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Eustachian tube dysfunction

Eustachian tube dysfunction
Literature review current through: Jan 2024.
This topic last updated: Nov 30, 2023.

INTRODUCTION — The middle ear is an air-filled chamber within the skull that is periodically vented when the Eustachian tube (ET) opens. Middle ear disease may be due, at least in part, to failure or inadequacy of ET function.

A normally functioning ET ventilates the middle ear space, allows drainage of middle ear secretions, and protects the middle ear from sound and the reflux of nasopharyngeal contents [1]. ET dysfunction represents a spectrum of disease ranging from obstructive dysfunction, in which there is failure to open to provide adequate ventilation to the middle ear, to the opposite extreme, patulous dysfunction, in which there is failure of the ET to close. It has become increasingly clear that the underlying pathophysiology that causes ET dysfunction may lead to either obstructive or patulous pathology, and that patients may move back and forth on this spectrum, creating difficulties in diagnosis and appropriate treatment; careful evaluation is necessary to make the correct diagnosis.

This topic will discuss the pathophysiology, evaluation, and treatment of ET dysfunction. Specific diseases associated with ET dysfunction are discussed elsewhere:

(See "Acute otitis media in adults".)

(See "Chronic otitis media and cholesteatoma in adults".)

(See "Etiology of hearing loss in adults".)

(See "Ear barotrauma".)

(See "Acute otitis media in children: Clinical manifestations and diagnosis".)

(See "Acute otitis media in children: Treatment".)

(See "Acute otitis media in children: Prevention of recurrence".)

(See "Otitis media with effusion (serous otitis media) in children: Management".)

ANATOMY — The Eustachian tube (ET) originates from the anterior wall of the middle ear cavity (called the protympanum) and passes anteroinferiorly to open into the nasopharynx (figure 1 and picture 1). The nasopharyngeal and tympanic ends are wider than the middle of the ET, with the bony isthmus being the narrowest portion. The ET passes superiorly, posteriorly, and laterally from the nasopharynx to the middle ear [2]. Its total length in adults ranges from 36 to 38 mm. Children have shorter, more horizontal tubes, immature floppy elastic cartilage, and larger adenoids compared with adults. This places them at a higher risk for ET obstruction as well as reflux of nasopharyngeal secretions and pathogens (figure 2) [3,4]. The ET in children usually reaches adult length by age 8 [5], but function may continue to mature with further development of the skull. In addition, the height of the ET orifice above the floor of the nasal cavity appears to reach adult dimension around age 18.

The ET is not a static pipe; it is a dynamic structure with a lumen, skeleton, mucosal lining, and surrounding soft tissue and muscles (figure 3) [6,7]. The skeleton of the tube is formed of cartilage in its inferior and medial two-thirds, and bone in the superior and lateral one-third. The bony portion lies within the petrous part of the temporal bone, while the cartilaginous portion is firmly attached superiorly to the sphenoid bone [8]. The bony portion is normally patent and does not open and close dynamically as does the cartilaginous portion [9]. Within the bone and cartilage are the four muscles related to ET function: tensor veli palatini (TVP), levator veli palatini (LVP), tensor tympani, and salpingopharyngeus. The most important muscles for tube dilation are the TVP, the principal active tubal dilator, and the LVP, which sets the cartilaginous skeleton into position against which the TVP can complete the dilation [8]. The anterolateral wall is membranous and consists of the luminal mucosa, submucosa, adipose tissue (called Ostmann’s fat pad), and the TVP muscle [2]. The mucosal lining of the ET is continuous with the rest of the respiratory tract.

Viewing the ET orifice from the nasopharynx with an endoscope (picture 2), the lumen lies just anterior and lateral to the posterior cushion. The adenoid pad is situated in the midline of the nasopharynx [10].

NORMAL EUSTACHIAN TUBE FUNCTION — The Eustachian tube (ET) has three functional roles [1,2,8]:

Equalization of pressure across the tympanic membrane (TM), which is considered the most important function of the ET, as gas pressure homeostasis is essential for optimal auditory function

Protection of the middle ear from infection and reflux of nasopharyngeal contents

Clearance of middle ear secretions

These three functions are mediated by opening and closing of the ET (picture 3). The tube ordinarily opens with swallowing and yawning, which occur approximately 84 times per hour while awake and less frequently during sleep [8,10], although not every swallow or yawn is accompanied by ET opening.

The recoiling memory properties of the cartilaginous ET, relaxing bulk of the tensor veli palatini (TVP) muscle, and pressure of neighboring extraluminal tissue cause the tube to close passively. The closed tube lumen is likely maintained by these factors, as well as by the overlying Ostmann’s fat pad and the surface tension of the apposed wet mucosal surfaces, which in aggregate serve as a functional valve that opens intermittently for ventilation [11]. This functional valve in the middle of the cartilaginous portion of the tube is roughly 15 to 20 mm in length [12].

PATHOPHYSIOLOGY OF EUSTACHIAN TUBE DYSFUNCTION — Eustachian tube (ET) dysfunction can be separated into three pathophysiologic processes: pressure dysregulation/impaired ventilation, impaired protective function, and impaired clearance [1,2,6].

Pressure dysregulation/impaired ventilation — The ET may fail to open adequately to allow for ventilation of the middle ear space, leading to pressure dysregulation [6]. Failure of the ET to open generally occurs due to functional or anatomic obstruction.

Functional obstruction – Functional obstruction refers to compromise of normal tubal dilation in the absence of a fixed physical blockage of the lumen. Chronic functional obstruction is most commonly due to mucosal inflammation with edema and secretions which limit the ability of the functional valve to open.

Less commonly, failure of muscular actions may limit the dilatory ability of the ET [10]. Impaired muscular function is common in cleft palate and other craniofacial syndromes in which the abnormal muscular and skull anatomy lead to reduced efficiency of the dilation action [13]. True muscular dysfunction or weakness can also occur in conditions such as in amyotrophic lateral sclerosis or myasthenia gravis. (See "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Clinical symptoms and signs' and "Overview of craniofacial clefts and holoprosencephaly", section on 'Problems associated with clefts'.)

In the middle ear, negative pressure is induced by the continuous absorption of middle ear gasses and can also be exacerbated under certain circumstances (eg, descent during air travel, scuba diving). It can also occur secondary to behaviors such as habitual sniffing and thumb sucking with obstructed nasal passages. Further, the negative pressure present within the elastic ET makes it more difficult for the tubal muscles to dilate the lumen. A functionally impaired ET may be able to partially open, but dilation may be insufficient to adequately ventilate the continually accumulating negative pressure within the middle ear. Once excessive negative pressure occurs within the middle ear, it becomes a self-perpetuating cycle in which the absence of ET opening makes it increasingly difficult to dilate the tube, and the failure to open further increases the negative pressure. Unless this cycle is interrupted, pressures may exceed negative 400 dekapascals (daPa) and cause transudate to fill the space. Conversely, positive middle ear pressure (relative to ambient pressure, as occurs with ascending from deep water, in an airplane, or in the mountains), facilitates opening of the tubal lumen.

Anatomic obstruction – True anatomic obstruction occurs infrequently. Intrinsic obstruction may be due to severe inflammation with swelling of mucosa, polyps, or neoplasms within the ET lumen; synechiae (intranasal adhesions or scar tissue); or congenital or acquired stenosis. ET lumen or orifice obliteration is most commonly the result of trauma but can also be a complication of surgical procedures, such as adenoidectomy, turbinectomy and maxillary osteotomy. It can also occur from inflammatory disease (eg, granulomatosis with polyangiitis [GPA] and mucosal pemphigus). Extrinsic obstruction can occur from a large adenoidal mass or nasopharyngeal neoplasm. (See "Granulomatosis with polyangiitis and microscopic polyangiitis: Respiratory tract involvement", section on 'Nasal, sinus, and ear disease' and "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma" and "Pathogenesis, clinical manifestations, and diagnosis of pemphigus", section on 'Clinical features' and "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical manifestations and diagnosis", section on 'Ear, nose, and throat involvement'.)

Impaired protective function — The ET normally protects against the reflux of nasopharyngeal pathogens, allergy-inducing proteins, and gastric secretions into the middle ear. If refluxed gastric secretions reach the ET, there may be loss of mucosal protection; nasopharyngeal and ET mucosa do not contain the protective proteins found in the stomach mucosa. The ET also serves to limit hearing the sounds of one's own breathing and speaking (autophony).

