhibition of respiration, and closure of the vocal folds to prevent aspiration of ingested material.
●Valsalva maneuver represents generation of increased pressure against a tightly closed glottis. This enables functions such as cough, straining, throat clearing, and defecation.
Anatomy of the larynx — The larynx is comprised of a cartilaginous skeleton, muscles (extrinsic and intrinsic), and a mucosal lining (figure 1) [1].
Cartilages — The larynx is suspended from the hyoid bone in the anterior neck by soft tissue attachments. The laryngeal skeleton consists of nine cartilages. The arytenoid, corniculate, and cuneiform cartilages are paired, whereas the thyroid, cricoid, and epiglottis are unpaired (figure 2).
The thyroid cartilage is the largest and forms a protective shield-like shape in front of the vocal folds. Its midline projection is commonly referred to as the "Adam's apple" and tends to be more prominent in men.
The cricoid cartilage, which lies below the thyroid cartilage and above the entrance to the trachea, is the only complete ring of the laryngeal skeleton. The cricoid cartilage encloses the subglottic region of the larynx. Stenosis may form if the mucosa in this region is injured, as can occur with prolonged endotracheal tube intubation.
The arytenoids are pyramidal-shaped cartilages positioned on the upper border of the posterior cricoid cartilage; these attach at the synovial cricoarytenoid joints (figure 2). The arytenoids serve as attachment sites for some of the intrinsic muscles of the larynx and allow complex movement and fine adjustment of the vocal folds. Fibrosis or fixation of the cricoarytenoid joint, as can be seen with rheumatoid arthritis or following trauma, can result in vocal fold immobility and respiratory or phonatory impairment.
Vocal folds — The true vocal folds are bands of tissue comprised of muscle, fibrous ligament, and mucosa extending from the arytenoids posteriorly to the midline thyroid cartilage anteriorly.
The false (or "ventricular") vocal folds are situated superior to the true vocal folds and are separated from them by a lateral recess termed the laryngeal ventricle. The ventricle contains mucus-producing glands that provide lubrication for the true vocal folds, which are themselves devoid of glandular elements. The false vocal folds are adducted only during effortful closure, as with Valsalva and reflex laryngeal closure due to noxious stimuli. They do not normally approximate during phonation; however, this may be observed in pathologic conditions, such as in patients with incompetent true vocal fold closure due to vocal fold paralysis, mass lesion, or presbyphonia (vocal fold changes due to aging of the larynx).
The larynx is subdivided into three regions: the supraglottis, glottis, and subglottis. The supraglottis encompasses the area above the true vocal folds and includes the epiglottis, false vocal folds, aryepiglottic folds, and arytenoids. The glottis consists of the true vocal folds and the immediate subjacent area extending 1 cm inferiorly. The subglottis refers to the region beginning at the inferior edge of the glottis and extending down to the inferior border of the cricoid cartilage.
Extrinsic and intrinsic muscles — The muscles of the larynx are divided into extrinsic and intrinsic muscles. The extrinsic group, including the anterior strap muscles and digastrics, affects the position of the entire larynx in the neck. This is important for laryngeal elevation during swallowing and fixation of the larynx during Valsalva. The intrinsic muscles are much more delicate and are responsible for movement of the vocal folds within the larynx as well as subtle tension adjustments related to phonation. The main intrinsic muscles are: posterior cricoarytenoid, lateral cricoarytenoid, interarytenoid, thyroarytenoid, and cricothyroid.
The thyroarytenoid muscle makes up the bulk of the true vocal fold. Movement at the cricoarytenoid joint allows the vocal folds to be approximated in the midline (adducted) during phonation or drawn apart laterally (abducted) during inspiration.
The vocal fold mucosa is composed of non-keratinizing stratified squamous epithelium, whereas the remainder of the larynx is lined by respiratory (ciliated pseudostratified columnar) epithelium; this enables the surface of the vocal fold to better withstand the repetitive trauma of high-velocity contact with the contralateral vocal fold. The subepithelial layer, known as Reinke's space or superficial lamina propria, contains mucopolysaccharides and mucoproteins that give it a viscous consistency. This facilitates vibration of the vocal fold mucosa over the deeper tissue layers which are more dense and fibrous. Scarring and stiffness of these layers can impair vibration with subsequent degradation of vocal quality.
Nerve supply — The vagus nerve innervates the laryngopharynx. The recurrent laryngeal nerves branch from the vagus in the upper chest and reenter the neck in the thoracic inlet. The recurrent laryngeal nerve travels underneath the subclavian artery on the right side, and around the arch of the aorta on the left side.
The recurrent laryngeal nerve innervates all intrinsic muscles except for the cricothyroid muscle, which is innervated by the external branch of the superior laryngeal nerve. Additional motor function of the lower pharynx and upper esophagus is supplied by direct pharyngeal branches of the vagus and recurrent laryngeal nerve. A mass lesion along the course of these nerves can result in vocal fold paralysis.