Protection against reflux depends upon competence of the functional valve of the ET. Valve closure progresses proximally to distally (from the ear toward the nasopharyngeal orifice), creating a pumping action that further serves to prevent reflux [14].

ET reflux occurs in the following conditions:

An abnormally patent ET (congenital or acquired).

Short, "floppy" ETs, as typically seen in young children and in some patients with craniofacial anomalies. Bottle-fed children are at higher risk for ET reflux compared with breast-fed children, especially if conventional nonventilated bottles are used [15,16]. (See "Acute otitis media in children: Epidemiology, microbiology, and complications", section on 'Risk and protective factors'.)

Elevated pressure in the nasopharynx can force material into the tube lumen; nasopharyngeal obstruction, blowing the nose, and crying can induce abnormal positive pressures at the nasopharyngeal end of the tube.

Impaired clearance — Impaired ET mucociliary function can result in the inability to clear viscous material and pathogens from the middle ear.

Loss of ciliary function can occur from bacteria and bacterial toxins, viruses, smoking, toxin exposure, allergic disease, and other sources of inflammation [17]. Ciliary function may also be impaired in inflammatory conditions such as Samter's triad (ie, asthma, nasal polyps, and aspirin sensitivity). Less commonly, primary loss of mucociliary function occurs in cystic fibrosis and other ciliary dysmotility disorders. (See "Cystic fibrosis: Clinical manifestations and diagnosis", section on 'Sinus and nasopharyngeal disease' and "Primary ciliary dyskinesia (immotile-cilia syndrome)", section on 'Clinical manifestations' and "Aspirin-exacerbated respiratory disease", section on 'Chronic rhinosinusitis with nasal polyposis'.)

Copious or viscous mucosal secretions within the middle ear and ET lumen may impair the adequate expulsion of pathogens from the middle ear.

ET clearance can have postural variation as well. Venous engorgement occurs when the head is in a dependent position; this may not be physiologically significant for most people, but patients with a patulous ET (in which the functional valve fails to close) may find symptomatic relief by lying down.

Impaired ET clearance may also have a seasonal variation due to the increased incidence of upper respiratory infections in the fall and winter months, as well as seasonal environmental allergies (eg, pollens in spring and summer and dust and molds in fall and winter) [18].

ETIOLOGIES OF EUSTACHIAN TUBE DYSFUNCTION

Spectrum of Eustachian tube dysfunction — Eustachian tube (ET) dysfunction represents a spectrum of disease ranging from obstructive dysfunction, in which there is failure of opening to provide adequate ventilation to the middle ear, to the opposite extreme, patulous dysfunction, in which there is failure of the ET to close [19].

Obstructive dysfunction is believed to be responsible for a large proportion of otitis media and chronic ear disease and is more common than patulous dysfunction. However, patulous dysfunction is probably far more common than previously realized [20], and it can cause bothersome symptoms that may be mistaken for obstructive dysfunction. Although the symptoms may be profoundly disturbing to patients, patulous dysfunction generally does not lead to any significant acute or chronic ear disease.

It has become increasingly clear that the underlying pathophysiology that causes ET dysfunction may lead to either obstructive or patulous pathology and that patients may move back and forth on this spectrum, creating difficulties in diagnosis and appropriate treatment. For example, in a series of 239 ETs with patulous dysfunction, 30 percent had evidence of chronic ear disease associated with past obstructive ET dysfunction, including tympanosclerosis, middle ear effusion, fixed retraction pockets, atelectasis of the tympanic membrane (TM), and cholesteatoma [20,21]. A careful evaluation is thus necessary to establish a correct diagnosis.

In some cases, however, the etiology of ET dysfunction is not identified, and the condition may resolve spontaneously without ever being diagnosed.

Obstructive dysfunction — Obstructive ET dysfunction is defined as the impaired ability to equalize pressure between the middle ear and nasopharynx, often associated with visible retraction of the TM or evidence of negative pressure in the middle ear (picture 4) [1].

There are several well-described factors that are associated with obstructive failure of the ET in both adults and children [8,19,22]:

Any cause of inflammation affecting the oropharyngeal mucosa:

Infection affecting the adenoids, nasopharynx, nose, and sinuses. Several chronic infections such as acute and chronic rhinosinusitis are frequently associated with obstructive dysfunction and middle ear effusion [23,24]. (See "Chronic rhinosinusitis: Clinical manifestations, pathophysiology, and diagnosis", section on 'Signs and symptoms' and "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis", section on 'Clinical features'.)

Seasonal and environmental allergies. (See "Allergic rhinitis: Clinical manifestations, epidemiology, and diagnosis", section on 'Clinical manifestations'.)

Irritants such as tobacco smoke, electronic cigarette aerosol, wood burning stoves, and air pollution [25]. (See "Chronic nonallergic rhinitis", section on 'Characteristic triggers'.)

Laryngopharyngeal and gastroesophageal reflux. (See "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management" and "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".)

Hormonal changes (eg, "pregnancy rhinitis", particularly in the third trimester when progesterone levels are peaking). (See "Recognition and management of allergic disease during pregnancy", section on 'Pregnancy rhinitis'.)

Primary mucosal disease (eg, aspirin-exacerbated respiratory disease [AERD or Samter’s triad], granulomatosis with polyangiitis [GPA]). (See "Aspirin-exacerbated respiratory disease", section on 'Chronic rhinosinusitis with nasal polyposis' and "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical manifestations and diagnosis", section on 'Ear, nose, and throat involvement'.)

Ciliary disorders (eg, primary ciliary dyskinesia). (See "Primary ciliary dyskinesia (immotile-cilia syndrome)", section on 'Rhinosinusitis'.)

Pressure dysregulation during scuba diving or air travel, also known as baro-challenged ET dysfunction. (See "Complications of SCUBA diving", section on 'Ear barotrauma' and "Ear barotrauma", section on 'Etiologies'.)

Acquired anatomic abnormalities:

Nasopharyngeal masses, including neoplasms, can physically block the orifice, invade or compress the tube lumen, interfere with the tensor veli palatini (TVP) and levator veli palatini (LVP) dilatory muscles, or impinge on nerves. (See "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma", section on 'Clinical presentation'.)

Trauma, surgery (eg, adenoidectomy, turbinectomy, maxillofacial, or cleft palate repair), or intubation (nasogastric or nasotracheal) might lead to injury of the ET, surrounding muscles, or palatopterygoid bone. Injury to the trigeminal nerve or its mandibular branch can lead to functional obstruction due to impaired TVP muscle function.

Chronically hypertrophied adenoids may functionally or, more rarely, anatomically occlude the tubal orifice (picture 5). Contact of the adenoid with the torus tubarius of the ET may cause anterior displacement of the torus during swallowing, which functionally occludes the lumen at the time it should be dilating (called “anterior thrusting”).

Congenital abnormalities include congenital cholesteatoma, dermoid cysts, cleft palates, and other craniofacial syndromes such as Down, Crouzon, Apert, Treacher-Collins, and Turner syndromes.

Degenerative neurologic and neuromuscular diseases (eg, multiple sclerosis, Parkinson disease, myasthenia gravis, amyotrophic lateral sclerosis), and metabolic diseases (eg, diabetes, glycogen storage diseases) affecting the tubal musculature. (See "Clinical presentation, course, and prognosis of multiple sclerosis in adults" and "Clinical manifestations of Parkinson disease" and "Clinical manifestations of myasthenia gravis" and "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease" and "Overview of inherited disorders of glucose and glycogen metabolism", section on 'Muscle symptoms'.)

Patulous dysfunction — Patulous dysfunction (chronic ET patency) is much more common than previously believed, as it is underrecognized and often misdiagnosed as obstructive ET dysfunction. It is estimated that 6 to 7 percent of the population has some degree of patulous ET dysfunction [26,27].

Differentiating between obstructive and patulous conditions is important in order to offer the appropriate treatment. The differential diagnosis can be challenging; patients will often complain of blockage or aural fullness or pressure and may not volunteer symptoms of autophony. Furthermore, many patients initially suffer from obstructive ET dysfunction but can progress to patulous dysfunction over time. This may be due to atrophy of the ET luminal mucosa and submucosa that also occurs within the nose and sinuses [28-30].

Several associated and causative factors have been reported [11,31-36]. As an example, in a review of 190 patients with confirmed patulous ET, the following associations were found [20]:

Allergic disease (50 percent of patients) – Chronic inflammation from allergic disease is known to cause patches of mucosal burnout with mucosal and submucosal atrophy in the nose and sinuses. Similar patchy atrophy has been observed within the functional valve of the ET and is suspected of causing incompetence of the valve. (See "Allergic rhinitis: Clinical manifestations, epidemiology, and diagnosis".)

Weight loss (38 percent of patients) – As little as a six-pound weight loss may be sufficient to produce tissue atrophy and patulous ETs. This may be due to a variety of chronic illnesses, especially rheumatologic diseases, but also from intentional weight loss.

Laryngopharyngeal reflux (33 percent of patients) – Laryngopharyngeal reflux (LPR) may induce mucosal atrophy, leading to patulous dysfunction. (See "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management".)

Stress and anxiety (31 percent of patients) – Chronic lateralization of the anterolateral wall in the valve, possibly due to tension in the TVP muscle or underlying medial pterygoid muscle, has been observed in patient with patulous ETs. The medial pterygoid muscle may serve as an auxiliary dilator of the ET. Excessive muscular tension may be related to recurrent clenching of facial and jaw muscles (eg, with stress or anxiety), bruxism, or other forms of temporomandibular disorders (TMD), including temporomandibular joint (TMJ) dysfunction.

In addition, other factors associated with or contributing to patulous dysfunction include:

Dehydration (eg, due to exercise, caffeine, or diuretics).

Neuromuscular disorders leading to muscle atrophy (eg, stroke, multiple sclerosis, poliomyelitis, traumatic injury to the trigeminal nerve).

Scarring or atrophy of mucosa as a result of previous surgical procedures, instrumentation, inflammation, or radiation [37].

Allergic rhinitis is thought to predispose to patulous ET dysfunction. Chronic allergic rhinitis is associated with patchy atrophy of nasal and sinus mucosa [28-30]. Such atrophy can be recognized within the lumen of the ET, even when the orifice, torus tubarius, or adenoid shows significant inflammation. If mucosal and submucosal atrophy occurs within the functional valve of the ET, it can lead to incompetence and patulous symptoms.

Hormonal factors, such as high estrogen levels in pregnancy.

Drugs, including stimulants (eg, topical [nasal] or systemic decongestants, nicotine, topical [nasal] or systemic cocaine), topical (nasal) steroid sprays, systemic antihistamines.

CLINICAL EVALUATION — Eustachian tube (ET) dysfunction is a generally a clinical diagnosis, based upon the history and physical examination. The diagnosis can be confirmed by nasal endoscopy and audiology studies. Other tests assessing for the etiology of the dysfunction are conducted based upon the patient's clinical situation (eg, allergy testing in a patient with persistent allergic symptoms). When available, additional testing modalities such as tympanometry, sonotubometry, and tubomanometry may aid diagnosing ET dysfunction, although there is no gold standard diagnostic test [1,21]. (See 'Physical examination' below.)

Many patients, particularly younger children, do not complain of ear problems but are discovered incidentally to have otitis media with effusion (OME) on a routine examination. In children ages 6 and older who have OME, allergies causing obstructive ET dysfunction should be suspected [38]. Additionally, in children who have delayed speech or language development or abnormal hearing screening tests, ET dysfunction should be considered.

History — In the evaluation of possible ET dysfunction, we inquire about specific symptoms, particularly those that may distinguish obstructive from patulous tubal dysfunction, as well as underlying causes and possible complications. (See 'Complications of Eustachian tube dysfunction' below.)

Hallmarks of obstructive ET dysfunction include symptoms during baro-challenge (eg, consistent difficulty equalizing ear pressure during air travel or with altitude changes) and a history of otitis media. Additional symptoms may include ear pain, a sensation of aural fullness or pressure, hearing loss, and tinnitus. Patients commonly describe their ear(s) as feeling "plugged" and may also report ear popping and snapping noises. Vertigo and disequilibrium may be reported in severe cases of negative pressure or in association with otitis media.

Patulous ET dysfunction can be asymptomatic or may present with symptoms that range from minimal and intermittent to persistent and severely disturbing; for some patients, symptoms may be disabling. In patulous ET dysfunction, patients classically experience a loud perception of their own internal sounds (autophony), most specifically of their own voice and breathing (autophony can be simulated by listening through a stethoscope while talking, or while breathing close to the stethoscope diaphragm). The patient may describe hearing their own voice as if "talking into a barrel.” For patients, hearing one’s own voice is generally more bothersome than hearing one's own breathing sounds. Symptoms of patulous dysfunction often fluctuate. For example, they may be relieved with the head in a dependent position and may be aggravated by activities that cause mucosal dehydration, such as exercise and prolonged speaking or singing. There can be a decongestive effect on mucosa from the epinephrine-like hormones released with exercise [11].

Pulsatile tinnitus is also common in patulous ET dysfunction. Importantly, patients with patulous dysfunction may also complain of aural fullness similar to patients with obstructive dysfunction.

We inquire about symptoms and pertinent medical history that may suggest a direct cause of or exacerbating factors for the ET dysfunction. As examples:

Nasal itch, frequent sneezing, and rhinorrhea suggest allergies. (See "Allergic rhinitis: Clinical manifestations, epidemiology, and diagnosis".)

Discolored nasopharyngeal discharge and sinus pressure may suggest recurrent or chronic rhinosinusitis. (See "Chronic rhinosinusitis: Clinical manifestations, pathophysiology, and diagnosis".)

Sore throat, cough, heartburn, frequent choking, voice changes, and excessive salivation suggest laryngopharyngeal reflux (LPR). (See "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management".)

Nasal obstruction might be a symptom of a mass lesion, particularly if it is unilateral. (See "Nasal obstruction: Diagnosis and management".)

Smoking, or exposure to secondhand smoke or other irritants, may be a contributing factor.

A history of head and neck radiation therapy.

In persistent cases, we ask patients about habits that may precipitate or exacerbate ET dysfunction, such as habitual sniffing or forceful attempts to aerate their middle ears and relieve the sense of pressure/obstruction. Habitual sniffing can cause chronic negative pressure in the middle ear that may lead to retraction of the tympanic membrane (TM). In addition, forceful nose blowing or autoinsufflation can force the ET open, but repetition over time may distend and weaken the ET and potentially result in a patulous tube.

The ET dysfunction questionnaire (ETDQ-7) is a validated seven-item scoring questionnaire for rating the severity of symptoms associated with ET obstructive dysfunction. It assesses ear pressure, ear pain, sensation of clogging, ear symptoms with a cold or sinusitis, popping or crackling sensation, ringing in the ear, and muffled hearing. In a small sample of patients, it had reasonable validity in distinguishing patients with and without ET dysfunction compared with tympanometry [39]. However, it is a nonspecific instrument that cannot distinguish between obstructive and patulous ET dysfunction; it cannot be used as a diagnostic aid, and it is best used to compare pre- and posttreatment symptom scores as an outcome measure [1,40].

Physical examination — We perform a focused head and neck examination, including a hearing evaluation, on every patient with a possible ET problem. Particular attention is given to the ear examination as this is most likely to reveal any underlying etiology and/or complications of ET dysfunction [41]. However, normal otoscopic findings do not rule out ET disease.

Otoscopy – With the patient seated upright, we perform an ear examination using an otoscope, with attention to the TM. A normal TM has a shiny translucent appearance (picture 6). A dull bluish gray or yellowish coloration denotes an effusion behind the TM; an air-fluid level may also be seen (picture 7). A reddish coloration and engorged TM vessels may indicate inflammation, although straining (eg, a child crying or blowing their nose) can also lead to visibly engorged vessels. The light reflection on the anteroinferior quadrant of the TM is not a reliable indicator of changes in the TM, as it is often present despite significant pathology. Scarring and thickening of the TM can alter the shape of the cone of light, so the entire TM should be evaluated systematically.