Sensory function above the level of the vocal folds is mediated by the internal branch of the superior laryngeal nerve. Sensory function below the level of the vocal folds is transmitted through the recurrent laryngeal nerve. The vagus nerve receives sensory information from the external auditory canal as well as the hypopharynx. Thus, a reflex cough can be provoked by instrumenting the ear during cleaning, and cancer present in the hypopharynx may result in ear pain.
Phonation — Phonation is generated by the interaction of aerodynamic forces of the exhaled air column with the viscoelastic properties of the true vocal fold mucosa as the vocal folds are held approximated (adducted) in the midline. This results in a vibratory, oscillating wave in the superficial layers of the vocal fold as air is expelled from the lungs.
Oscillation occurs about 100 to 300 times per second (Hz) during speech, and is greater than 1000 Hz in a soprano while singing. This is too fast for the human eye to perceive, and special techniques (such as videostroboscopy) are needed to capture vocal fold vibration. The frequency of vibration is perceived by the ear as pitch. Pitch is mainly determined by vocal fold length and tension and is regulated by minute adjustments of the cricothyroid muscle. Increase in mass of the vocal fold can also alter pitch, as seen with polyps or an increased amount of tissue in Reinke's space in smokers.
The glottic vocal tone is produced at the level of the glottis (true vocal folds); it then resonates in the pharynx and nose, adding harmonics and timbre, and is articulated by fine motor control of the tongue, palate, and lips. A patient with cleft palate may have normal vocal fold function but will have a hypernasal voice due to the palatal defect and poor velopharyngeal closure (resulting in excess air escape through the nose). By contrast, a patient with nasal congestion may exhibit hyponasal resonance due to inadequate air escape through the nose. The dysarthric patient may have normal vocal fold function but abnormal articulation secondary to neurologic dysfunction of the tongue or lips.
CAUSES OF HOARSENESS — Hoarseness may be due to either functional or organic causes. Any patient with persistent hoarseness should be evaluated in order to establish a diagnosis. In the absence of symptoms of an acute upper respiratory infection, patients with hoarseness persisting for more than two weeks should be referred for a complete otolaryngologic examination. This is especially important in the setting of associated risk factors for head and neck cancer (primarily tobacco and alcohol use), or worrisome coexistent symptomatology such as severe cough, hemoptysis, unilateral ear or throat pain, odynophagia, dysphagia, or unexplained weight loss [2].
Causes of hoarseness may be categorized as follows:
●Acute laryngitis, which is self-limited and related to acute respiratory illness or acute voice misuse
●Chronic laryngitis, which is related to irritants, reflux, chronic infection (such as fungal), or habitual vocal misuse
●Benign vocal fold lesions
●Malignancy
●Neurologic dysfunction
●Non-organic ("functional") issues
●Systemic conditions and rare causes
Acute laryngitis — Acute laryngitis is a common and self-limited inflammatory condition lasting less than three weeks and usually associated with either an upper respiratory tract infection or acute vocal strain. Moraxella catarrhalis, Haemophilus influenzae, and Streptococcus pneumoniae have been isolated from the nasopharynx of adults with acute laryngitis, even though the etiology of infection in most cases is thought to be viral [3]. Hoarseness resulting from an upper respiratory tract infection is often associated with rhinorrhea, cough, and mild sore throat. Acute vocal strain due to screaming or protracted coughing can also result in submucosal microtrauma of the vocal fold, with focal edema and hemorrhage.
Chronic laryngitis — When laryngitis persists beyond three weeks, it is defined as chronic laryngitis [4].
Irritants — Chronic laryngitis is typically associated with one or more chronic irritants which, over time, lead to persistent inflammation. Examples include inhaled toxins (such as chemical fumes), gastroesophageal reflux disease (GERD), chronic sinusitis with postnasal drip, chronic alcohol use, and chronic vocal strain. In addition to increasing the risk of squamous cell carcinoma of the larynx, tobacco smoke irritates the vocal folds and can cause benign changes such as keratosis and polypoid corditis. (See 'Polypoid corditis' below.)
Laryngopharyngeal reflux — Laryngopharyngeal reflux (LPR) results from the retrograde movement of gastric contents (acid and enzymes such as pepsin) beyond the upper esophageal sphincter, leading to morphologic and functional changes in the larynx and pharynx [5,6]. Substantial evidence suggests a relationship between reflux and posterior laryngitis, including interarytenoid hypertrophy and contact ulceration with or without granuloma formation [7]. (See "Complications of gastroesophageal reflux in adults" and "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management".)