The short process of malleus is visible as a mild protrusion near the "twelve-o-clock" position in the healthy transparent TM (picture 6 and figure 4). With high negative pressure, the TM is retracted, the short process appears more prominent, and the manubrium (or handle) of the malleus appears shorter because it is medially rotated (picture 4). A middle ear effusion, if present, may obscure the view of the short process. The fullness or retraction of the TM is most clearly appreciated at the posterosuperior aspect, as it has the highest compliance.

The TM is examined for any retractions (picture 4), effusions (picture 8), atelectasis (picture 9), cholesteatomas (picture 10), perforations (picture 11), or myringosclerotic plaques (picture 12 and picture 13). Any of these findings can be seen with obstructive ET dysfunction.

In addition, we observe the TM for movement with respiration. When there is an actively patulous ET, excursions of an intact (ie, nonperforated) TM will accompany the patient's breathing, especially if the contralateral nostril is held closed. Lying in the supine position may temporarily close the ET with the patulous defect and eliminate the breathing-induced excursions. Thus, it is important to perform the otoscopic examination with the patient in an upright position.

We suspect patulous dysfunction in patients who are observed to be frequently sniffing yet have evidence of negative middle ear pressure on examination. Such sniffing represents attempts to close patulous ETs by temporarily generating enough negative pressure to close the ET lumen. The resultant negative pressure, however, may be severe enough to cause retraction of the TM (picture 4) and even middle ear effusion and ultimately middle ear cholesteatoma.

Pneumatic otoscopy – The ear examination is greatly aided with pneumatic otoscopy (picture 14). With gentle application of positive and then negative pressure with the pneumatic otoscope, a normal, intact (nonperforated) TM moves inwards then outwards respectively (movie 1). The movement of the TM is most evident posterosuperiorly. A fluid-filled middle ear will minimize any TM excursions (movie 2). When there is negative pressure within the middle ear, the retracted TM will mobilize laterally and become more compliant with the application of negative pressure.

A fixed retraction pocket or adhesive middle ear disease may persist after resolution of obstructive ET dysfunction or in active patulous ET dysfunction. Evidence of negative pressure on pneumatic otoscopy or tympanogram are indicative of active obstructive ET dysfunction.

Newborn infants have a thicker and more opaque TM than older infants and children; care should be taken not to mistake a normal newborn infant TM for a retracted TM.

Nasal cavity inspection – Inspection of the nasal cavity for abnormalities, including evidence of inflammation, allergic changes, masses [42], bleeding, mucosal granulomatous disease, and polyps.

Neck examination – Neck examination includes visual inspection and palpation for enlarged lymph nodes, masses, or congenital cysts. These findings may indicate inflammatory conditions or neoplasms, especially nasopharyngeal tumors.

Additional components of the physical examination include:

Hearing evaluation – All patients with ET dysfunction should have a hearing evaluation.

We ask all patients with suspected ET dysfunction about hearing loss. In the absence of subjective hearing loss, a screening hearing evaluation can be done with a whispered voice test, or if available, a tone-emitting otoscope. For patients with subjective hearing loss or hearing loss detected with a whispered voice test or tone-emitting otoscope, tuning fork evaluation can determine if the hearing loss is conductive or sensorineural (figure 5 and table 1). For all patients with hearing loss, formal audiology testing is necessary to determine the nature and extent of the hearing loss. (See "Evaluation of hearing loss in adults", section on 'Office hearing evaluation' and "Hearing loss in children: Screening and evaluation", section on 'Evaluation of the child with hearing loss'.)

Conductive hearing loss commonly occurs with obstructive, but not typically with patulous ET dysfunction. However, patients with patulous ET might complain of subjective hearing loss as their hearing is being “distracted” (ie, masked) by autophony.

Nasal endoscopy – Nasal endoscopy, typically performed by an otolaryngologist, may provide helpful diagnostic information in some patients, such as those with severe ear complaints (eg, significant hearing loss or intense otalgia), recurrent otitis media (including acute otitis media and otitis media with effusion [OME]), and persistent unilateral otitis media with effusion. Endoscopy can be used to evaluate the nasopharynx as well as ET anatomy and function. (See 'When to refer to a specialist' below.)

We find it useful to begin the examination using the flexible endoscope and, if more detailed views are needed, the rigid endoscopes (30 or 45 degree view angle) may be used to provide the optimal view. The flexible endoscope is first used to survey the nasal cavity and inspect the sinus orifices for inflammation, secretions, or allergic manifestations. The nasopharynx is also examined for evidence of enlarged or inflamed adenoids or other masses. The relationship of any adenoidal mass to the posterior cushion is noted to determine if may cause impingement on tubal opening at rest or with swallowing. The endoscope is then passed towards the oropharynx, hypopharynx, and larynx to check for evidence of acid reflux, such as thickening, edema, and erythema of the vocal cords.

Examination of the ET is performed last. The best view into the ET lumen is often obtained by passing the flexible endoscope from the contralateral nares, curving around the vomer bone to come in line with the longitudinal axis of the ET (picture 15 and picture 5 and picture 2). Patients are asked to perform a series of swallows and yawns to assess the quality and dynamics of the opening of the tube (picture 3). The lumen is inspected with an angled view to assess for inflammation and compromise of valve function. We also assess whether hypertrophy of the adenoid or tubal tonsil tissue may compromise opening of the ET during swallows due to the muscular compression exerted from the lateral pharyngeal wall. Hypertrophy of the torus tubarius or adenoid may cause anterior thrusting of the torus due to this compression, paradoxically forcing the lumen closed when it should be opening. This dynamic process will be missed unless an angled view is obtained and observation done during swallows and yawns.

Tympanometry and audiometry – Both tympanometry (to measure the middle ear pressure) and pure tone audiometry (to assess for hearing loss) are important tools in evaluation of ET dysfunction; they can be used both to help diagnose ET dysfunction and to provide an objective measurement of response to therapy.

Tympanometry is a reliable instrument that determines normal versus abnormal pressures within the middle ear; it can indirectly measure middle ear pressure by comparing changes in TM compliance with changes in external ear canal pressure. The presence of a middle ear effusion stiffens the system (decreases the compliance). Actively patulous ETs can sometimes be identified on tympanometry by a sawtoothed pattern; this reflects changes in TM compliance as the patient's breathing causes shifts in middle ear pressure.

Although audiometry is important in measuring the impact that ET dysfunction may have on hearing, these changes do not correlate with the severity of tubal pathology. Mild to moderate conductive hearing loss is expected in cases of TM retraction and middle ear effusion.

Additional testing options may assist in the diagnosis of challenging cases or in the evaluation of the severity of persistent ET dysfunction but are not universally available for clinical use. As examples, nine-step tympanometry (repeated tympanometry with a series of changes in ear canal pressure followed by swallows), sonotubometry, and tubomanometry can indicate opening of the ET, but these tests have not been shown to have a strong correlation for predicting clinical outcomes for middle ear function. Among these tests, tubomanometry has been found to be the most reliable in detecting opening of the ET; during such testing, a dry swallow yields stronger ET opening than swallowing liquids [1,43-46]. In a review of the accuracy of available tests, it was determined that each test measures different components that contribute to overall ET function, but no single test serves as a gold standard for diagnosing disorders of ET function [44].

Imaging for patients with persistent unilateral symptoms — For patients with more than three months of unilateral symptoms and a persistent middle ear effusion, imaging is indicated to rule out neoplasm, especially in adults.

Magnetic resonance imaging (MRI) with contrast of the nasopharynx has the greatest sensitivity for neoplasms, although, if this protocol is not available, sinus or temporal bone MRI with contrast is generally acceptable. Computed tomography (CT) without contrast may also be used to provide additional information about surrounding structures. Unilateral symptoms and middle ear effusion in an adult raise suspicion for an obstructing neoplasm, and submucosal spread of nasopharyngeal carcinoma or lymphoma may be missed with endoscopy alone or imaging without contrast [42].

DIFFERENTIAL DIAGNOSIS — Many conditions can cause ear symptoms (eg, hearing loss, tinnitus, aural fullness, or otalgia) in adults and children. The evaluation of these symptoms is discussed in detail separately. (See "Evaluation of hearing loss in adults" and "Acute otitis media in adults" and "Etiology and diagnosis of tinnitus" and "Hearing loss in children: Screening and evaluation" and "Evaluation of earache in children".)

In particular, clinicians should be aware of other causes of aural fullness, including temporomandibular disorders (TMD), Meniere disease (MD), and Minor’s syndrome (superior semicircular canal dehiscence [SSCD]).

Temporomandibular disorders – Dysfunction in the muscles of mastication and the temporomandibular joint (TMJ) are collectively called temporomandibular disorders and may produce ear blockage symptoms that are commonly misdiagnosed as Eustachian tube (ET) dysfunction. In TMD, there can be pain deep within the ear, headaches, and tenderness to palpation around the ear canal or pre-auricular area. TMD is also characterized by discomfort just posteriorly and superiorly to and overlying the joint space with mouth opening. Intraoral examination will often reveal tenderness over the pterygoid muscles where they insert into the mandible (picture 16). Furthermore, in contrast to patients with ET dysfunction, otoscopic examination, pneumatic insufflation, and tympanometry will be normal in TMD despite the patient's otologic complaints. The evaluation, diagnosis, and management of TMD is reviewed in detail elsewhere. (See "Temporomandibular disorders in adults".)

Meniere disease – Patients with early MD may present with a sensation of fluctuating aural fullness or blockage, with or without the accompanying intermittent hearing loss, tinnitus, or vertigo which are classical for MD. The diagnosis is made by observing the patient over time, as MD symptoms typically remit and recur in contrast to the relatively stable symptoms of ET dysfunction. (See "Meniere disease: Evaluation, diagnosis, and management", section on 'Clinical presentation'.)

In most cases, the otologic examination and tympanometry will be normal. The most common audiometric pattern in early MD is a low-frequency or combined low- and high-frequency sensorineural hearing loss with normal hearing in the mid-frequencies. Over time, the hearing loss "flattens out" with hearing loss in all frequency ranges. The evaluation, diagnosis, and management of MD is reviewed elsewhere. (See "Meniere disease: Evaluation, diagnosis, and management", section on 'Diagnostic criteria and testing'.)

Otic capsule dehiscence – Minor's syndrome, or otic capsule dehiscence, including the most common presentation, SSCD, should also be considered in the differential diagnosis of ET dysfunction, particularly in patulous ET dysfunction [47]. These two conditions can present with similar symptoms, including autophony to both voice and breath; however, breathing autophony is much more pronounced in patulous ET dysfunction.

Vestibular symptoms are more prevalent in SSCD than ET dysfunction. In SSCD, vertigo can be provoked by coughing, sneezing, Valsalva maneuver, and even loud noises. Vestibular evoked potentials can help with diagnosis, and high-resolution computed tomography (CT) of the temporal bone is used to confirm a bony dehiscence. (See "Causes of vertigo", section on 'Semicircular canal dehiscence syndrome' and "Evaluation of the patient with vertigo", section on 'Vestibular evoked myogenic potentials'.)

TREATMENT — The treatment of Eustachian tube (ET) dysfunction should be directed at the underlying etiology, if identified, and at any complications [8]. If possible, obstructive dysfunction should be differentiated from patulous dysfunction during the evaluation. Treatments for obstructive dysfunction used in patients with patulous dysfunction will not improve symptoms and may potentially exacerbate them.

Medical treatment for "non-specific" ET dysfunction (ie, ET dysfunction without an identified underlying etiology) has not been shown to be effective and is not recommended [1,48]. There are few high-quality, data-informing treatment studies; randomized trial data are limited and much of what is known about the treatment of ET dysfunction comes from animal rather than human studies [49-51].

Obstructive dysfunction

Treat the cause of obstruction — In patients with obstructive ET dysfunction, identification and treatment of the cause of the obstruction and management with appropriate therapy is typically successful in improving ET function (see 'Etiologies of Eustachian tube dysfunction' above):

Rhinosinusitis – Treatment for acute viral rhinosinusitis and mild cases of acute bacterial rhinosinusitis is usually directed at management of symptoms (facial pain and pressure, postnasal drip, nasal congestion) with topical nasal steroids, intranasal/sinus rinses and pain medications. Moderate to severe cases of acute bacterial rhinosinusitis are typically treated with antibiotics. Nasal decongestants may be helpful in promoting opening of congested sinus orifices. (See "Uncomplicated acute sinusitis and rhinosinusitis in adults: Treatment" and "Acute bacterial rhinosinusitis in children: Microbiology and management".)

Medical management of chronic rhinosinusitis has not been specifically evaluated for managing ET dysfunction, but surgical treatment of chronic rhinosinusitis with and without nasal polyps has been shown to improve ET dysfunction symptoms [52,53]. As medical management of chronic rhinosinusitis is indicated before considering sinus surgery, treatment with nasal steroid sprays, nasal irrigations (with or without corticosteroids), antifungal agents, oral steroids, and other agents as appropriate, might provide some secondary benefit in improving ET function. The treatment of chronic rhinosinusitis is discussed in detail separately. (See "Chronic rhinosinusitis without nasal polyposis: Management and prognosis" and "Microbiology and antibiotic management of chronic rhinosinusitis" and "Chronic rhinosinusitis with nasal polyposis: Management and prognosis".)

Allergic and nonallergic rhinitis – Effective management of rhinitis, both allergic and nonallergic, can improve obstructive ET dysfunction. For most patients, trigger avoidance and, if needed, adjunctive pharmacotherapy are appropriate management strategies. For patients with nonallergic rhinitis and cigarette smoke exposure, counseling on smoking cessation and avoiding secondhand smoking is provided. Many patients with vasomotor rhinitis may also have allergies that have not been identified by testing and may respond to the above measures as well. The management of allergic and nonallergic rhinitis are reviewed in detail elsewhere. (See "Allergen avoidance in the treatment of asthma and allergic rhinitis" and "Pharmacotherapy of allergic rhinitis", section on 'Overview of treatment' and "Chronic nonallergic rhinitis", section on 'Management'.)

Laryngopharyngeal reflux – In patients with ET dysfunction and laryngopharyngeal reflux (LPR), treatment of the underlying condition can improve symptoms. In LPR, initial treatment is geared towards lifestyle and dietary modifications (eg, avoidance of caffeine, alcohol, chocolate, mints, carbonated beverages, spicy foods; instruction to eat smaller meals and avoid eating immediately before sleep; maintaining a healthy weight; avoidance of nicotine). Patients with persistent or severe LPR are treated with proton pump inhibitors. The evaluation and management of LPR is discussed in detail elsewhere. (See "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management".)

Mass lesions – Mass lesions blocking the ET orifice or compressing the lumen are managed according to the nature of the mass.

Adenoid hypertrophy is the most common entity causing ET obstruction; the enlarged adenoid may physically impair the opening of the tubal orifice or may contribute to inflammation within the ET itself. Excision of enlarged adenoids is effective in reducing the incidence of otitis media with effusion (OME), especially in children. (See "Etiologies of nasal obstruction: An overview", section on 'Enlarged adenoids' and "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications".)

Tumors are uncommon but should be suspected in cases of persistent unilateral symptoms. Nasopharyngeal carcinoma is the most common malignancy affecting the ET. (See "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma", section on 'Clinical presentation' and "Treatment of early and locoregionally advanced nasopharyngeal carcinoma", section on 'Principles of radiation therapy'.)

If the cause of obstructive dysfunction is unknown — In the absence of a specific etiology for obstructive ET dysfunction (eg, isolated ET dysfunction), we agree with clinical practice guidelines and clinical consensus statements [1,48] and do not treat presumptively with systemic decongestants, antihistamines, or nasal steroid sprays, as evidence of benefit is lacking [54,55]. We suggest treatment with intermittent ET insufflation; if done on a regular basis, this may be effective in improving symptoms and aid in relieving retraction of the tympanic membrane (TM) and middle ear effusion.

In addition, patients with persistent ET dysfunction without an identifiable underlying cause should be referred to otolaryngology for further evaluation.

Medical management — There is little evidence to support the use of pharmacologic and nonsurgical interventional therapies for isolated ET dysfunction (ie, ET dysfunction not associated with any of the conditions described above) [1,48,49,54,55].

Decongestants – Systemic decongestants, such as pseudoephedrine or phenylephrine, may be helpful in managing nasal congestive symptoms, but evidence is lacking that these agents will help resolve TM retraction or middle ear effusion. Similarly, systemic or topical (nasal) decongestants are not effective in treating OME [56,57].