The most common symptoms associated with LPR are throat clearing (98.3 percent), persistent cough (96.6 percent), heartburn/dyspepsia (95.7 percent), globus sensation (lump in the throat feeling; 94.9 percent), and change in voice quality (hoarseness; 94.9 percent) [5]. Other symptoms include sore throat, dysphagia, and laryngospasm or choking sensation. Symptoms characteristically vary over time. Reflux esophagitis may not be present in patients with symptomatic reflux affecting the laryngopharynx and testing may not definitively demonstrate the presence of acid. The diagnosis of LPR is discussed in detail separately. (See "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management", section on 'Diagnosis' and "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management".)
Muscle tension dysphonia — The larynx can be affected by abnormal hyperfunctional mechanisms and imbalance of tension in muscles involved in voice production leading to dysphonia. Muscle tension dysphonia is considered either a psychologic or neurologic dystonic disorder.
In the primary form of vocal hyperfunction, true vocal fold morphology and motion are observed to be normal. Inappropriate contraction and closure (adduction) of the false vocal folds occurs during phonation, with generation of excessive strain and effort. There may also be contraction of the entire supraglottis, obscuring visualization of the true vocal folds.
In the secondary form, false vocal fold compression may be seen as a compensatory mechanism for incompetence at the level of the true vocal folds. Such incomplete closure of the true vocal folds may be due to vocal fold paralysis, atrophy (as seen with aging, where superficial lamina propria is lost from Reinke's space), and mass lesions preventing approximation of the vocal fold edges (such as nodules or polyps).
Benign vocal fold lesions
Polypoid corditis — Polypoid corditis is also known as Reinke's edema (picture 1). Viscous material accumulates in the superficial lamina propria (Reinke's space) of the true vocal folds as a result of chronic irritation and inflammation secondary to smoking. The vocal folds appear swollen and "floppy" and may cause respiratory symptoms in severe cases. The condition is frequently seen in middle-aged women and causes a husky, low-pitched voice [8]. In these cases, the patient often complains of "sounding like a man." A similar clinical appearance can be seen in patients with hypothyroidism.
Recurrent respiratory papillomatosis — Recurrent respiratory papillomatosis (RRP) is a condition characterized by the development of papillomas in the respiratory tract, and it is associated with human papillomavirus types 6 and 11. The disease may occur in both children and adults, and patients may present with symptoms ranging from hoarseness to respiratory distress, depending upon the location and severity of disease [9,10]. The evaluation and treatment of RRP is discussed in detailed elsewhere. (See "Human papillomavirus infections: Epidemiology and disease associations", section on 'Recurrent respiratory papillomatosis' and "Common causes of hoarseness in children", section on 'Papillomatosis' and "Pathology of head and neck neoplasms", section on 'Recurrent respiratory papillomatosis'.)
Polyps and nodules — Both polyps and nodules on the vocal fold are manifestations of chronic vocal fold irritation. Etiologic factors include smoking, reflux, and muscle tension dysphonia. Some polyps form following traumatic hemorrhage into the vocal fold from vocal abuse or coughing ("hemorrhagic polyp"). Polyps tend to be unilateral, although a contralateral smaller "contact lesion" is often seen which arises from damage to the opposing vocal fold in the setting of repeated contact against the primary mass lesion (picture 2A-B). They present in the anterior one-third of the vocal fold and are seen more frequently in men.
Nodules are sometimes also called "singer's" or "screamer's" nodes. They occur bilaterally and generally appear relatively symmetric (picture 3) [11]. They are more common in women and children and are also frequently seen in the setting of vocal abuse. The early nodule is edematous and becomes thickened and fibrotic with ongoing vocal fold microtrauma.
Laryngeal cancer — The vast majority of laryngeal cancer is squamous cell carcinoma (picture 4). Major risk factors include smoking and alcohol abuse. (See "Epidemiology and risk factors for head and neck cancer".)
Squamous cell carcinoma is epithelial, arising from the mucosal surface of the larynx, and tends to metastasize to regional cervical nodes. Early lesions may appear initially as white (leukoplakic) plaques; they can be asymptomatic or present with hoarseness depending on location within the larynx. Advanced malignant lesions can be large and exophytic or deeply ulcerative.
Neurologic dysfunction — Injury to the vagus or recurrent laryngeal nerve can cause vocal fold dysfunction or paralysis. In a 20-year retrospective study, non-thyroid neck surgery has replaced extralaryngeal malignancies as the most common cause of unilateral and bilateral vocal fold paralysis [12,13].
Unilateral vocal fold paralysis — Unilateral recurrent laryngeal nerve injury causes the affected vocal fold to rest in the paramedian (or partially lateralized) position. The glottic airway is usually adequate and airway complaints are rare. The contralateral vocal fold may or may not compensate to provide adequate glottic closure during phonation. If closure is not achieved, the residual glottal gap results in air escape with a weak, breathy voice secondary to a "leaky valve" phenomenon. Glottal incompetence also presents risk of aspiration, particularly with thin liquids. Cough, which requires transient tight glottic closure, may be ineffectual. Associated sensory loss (particularly in the case of stroke) may also complicate swallowing.