Topical nasal decongestant sprays or drops may provide symptomatic relief of nasal congestion or rhinitis, but they have not been shown to improve obstructive ET dysfunction [58,59].

However, topical decongestants may be helpful for reducing difficulty in clearing ("popping") the ears during baro-challenge (eg, airplane flights and scuba diving) and preventing barotrauma. If used for this purpose, however, patients are counseled not to exceed three consecutive days of topical nasal decongestant treatment in order to avoid nasal mucosal dependency and rhinitis medicamentosa. (See "An overview of rhinitis", section on 'Nasal decongestant sprays'.)

Glucocorticoids

Systemic glucocorticoids – The use of systemic glucocorticoids has not been shown to be beneficial for the management of chronic ET dysfunction or OME. Oral corticosteroids have shown short-term benefit for acute-onset middle ear effusion, such as from barotrauma, but evidence is lacking for long-term benefit. Although animal studies have found that oral methylprednisolone may be effective in relieving effusion and improving acute ET obstructive dysfunction [51], this has not been demonstrated in human studies [60]. In the absence of evidence for benefit and given the risks of adverse effects, we agree with 2016 clinical practice which recommend against the use of systemic or nasal glucocorticoids for the treatment of middle ear effusion in children [48].

Topical nasal glucocorticoids – Although commonly used to treat ET dysfunction, topical nasal steroids have failed to demonstrate benefit in the absence of sinonasal inflammation. In a randomized trial including 91 individuals aged >6 years with ET dysfunction (negative middle ear pressure or middle ear effusion), treatment with six weeks of intranasal aqueous triamcinolone acetonide did not reverse the sequelae of ET dysfunction compared with placebo [55].

Eustachian tube insufflation – Once negative pressure has accumulated within the middle ear, it makes it more difficult to open the functional valve of the ET, as the negative pressure relative to ambient air pressure acts to keep the valve closed. If air can be insufflated into the middle ear to reduce the negative pressure, it may become easier to subsequently open the ET. Insufflation on a regular basis can be effective in improving symptoms of obstructive ET dysfunction and can aid in relieving retraction of the TM or middle ear effusion.

Patients can be instructed in performing a modified Valsalva maneuver. Forceful autoinsufflation is never advised as permanent injury to the inner ear can occur, but the modified Valsalva maneuver technique is safe and more effective: Patients are instructed to hold their nose and mouth closed, slowly and gently elevate intranasal pressure with a sustained, gentle nose-blow and a simultaneous swallow at the point of maximum pressure, which activates the dilatory muscles of the ET (table 2).This maneuver can performed as needed or on a regular basis and can be particularly helpful for patients who experience symptoms with baro-challenge.

For patients who are unable to perform the modified Valsalva maneuver, insufflation of the ET by using a device to apply positive pressure to the ET orifice via the nasal cavity while swallowing (the Politzer maneuver) can temporarily relieve negative middle ear pressure. "Politzerization" devices include powered nasal insufflators and a device allowing the inflation of a balloon using air exhaled via one nostril at a time.

In a systematic review including eight trials and approximately 700 children, the use of nasal insufflation devices were effective in the management of OME in children, with improvement in tympanometry and audiometry [61]. However, it is uncertain whether these results are generalizable to the adult population.

In one prospective cohort trial including 28 adults with ET dysfunction following airplane travel, use of a Politzer device twice weekly for six weeks improved tympanometric pressures compared with those who did not use the device [62].

Politzer devices for home use are available over the counter without a prescription. In general, we have found better acceptance of nasal balloon devices in children and with powered insufflators in adults. Although adherence may be a challenge and impractical for long-term use in many patients, Politzer devices can be useful in certain circumstances (eg, in anticipation of expected baro-challenge).

Surgical management if symptoms persist despite medical therapy — Surgical intervention is generally indicated when medical management of obstructive ET dysfunction is unsuccessful.

Tympanostomy tubes – Tympanostomy tubes equilibrate middle ear pressure with external air pressure, thus neutralizing the negative pressure within the middle ear and providing relief from the effects of obstructive ET dysfunction. Tympanostomy tubes are commonly performed for the management of ET dysfunction, particularly with persistent OME. (See "Acute otitis media in adults", section on 'Otitis media with effusion'.)

In children with OME with persistent symptoms over 90 days despite medical therapy, tympanostomy tubes are typically indicated [48]. (See "Otitis media with effusion (serous otitis media) in children: Management", section on 'Tympanostomy tubes'.)

The indication for tympanostomy tubes in adults with ET dysfunction is more variable, however, and depends upon the severity of symptoms and likelihood of improvement. In adults, an audiogram and tympanogram (initial or follow-up) may be done after 3 to 12 months of medical therapy, depending upon the severity of symptoms and the degree of improvement. As an example, in an adult with persistent, severe symptoms that do not respond to three months of medical therapy, we obtain audiogram and tympanogram with consideration for more aggressive medical care or a tympanostomy tube.

Tympanostomy tubes are effective in preventing sequelae of negative middle ear pressure and, and in most cases, middle ear effusion (if present) will not recur upon tube extrusion. However, if ET pathology persists, recurrence of signs and symptoms of ET dysfunction is likely, and replacement of tympanostomy tubes may be necessary. Longer-term tympanostomy tubes that remain in place for several years may be used, but these have a higher risk for subsequent TM perforation [49].

Balloon dilation of the Eustachian tube – Balloon dilation of the ET (BDET) is used to directly treat the pathology within the lumen of the ET lumen that is causing obstructive dysfunction.

In this procedure, a balloon catheter is used to dilate the cartilaginous portion of the tube through a minimally invasive transnasal endoscopic approach (picture 17). Balloon dilation reduces inflammation within the lumen; the mechanism of action may be through regeneration of healthy ciliated pseudocolumnar epithelium, reduction of submucosal inflammatory infiltrate and elimination of lymphoid follicles, replacing them with a thin layer of fibrosis [63,64]. These histological changes are similar to those seen post-adenoidectomy, suggesting that long-term resolution of inflammation is possible as long as contributing medical conditions (eg, allergic rhinitis, chronic rhinosinusitis, LPR) are effectively controlled.

The American Academy of Otolaryngology Head and Neck Surgery Clinical Consensus Statement states that BDET is indicated for chronic obstructive ET dysfunction (ie, ≥3 months) with type B (flat) or C (negative pressure) tympanograms (figure 6) [1]. However, there is an exception if symptoms only occur under baro-challenge since these patients may have normal tympanometry results on testing. These patients will typically have a history of significant pain with or sequelae from baro-challenge. Importantly, if a patient has had a tympanostomy tube but it did not help relieve their symptoms, it is probable that there is a diagnosis other than obstructive ET dysfunction and BDET is not indicated.

Two randomized controlled trials in adults with refractory chronic obstructive ET dysfunction have demonstrated the efficacy of BDET [65,66]. In the first trial including 323 subjects, BDET plus intranasal corticosteroids were compared with intranasal corticosteroids alone, and tympanogram and ET dysfunction questionnaire (ETDQ-7) symptom scores were measured. More patients in the BDET group demonstrated normalization of tympanograms and ETDQ-7 scores compared with the control group (52 versus 14 percent and 56 versus 9 percent, respectively) [65]. Tympanogram improvements, but not a significant difference in normalization of ETDQ-7 scores, were sustained at 12 months [66]. Subsequent trials including 60 adults showed similar results with durable improvements in both tympanograms and ETDQ-7 scores at 29 months’ follow-up [67,68].

Systematic reviews and meta-analyses of observational studies have shown benefit in improvement of all outcome measures, including patient-reported symptoms or ET function scores, otoscopy, tympanometry, and successful Valsalva maneuver [69-73]. Four cases series have demonstrated the durability of improvements [68,72,74,75].

Observational studies suggest that BDET may have a role in the management of children with ET dysfunction, particularly in those who have persistent otitis media with effusion (OME) or chronic negative pressure obstructive ET dysfunction, who have had previous tympanostomy tubes (with or without adenoidectomy) [76-78].