The etiology of unilateral vocal fold paralysis includes [14]:
●Extra-laryngeal malignancy of the skull base, neck, or thorax, with invasion of the vagus or recurrent laryngeal nerve (image 1).
The recurrent laryngeal nerve is among the most frequent sites affected by invasive, differentiated thyroid cancer (due to invasion by the primary tumor or from central neck lymph node metastases) [15]. Vocal fold paralysis in the setting of a thyroid nodule should raise suspicion of invasive thyroid cancer [16]. Recurrent laryngeal nerve invasion may present with hoarseness, but the associated voice change can be variable and the voice may even be normal; the variability in voice change may be due to a compensatory mechanism by the contralateral vocal cord. Symptoms of aspiration may also be present. (See "Differentiated thyroid cancer: Surgical treatment".)
●Iatrogenic injury to the recurrent laryngeal or vagus nerves during procedures in the neck, chest, and skull base (eg, thyroid and parathyroid surgery, carotid endarterectomy, cardiothoracic procedures and anterior cervical approaches to the cervical spine for disk surgery) [17,18]. Unilateral vocal cord immobility can also occur as a complication of endotracheal intubation; the recurrent laryngeal nerve may be injured by compression, the intubation, endotracheal cuff, or through a twist or stretch secondary to arytenoid dislocation [19]. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Vocal cord paralysis'.)
●Neck and chest trauma, or laryngeal trauma.
●Degenerative neural disorders including bulbar palsies (eg, polio, amyotrophic lateral sclerosis) and demyelinating disease.
●Brainstem stroke syndrome, specifically lateral medullary (Wallenberg) syndrome.
Patients with lateral medullary infarct often present with additional neurologic symptoms including ataxia, vertigo, ipsilateral Horner syndrome, dysphagia, and vomiting. However, if the infarct is small, the clinical syndrome may not be complete, and hoarseness may be the most prominent presenting symptom [20].
●Approximately one-third of cases of unilateral vocal fold paralysis are idiopathic, although many of these may be of viral etiology.
A review of over 700 cases of idiopathic unilateral paralysis found that complete and partial recovery of motion occurred in approximately 40 percent of patients, with complete and partial voice recovery in 60 percent; spontaneous recovery was rare after one year [21].
●Ortner's (or cardiovocal) syndrome is a rare cause of unilateral vocal fold paralysis and occurs due to compression of the left recurrent laryngeal nerve by enlarged vascular structures (eg, enlarged left atrium due to mitral stenosis or enlarged pulmonary artery in pulmonary hypertension) [22,23]. In such cases, hoarseness rarely occurs in the absence of other symptoms but may be a prominent, early complaint. (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Symptoms' and "Rheumatic mitral stenosis: Clinical manifestations and diagnosis", section on 'Hoarseness'.)
Bilateral vocal fold paralysis — Bilateral vocal fold paralysis causes a different constellation of symptoms. The bilaterally denervated vocal folds may be positioned near the midline, with a narrow glottic aperture. Voice is usually good with this glottic configuration, but respiratory function can be compromised. Symptoms range from minimal dyspnea or inspiratory stridor to severe respiratory distress [24].
Bilateral vocal fold paralysis is usually iatrogenic, secondary to neck surgery or tracheal intubation. Neurologic disorders, including ALS, diabetic neuropathy, myasthenia gravis, neurologic sequelae of organophosphate pesticide toxicity or therapeutic administration of vinca alkaloids, stroke, head injury, and hydrocephalus or brainstem compression associated with Arnold-Chiari malformation may also be etiologic [25,26]. Bilateral cricoarytenoid joint fixation can occur in association with rheumatoid arthritis.
Spasmodic dysphonia — Spasmodic (previously called spastic) dysphonia is a voice disorder believed to represent a focal laryngeal dystonia and can be associated with other dystonic disorders. It results in involuntary contraction of the laryngeal muscles and is often characterized by a halting, strained, strangled voice quality. This is especially notable with vowels and results from uncoordinated forceful adduction during phonation (adductor type). The less common abductor type of spasmodic dysphonia results in voiceless gaps in speech secondary to dysregulation of vocal fold abduction. Spasmodic dysphonia is not felt to be psychogenic in origin, although many patients report initial onset of symptoms following a stressful life event. Symptoms may improve with whispering, laughing, or singing. Diagnosis is based on clinical presentation and treatment usually involves botulinum toxin injection into the larynx. (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Laryngeal dystonia'.)
Neurologic disease associated with voice disorders
Parkinson disease — Approximately 70 to 90 percent of patients with Parkinson disease exhibit laryngeal findings. The voice is typically hypophonic with a soft breathy and monotone quality. Resting vocal fold tremor occurs in about 55 percent of patients [27,28]. The speech abnormalities associated with Parkinson disease are collectively termed hypokinetic dysarthria and are caused by three important underlying factors: aerodynamic deficits, inefficient vibratory function, and weak muscle activity [29] (see "Clinical manifestations of Parkinson disease", section on 'Other motor features'). The finding of vocal fold paralysis should raise the possibility of a Parkinson-related syndrome.
Motor neuron diseases — Weakness secondary to progressive degeneration of upper and/or lower motor neurons frequently affects the laryngopharyngeal complex, causing dysphagia, aspiration, dysphonia, and vocal fold paralysis. Approximately one-quarter of patients with amyotrophic lateral sclerosis present with voice or other otolaryngologic symptoms as their initial complaint [27,30].
Tremor — Tremor is a rhythmic, oscillatory movement occurring at rest or with action. Several primary neurodegenerative disorders, including Parkinson disease and multiple sclerosis, can cause resting and intention laryngeal tremors. Tremors may also occur with stroke and tumor. Approximately 25 to 30 percent of patients with essential tremor have laryngeal tremor; laryngeal tremor may present in isolation but more commonly occurs with tremor elsewhere in the body [27].
Myasthenia gravis — Patients with myasthenia gravis may develop fluctuating hoarseness, sometimes associated with dysphagia and stridor. The voice tends to fatigue with repetitive use and recover with rest. Rarely, laryngeal symptoms may precede the appearance of ocular symptoms, in which case the diagnosis can be made with an anticholinesterase test [31].
Functional voice disorders
Functional dysphonia — Functional dysphonia is impairment of voice production without an identifiable organic lesion [32]. Functional dysphonia often affects people in occupations that cause vocal stress, with teachers representing the largest occupational group seeking help in vocal clinics.
Laryngeal conversion disorder — The larynx and throat are potential somatization targets for patients with psychological issues. Findings vary, but patients may present with intermittent episodes of respiratory distress, stridor, hoarseness, or aphonia, without a clear-cut diagnosis. Episodes may be triggered by illness such as upper respiratory tract infections or asthma.
Paradoxical vocal cord motion — Vocal fold adduction occurring with inspiration and abduction occurring with expiration results in marked inspiratory stridor and can be mistaken for asthmatic wheezing. Paradoxical vocal cord motion is discussed in detail separately. (See "Inducible laryngeal obstruction (paradoxical vocal fold motion)".)
Other conditions
Leukoplakia — Leukoplakia is a clinical description of a white lesion representing a thickened patch of epithelium. Focal leukoplakic lesions may be benign (keratosis), precancerous (dysplasia), or frankly malignant and require biopsy for definitive tissue diagnosis. Benign lesions typically result from chronic exposure to smoking, alcohol, vocal strain, chemical irritants, and GERD.
A keratotic lesion implies the development of keratin on the normally non-keratinized stratified squamous epithelium of the vocal cord. Lesions with increasing degrees of atypia carry an increased risk of developing carcinoma. Approximately 2 to 10 percent of keratotic lesions ultimately develop into carcinoma.
Laryngeal amyloidosis — Laryngeal amyloidosis most often represents a localized form of amyloidosis, though it can occasionally be associated with systemic disease [33]. Laryngeal amyloidosis usually causes hoarseness or progressive dysphonia, though patients may also present with dyspnea, cough, stridor, odynophagia, and rarely hemoptysis. Laryngeal examination typically reveals a firm orange-yellow to grey epithelial nodule. Primary treatment is with endoscopic microsurgical removal of deposits [34,35].
Long-term follow-up is important, as localized disease may be slowly progressive [34]. Patient evaluation should include blood and urine tests to exclude systemic amyloidosis. (See "Clinical presentation, laboratory manifestations, and diagnosis of immunoglobulin light chain (AL) amyloidosis".)
Infections and inflammatory disease — Inflammatory or infectious disorders of the neck, skull base, and mediastinum, including radiation-induced fibrosis and tuberculosis, may cause unilateral vocal fold paralysis. Vocal fold paralysis can also be seen following viral upper respiratory tract infection. Unilateral vocal fold paralysis associated with herpesvirus infection has been reported [36,37]. (See "Clinical manifestations and complications of pulmonary tuberculosis", section on 'Laryngeal tuberculosis'.)
Other less common etiologies for chronic laryngitis include autoimmune disorders or systemic diseases (eg, rheumatoid arthritis, pemphigoid, systemic lupus erythematosus, or sarcoid) [4]. These etiologies may be considered when patients have systemic symptoms in addition to chronic laryngitis. Rheumatoid arthritis can arise in the cricoarytenoid joints resulting in joint fixation with vocal fold immobility. Rheumatoid nodules can also be seen on the true vocal folds.