Eustachian tuboplasty – Eustachian tuboplasty is a procedure that reduces the thickness of the mucosa and submucosa of the posterior-medial wall of the tubal orifice and lumen in order to facilitate tubal dilation [9]. Small case series have shown that Eustachian tuboplasty is effective in treating tubal dysfunction [79-81]; it is sometimes done in conjunction with sinus surgery as it can be accomplished using a microdebrider [82]. The procedure is less commonly performed than BDET.

Patulous dysfunction

Initial management for all patients — Patients with patulous ET dysfunction have often been empirically treated with decongestants or nasal steroid therapy, but these should be discontinued as they are not generally effective and may worsen symptoms, even in patients with allergic rhinitis [49].

We encourage all patients with patulous ET dysfunction to maintain adequate hydration. In addition, we provide reassurance to patients who have only mild symptoms about the benign nature of the condition, explaining that symptoms often fluctuate depending upon the patient's underlying medical condition and hydration status. Autophony very commonly occurs during exercise due to the combination of dehydration, adrenaline or other stimulant hormones, and copious airflow past through the nasopharynx. If symptoms only occur with exercise and subside shortly thereafter, patients are reassured that this is considered normal and are advised that the best treatment is adequate pre- and post-workout hydration.

Treat the underlying cause of patulous dysfunction — In patients with patulous ET dysfunction, treatment should be directed at the underlying medical condition(s); appropriate therapy can be effective in improving tube function and reducing or eliminating symptoms. (See 'Etiologies of Eustachian tube dysfunction' above.)

Allergies – For patients with allergies, environmental measures to minimize exposure (eg, dust-proofing bedding, using air filtration) and consultation with an allergist for testing and possible immunotherapy are recommended. The use of systemic antihistamines and nasal steroid sprays may be effective in improving allergy symptoms but may exacerbate patulous ET symptoms; nasal saline irrigation and topical nasal cromolyn spray are good alternatives, as they will not dry out mucous membranes and will not exacerbate symptoms. Management of allergic rhinitis is discussed in detail elsewhere. (See "Pharmacotherapy of allergic rhinitis", section on 'Overview of treatment'.)

Laryngopharyngeal reflux – The inflammation from LPR often initially causes obstructive ET dysfunction but, over time, may progress to patulous dysfunction. Treatment of LPR is reviewed in detail elsewhere. (See 'Medical management' above and "Laryngopharyngeal reflux in adults: Evaluation, diagnosis, and management", section on 'Treatment'.)

Temporomandibular disorders – Muscle spasm or tension in the muscles of mastication may provoke or exacerbate patulous ET dysfunction due to chronic tension in the tensor veli palatini (TVP) and medial pterygoid muscles. Bruxism, temporomandibular joint (TMJ) dysfunction, and other sources of tension in the head and neck can also be associated with patulous ET (see 'Patulous dysfunction' above). The muscle tension may affect the functional valve, forcing it into an open position and causing it to become partially or fully incompetent. Evaluation and management of temporomandibular disorders (TMD) is reviewed in detail elsewhere. (See "Temporomandibular disorders in adults".)

Anxiety – Patients with significant anxiety may have jaw clenching or other head and neck muscle tension (eg, TMD). In such patients, symptoms of autophony may be perceived as particularly disturbing, which may further exacerbate anxiety, worsening muscle tension and further exacerbating symptoms. Patients should be reassured that, as disturbing as the symptoms may be, patulous ET dysfunction is a generally benign condition. However, we validate patients' concerns, explore the extent to which symptoms are impairing their quality of life, and refer them to behavioral health providers for further management as needed. (See "Generalized anxiety disorder in adults: Management".)

Weight loss – Although many patients with patulous dysfunction have experienced a significant weight loss, weight gain is rarely effective in treating the condition and is generally not a treatment goal unless the patient is physiologically underweight.

Other – Neuromuscular disorders should be evaluated and managed accordingly. For patients who smoke, smoking cessation is encouraged.

Additional medical management for patients with persistent symptoms

Intranasal saline drops — For patients with more severe symptoms, or persistent symptoms lasting beyond six weeks that do not improve with adequate hydration or treatment of the underlying condition, we suggest treatment with intranasal saline drops [83]. Saline introduced to the ET orifice causes mucosal irritation, inflammation, edema, and increased secretions, thus helping "close" the patulous ET lumen.

We advise patients to use an over-the-counter intranasal saline drop preparation. Most nasal sprays will not reach the ET orifice in the nasopharynx; therefore, proper application of topical drops is important.

To achieve the best result, the saline drops should come directly into contact with the tubal orifice. Patients are instructed to lie supine on a bed or couch with their head just off the edge of the surface at approximately 15 degrees of neck extension. Three to four drops of saline are placed into the ipsilateral nostril with the neck still extended, the head rotated 45 degrees toward the floor to allow gravity to direct the drops to the ET orifice. (The final position resembles the Hallpike position, but with only 15 degrees of neck extension.) The patient should feel a "twinge" radiate to the ipsilateral ear when the solution makes contact with the ET orifice, although the saline does not typically enter the ear. Some patients may require more drops (ie, five to six) to feel an effect; application should be done a minimum of twice daily and as often as needed to achieve symptom control. This is done for eight weeks to achieve a lasting benefit, although we do not advise chronic use.

If regular saline is ineffective, a hypertonic saline solution (prepared with 4 teaspoons of table salt in a cup of tap water) can be used. It is more irritating and will generate more tissue edema and mucus secretion, although not all patients can tolerate it. If necessary, the concentration can be reduced to improve tolerability.

Other — For refractory cases, a topical ascorbic acid preparation can be used, although this is even more irritating and not tolerated by all patients [84,85].

For patients with allergic rhinitis, rhinosinusitis, or other nasal congestion symptoms, nasal saline nasal irrigations can be helpful.

Mass loading of the tympanic membrane has been shown to help many patients, and this can be done in an office setting [86]. Originally done by placing blue tack on the posterior surface of the TM, it can be more practically done by placing topical ointment or one or more stacked layers of reinforced adhesive skin closure strips.

Surgery for severe, persistent symptoms — Surgical management of patulous dysfunction is reserved for patients with severe symptoms who do not respond to medical management (eg, adequate hydration, treatment of the underlying etiology, intranasal saline).

Tympanostomy tubes – For patients who do not respond to medical therapy, tympanostomy tube insertion may provide symptomatic relief. In our experience, patients who are bothered more by breath autophony than voice autophony are more likely to benefit.

The reason for benefit from tympanostomy tube is not clear, but there is some evidence that mass loading of the tympanic membrane alters its mechanical resonance properties [87], and up to 50 percent of patients may experience symptomatic improvement [83]. To determine if a patient is a candidate, a dab of ointment or a moistened paper patch can be applied to the posterior aspect of the TM as a test; if the patient derives significant relief of symptoms, we offer tympanostomy tube insertion. Sometimes patients may experience troublesome hearing distortion, however, and the tympanostomy tube can be removed if desired.

Eustachian tube shim placement – For patients with patulous dysfunction who have persistent, severe symptoms despite medical therapy and tympanostomy tubes, we generally offer treatment with placement of an intraluminal catheter, or shim.

With shim placement, a sealed intravenous catheter is placed within the lumen to partially obstruct the patulous ET (picture 18). The catheter wedges into the isthmus but is not intended to completely obstruct the tube lumen; sufficient air should still be exchanged around the catheter. The shim can be sutured to the anterior pillar (anterolateral wall of the nasopharyngeal orifice) for added stability. In several case reports, this method was effective in eliminating or reducing bothersome autophony in most patients [8,32,88]. In a study evaluating different surgical procedures for patients with patulous ET, three-quarters of patients undergoing shim placement as a primary procedure had resolution of symptoms at 12 months [21]. 12 percent of shims spontaneously dislodged, but symptoms did not always recur. The catheter is inert and can remain in place for long periods of time, even decades [32]. In the event that the shim causes obstructive ET dysfunction, a tympanostomy tube can be placed.

Eustachian tube augmentation – ET augmentation using calcium hydroxyapatite cement is occasionally used as another option. It is only suitable for small, favorably located defects involving the anterolateral ET wall. Most patients have a defect that is either unfavorably located in the roof of the lumen where the mucosa is too thin to hold a filler, or the defect is too large to be adequately managed using a filler. Calcium hydroxyapatite is injected under direct endoscopic view in a submucosal plane within the lumen of the ET. It increases the soft tissue bulge of the mucosal walls within the ET valve, restoring valvular competence. The filler is absorbed over approximately eight months; as the microspheres of calcium resorb, a variable amount of scar may replace some of the volume, such that repeat injections are not always required.