CLINICAL EVALUATION
History — The history of a voice disorder should include the following components:
●Duration of voice complaints and whether symptoms are constant or intermittent
●Character of onset (ie, sudden or gradually progressive) and pattern (ie, worse with voice use or worse in the morning upon arising)
●Potential triggering factors (vocal abuse, concurrent upper respiratory tract infection, change in medications, exposure to known allergens or toxins)
●Exacerbating and ameliorating factors, such as improvement with voice rest, or fatigue with use
●Other head and neck symptoms (eg, dysphagia, otalgia, odynophagia, odynophonia, bleeding, throat pain, postnasal drip)
●History of smoking and alcohol use or use of medications which can affect the voice (eg, inhaled steroids for asthma)
●History of reflux or sinonasal disease
●History of past surgery involving the neck (especially thyroid, carotid, and cervical spine), base of skull, or chest
●History of trauma or endotracheal intubation
●Occupation, hobbies, and habits impacting voice use
●Medical comorbidities which may affect voice (eg, rheumatoid arthritis, tremor, hypothyroidism)
Symptoms that raise a flag for underlying malignancy, when not associated with an acute respiratory infection, include shortness of breath, stridor, cough, hemoptysis, throat pain, dysphagia, odynophagia, and weight loss. A history of smoking and alcohol use increases the risk for squamous cell carcinoma of the larynx. Referred ear pain via cranial nerves IX and X may represent one of the first symptoms of laryngopharyngeal cancer.
Physical examination — The physical examination should begin by noting the quality of the patient's voice. Many voice disturbances are typically described by the catch-all term "hoarseness," but should be more critically evaluated:
●Hoarseness is a coarse, scratchy sound that frequently correlates with irregularity of the medial, or vibratory, edge of the true vocal fold. Underlying pathology may relate to laryngitis, an early vocal fold malignancy, a benign mass lesion, vocal fold hemorrhage, or mucosal disruption.
●Breathiness is a term describing the perception of excessive air escape during phonation, in which the voice sounds or feels "weak." This is usually secondary to incomplete closure of the vocal folds, as seen with vocal fold paralysis, atrophy, mass lesions preventing contact of the vocal fold edges, and pathology of the cricoarytenoid joint.
●Vocal fatigue refers to degradation in vocal quality and loss of control of vocal quality with extended periods of voice use. This can be secondary to local anatomic or physiological factors at the level of the vocal folds; poor vocal technique with misuse of neck or abdominal musculature; or systemic conditions such as dehydration, neuromuscular disorders, generalized malaise, or de-conditioning.
●The voice may sound wet, gurgling, full, or "hot-potato-like," as with peritonsillar abscess or supraglottic tumor mass with salivary pooling.
●The voice may exhibit a tremulous quality, and tremor may be seen on examination. Inability to produce any sound is described as aphonia.
Although not absolutely definitive, various voice qualities may correlate with underlying etiologies for the voice disorder.
The physical examination should include an assessment of the ears, upper airway mucosa, oral cavity (including tongue mobility), cranial nerve function, and respiration. Systemic diseases should be considered when suggested by symptoms or examination, including hypothyroidism, neurologic conditions such as tremor, Parkinson disease, amyotrophic lateral sclerosis, or multiple sclerosis [38].
Patients with hoarseness persisting for more than two weeks, in the absence of symptoms of an acute respiratory infection, should have a complete head and neck examination with visualization of the laryngopharynx by an otolaryngologist. This may be performed on the awake patient by indirect laryngoscopy using a mirror or via transnasal or transoral laryngoscopy with a digital or fiberoptic endoscope. In some cases, examination under general anesthesia may be necessary.
The examination should emphasize complete visualization of the true and false vocal folds, epiglottis, pyriform sinus, and vallecula. Computed tomography (CT) scanning or other radiographic evaluation is not a substitute for direct laryngeal examination, although it may serve as a valuable adjunct. Additional evaluation of the vibratory characteristics of the vocal fold may be necessary and is most commonly achieved using high-magnification endoscopy under stroboscopic lighting (strobovideolaryngoscopy) [39].
MANAGEMENT — Treatment options for hoarseness vary depending on the underlying etiology. Treatment generally consists of voice rest, voice therapy, pharmacotherapy, and/or surgery [40].
Voice rest is used for acute laryngitis, vocal fold hemorrhage, and other conditions where there is acute laryngeal edema and swelling. During voice rest, patients refrain from abusive vocal behaviors to prevent further damage to the vocal folds from fibrosis and scarring. Duration ranges from one to several weeks depending on the problem and balancing other issues such as patient needing to use their voice for work.
Voice therapy involves teaching techniques to minimize harmful behaviors and altering voice production. One aim of therapy is to enable the patient to functionally adapt to laryngeal pathology that may be unalterable, such as vocal fold scarring. Voice therapy may be effective for select conditions such as vocal cord nodules and functional voice disorders.
Pharmacologic therapy includes antibiotics, glucocorticoids, mucolytics, antireflux medication, and nonsteroidal antiinflammatory drugs (NSAIDs). These drugs are usually used as ancillary therapy.
Surgical interventions include but are not limited to microlaryngoscopy with endolaryngeal excision, open neck procedures, and office-based procedures (eg, injections, laser treatments).
Acute laryngitis — Acute laryngitis resolves without specific treatment other than hydration, humidification, and voice rest.
Antibiotics for acute laryngitis are usually unnecessary and may lead to bacterial resistance. A systematic review of studies evaluating antibiotics for acute laryngitis found only three randomized trials that met inclusion criteria [41]. One of these trials found no difference in time to voice recovery in patients randomly assigned to penicillin or placebo [42]. The second trial found no difference in objective voice scores between patients who received erythromycin or placebo; however, subjective reports of voice and cough improvement at one week favored erythromycin [43]. The third trial found that compared with no treatment, antibiotics (fusafungine or fusafungine plus clindamycin) improved clinical cure rates at 5 days, but not at 8 or 28 days [44]. While antibiotic therapy may shorten the course of the voice complaints slightly, acute voice symptoms generally respond within one week regardless of therapy. Thus, antibiotics are not indicated unless there is clear evidence of coexistent bacterial pharyngitis [3,43]. (See "Treatment and prevention of streptococcal pharyngitis in adults and children".)
Systemic glucocorticoids have a limited role in the treatment of acute laryngitis and should be reserved for patients who have a pressing need to use their voice (eg, professional speaking engagement or vocal performance). Although clinical experience suggests that the administration of steroids can lead to rapid resolution of vocal fold inflammation and an improvement in vocal quality, there are no randomized trials of glucocorticoid use for laryngitis in adults. Glucocorticoid use should be balanced by the adverse systemic effects, as well as the risk of masking underlying vocal fold pathology. If the performer strains an already compromised larynx, it can lead to vocal fold hemorrhage with the potential for permanent scarring and voice change.
Chronic laryngitis — Chronic laryngitis due to irritants generally resolves with removal of the offending agent.
Treatment of chronic laryngitis due to laryngopharyngeal reflux is discussed separately. (See "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management", section on 'Treatment' and "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management".)
Muscle tension dysphonia may be amenable to voice therapy [45]. A typical course of voice therapy includes retraining of the vocal muscles, education regarding proper care of the voice (vocal hygiene), and avoidance of counterproductive vocal behaviors, such as yelling or straining to speak over background noise.
Benign vocal cord lesions — Treatment for polypoid corditis, polyps, and nodules includes smoking cessation, reflux management, and voice therapy. Intralesional steroid injection has been shown to be beneficial [46]. Surgical debulking/recontouring may be necessary in certain cases or when focal irregularity warrants biopsy.
The treatment of polyps usually requires surgery, whereas treatment for nodules is aimed at correcting vocal strain and maladaptive vocal habits and usually does not require surgery. Surgery is generally reserved for cases in which vocal quality is judged to be inadequate following voice therapy. A 2012 systematic review found no randomized trials that compared the effectiveness of surgical versus nonsurgical management for vocal cord nodules [47].
Laryngeal cancer — The five-year cure rate is over 90 percent for small, early-stage vocal fold lesions, with laryngeal and voice preservation. Cure rates are reduced by half once the lesion metastasizes to regional cervical lymph nodes. (See "Treatment of locoregionally advanced (stage III and IV) head and neck cancer: The larynx and hypopharynx".)
Vocal fold paralysis — A recurrent laryngeal nerve that has been surgically transected or infiltrated with malignancy will not resume function. However, speech and swallowing therapy can be helpful by developing compensatory behaviors. In nerves that have sustained bruising or stretch injury without transection (neurapraxia), function generally returns within six months to one year. Laryngeal electromyography (EMG) can offer prognostic information regarding the likelihood of return of function [48]. Permanent uncompensated unilateral vocal cord paralysis can be treated with surgical interventions. (See 'Surgical treatments' below.)
Medications — No medications are used to treat vocal cord paralysis. However, preliminary studies in patients with acute (<4 months’ duration) idiopathic or iatrogenic unilateral or bilateral vocal cord paralysis have suggested that nimodipine may improve recovery rates [49-51]. It is hypothesized that nimodipine may speed axonal regeneration by blocking the transient intracellular influxes of calcium ions within neurons to improve propagation of the growth cones in the injured nerve. Randomized trials are needed to further evaluate nimodipine for the treatment of vocal cord paralysis.
Surgical treatments
●Unilateral paralysis – Surgical procedures are available for unilateral fold paralysis to reposition (medialize) the immobile vocal fold in order to achieve adequate glottal closure and improve voice as well as swallowing and cough [52]. Techniques include [53,54]:
•Injection laryngoplasty, a transoral or transcervical injection of permanent or resorbable material (eg, autologous fat, collagen, hyaluronic acid, hydroxylapatite) lateral to the vocal fold
•Medialization thyroplasty, which involves transcervical placement of an implant (usually silicone or Gore-Tex) through a surgically created window in the thyroid cartilage
•Arytenoid adduction, performed when the vocal cord anatomic position is such that medialization alone is insufficient to improve glottis closure, requiring vocal fold repositioning
•Laryngeal reinnervation, which has been performed with varying degrees of success
●Bilateral paralysis – Treatment of bilateral vocal fold paralysis primarily relates to the need to provide an adequate airway. Procedures to widen the airway are usually performed at the expense of vocal quality. Available treatments include tracheotomy, vocal fold lateralization, resection of a portion of the posterior vocal fold and/or arytenoid, and laryngeal reinnervation.
Spasmodic dysphonia — Voice therapy is generally not effective, although it may help minimize vocal fatigue and improve breath control. Injection of botulinum toxin into the affected laryngeal muscles helps to reduce severity of symptoms [55-57]. (See "Treatment of dystonia in children and adults", section on 'Focal dystonia'.)
Neurologic disease associated with voice disorders — Treatments for voice disorders associated with neurologic diseases, such as Parkinson disease or laryngeal tremor, are aimed at the underlying illness. For Parkinson disease, the mainstay of treatment is behaviorally based intensive voice therapy (Lee Silverman Voice Treatment), designed to improve loudness by increasing phonatory effort. For patients with laryngeal tremor, injection of botulinum toxin is associated with improved patient-reported voice quality [55].
Functional dysphonia — A systematic review of six randomized trials in patients with functional dysphonia found that voice therapy, compared with no intervention, improved perceived and objective measures of vocal function that persisted for at least 14 weeks [32]. Prophylactic voice therapy for high-risk occupations was not effective.
REFERRAL — Patients who have hoarseness that lasts for more than two weeks, in the absence of symptoms of an acute upper respiratory infection, should have a complete otolaryngologic examination to rule out potentially serious causes such as malignancy. This is particularly a concern in patients with a history of tobacco or alcohol use who are at high risk for cancer of the head and neck. Patients with associated symptoms concerning for malignancy should also be referred to an otolaryngologist. (See 'Clinical evaluation' above.)
Patients with recent surgery involving the neck or recurrent laryngeal nerve or endotracheal intubation should also be referred for an otolaryngologic evaluation early [4].
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Laryngitis (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Anatomy – The laryngopharynx is composed of a cartilage framework, true and false vocal folds, extrinsic and intrinsic muscles, a neurovascular supply, and overlying soft tissues. It functions to allow phonation, Valsalva, airway patency during respiration, and airway protection during swallowing. (See 'Anatomy of the larynx' above.)
●Clinical evaluation – In a patient with voice disturbance not due to acute upper respiratory tract infection, symptoms of shortness of breath, stridor, cough, hemoptysis, throat pain, difficulty swallowing, unilateral otalgia, fever, night sweats, or weight loss should raise concern for cancer, and the patient should be promptly referred to an otolaryngologist. (See 'Clinical evaluation' above.)
●Etiology – The differential diagnosis of sustained hoarseness is broad and includes infection, laryngeal irritants, benign vocal fold lesions, laryngeal cancer, neurologic dysfunction, and functional disorders. Evaluation by an otolaryngologist with direct visualization of the vocal folds is necessary to determine the etiology and treatment of voice disorders. (See 'Causes of hoarseness' above.)
●Management – Management of hoarseness depends on the underlying cause. Treatment options include removal of offending agents, voice therapy, medications, treatment of underlying systemic disease, and surgery. (See 'Management' above.)
•Acute laryngitis, associated with an upper respiratory infection or acute vocal strain, generally lasts less than three weeks. We recommend not treating patients with antibiotics for acute laryngitis (Grade 1B). (See 'Acute laryngitis' above.)
•We suggest not routinely treating patients with glucocorticoids for acute laryngitis (Grade 2C). While clinical observation suggests that a course of oral glucocorticoids can speed the resolution of acute laryngitis, this may increase the risk of additional vocal fold damage such as hemorrhage and scarring. In certain circumstances (professional singers or speakers), it may be appropriate to offer such therapy with informed consent; such treatment it is best managed by a specialist in voice disorders. (See 'Acute laryngitis' above.)
●Referral – Hoarseness that lasts for more than two weeks, in the absence of symptoms of an acute upper respiratory infection, requires a complete otolaryngologic examination, particularly in patients with a history of tobacco or alcohol use. (See 'Referral' above.)