Eustachian tube reconstruction – Reconstruction of the patulous defect using cartilage grafting is another option for patients who have persistent symptoms despite medical therapy. In cartilage grafting, endoscopic approaches are used for reconstruction of the patulous defect while preserving ET function.

Cartilage grafts (eg, conchal or septal autologous cartilage or irradiated rib cartilage) are implanted to augment the concave defects that occur mostly within the posterolateral wall of the lumen. The cartilage can be implanted into a submucosal pocket, most commonly into the posteromedial wall where the cartilage skeleton of the torus tubarius serves to brace the implants. Cartilage can also be implanted into the opposite anterolateral wall (or both walls as required). Although long-term outcome data are not available [21], in observational studies the procedure has shown success, with all patients experiencing immediate relief of autophony, but with some return of symptoms in 66 percent by 12 months. In the event of return of bothersome symptoms, a second stage implantation of cartilage into the anterolateral wall may be offered, although data from staged reconstruction is not available [21,35].

Eustachian tube obliteration – For patients with persistent, intolerable symptoms despite medical therapy and all other surgical interventions, complete obliteration of the ET is a treatment of last resort. Because complete, irreversible obstruction of the ET is achieved, chronic middle ear effusions with associated autophony are common sequelae. As such, permanent tympanostomy tubes are generally required to avoid complications, including severe TM retraction, permanent effusion, or cholesteatoma [32,35]. Chronic thick mucoid effusions which can block the tympanostomy tubes can occur [21].

COMPLICATIONS OF EUSTACHIAN TUBE DYSFUNCTION — Complications of Eustachian tube (ET) dysfunction include conductive hearing loss, acute and chronic otitis media, tympanic membrane (TM) perforation, otitis media with effusion (OME), and cholesteatoma.

Hearing loss – In the initial stages of ET dysfunction, the retracted TM or middle ear effusion will cause a conductive hearing loss. Restoration of tubal function at this stage will usually reverse the hearing loss and permit normal hearing function. If ET dysfunction continues, permanent TM retraction may occur, in which case full restoration of the conductive hearing loss may not occur. (See "Etiology of hearing loss in adults", section on 'Eustachian tube dysfunction' and "Hearing loss in children: Etiology", section on 'Middle ear'.)

Otitis media (acute otitis media and otitis media with effusion) – Acute otitis media or OME may occur as a complication of ET dysfunction. The management of each condition is reviewed elsewhere:

(See "Acute otitis media in children: Treatment".)

(See "Acute otitis media in adults".)

(See "Otitis media with effusion (serous otitis media) in children: Management".)

(See "Acute otitis media in adults", section on 'Otitis media with effusion'.)

Tympanic membrane perforation – Negative pressure in the middle ear may result in a retracted TM and, in some cases, TM perforation. For most patients with acute rupture of the TM, treatment consists of systemic antibiotics and water precautions (preventing water from entering the ear canal). TM perforations will often heal spontaneously within six weeks. However, patients with TM perforation and associated hearing loss, otorrhea, nystagmus, or persistent perforation should be referred to an otolaryngologist. (See "Acute otitis media in children: Treatment", section on 'Tympanic membrane perforation' and "Acute otitis media in adults", section on 'Management of acute tympanic membrane rupture in acute otitis media'.)

Cholesteatomas – Persistent inflammation involving the middle ear and tympanic membrane due to ET dysfunction may lead to the formation of retraction pockets that retain debris with progressive deepening of the pockets into the roof of the middle ear and mastoid cavity. These may eventually develop into a continually expanding cyst of squamous epithelium, known as a cholesteatoma. Cholesteatomas are potentially destructive to the middle and inner ear, particularly when they become infected. Patients with cholesteatomas should be referred to an otolaryngologist for surgical management, usually removal in conjunction with tympanoplasty. (See "Cholesteatoma in children", section on 'Surgical treatment' and "Chronic otitis media and cholesteatoma in adults", section on 'Surgical treatment'.)

WHEN TO REFER TO A SPECIALIST — For patients with Eustachian tube (ET) dysfunction, indications for referral to an otolaryngologist include:

Persistent ET dysfunction without an identifiable underlying cause.

Severe ear complaints including hearing loss or troublesome, persistent otalgia.

Lack of improvement or worsening symptoms despite appropriate medical treatment.

Presence of cholesteatoma, recurrent otitis media, persistent effusion, or tympanic membrane (TM) perforation that is symptomatic or persistent.

Persistent unilateral otitis media with effusion (OME), which may indicate a concerning underlying etiology (eg, neoplasm).

For children with persistent allergic symptoms who have not "outgrown" their ET dysfunction by age 6, referral to an allergist for further evaluation may be appropriate.

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 topic (see "Patient education: Eustachian tube problems (The Basics)")

SUMMARY AND RECOMMENDATIONS

Anatomy and normal physiologic function – The Eustachian tube (ET) originates from the anterior wall of the middle ear cavity and passes anteroinferiorly to open into the nasopharynx (figure 3). The ET is a dynamic structure with a lumen, skeleton, mucosal lining, and surrounding soft tissue and muscles. The ET has three functional roles: equalization of pressure across the tympanic membrane (TM), protection of the middle ear from infection and reflux of nasopharyngeal contents, and clearance of middle ear secretions. (See 'Anatomy' above and 'Normal Eustachian tube function' above.)

Spectrum of Eustachian tube dysfunction: Obstructive versus patulous – ET dysfunction represents a spectrum of disease ranging from obstructive dysfunction (failure of ET opening to provide adequate ventilation to the middle ear) to the opposite extreme, patulous dysfunction (failure of the ET to close).

Obstructive dysfunction is responsible for a large proportion of otitis media and chronic ear disease and is more common than patulous dysfunction. However, patulous dysfunction is more common than previously realized and can cause bothersome symptoms that may be mistaken for obstructive dysfunction, but generally does not lead to any significant acute or chronic ear disease. The underlying pathophysiology may lead to either obstructive or patulous pathology and patients may move back and forth on this spectrum, creating difficulties in diagnosis and appropriate treatment. (See 'Spectrum of Eustachian tube dysfunction' above.)

Clinical evaluation and diagnosis – ET dysfunction is a generally a clinical diagnosis, which can be further evaluated and confirmed with nasal endoscopy and audiology studies. When available, additional testing modalities such as tympanometry, sonotubometry, and tubomanometry may aid diagnosing ET dysfunction, although there is no gold standard diagnostic test. (See 'Clinical evaluation' above.)

Treatment – Obstructive dysfunction should be differentiated from patulous dysfunction during the evaluation; treatments for obstructive dysfunction used in patients with patulous dysfunction will not improve symptoms and may potentially exacerbate them. Medical treatment for "nonspecific" ET dysfunction (ie, ET dysfunction without an identified underlying etiology) is not effective. (See 'Treatment' above.)

Obstructive Eustachian tube dysfunction treatment

-Identification and treatment of the underlying cause (eg, rhinosinusitis, allergic and nonallergic rhinitis, laryngopharyngeal reflux [LPR], obstructing mass lesions), and management with appropriate therapy is typically successful. (See 'Treat the cause of obstruction' above.)

-In the absence of an identifiable etiology for obstructive ET dysfunction, we do not treat presumptively with systemic decongestants, antihistamines, systemic glucocorticoids, or nasal steroid sprays. Evidence of benefit for these treatments is lacking, and this approach is consistent with clinical practice guidelines. (See 'If the cause of obstructive dysfunction is unknown' above and 'Medical management' above.)

For patients with obstructive ET dysfunction of unknown etiology, we suggest intermittent ET insufflation rather than other interventions (Grade 2C). When performed on a regular basis, this be effective in improving symptoms of obstructive ET dysfunction and aid in relieving retraction of the TM or middle ear effusion. Patients with persistent ET dysfunction without an identifiable underlying cause should be referred to otolaryngology for further evaluation. (See 'Medical management' above.)

-Surgical intervention is generally indicated when medical management of obstructive ET dysfunction is unsuccessful; surgical interventions include tympanostomy tubes and balloon dilation of the ET. (See 'Surgical management if symptoms persist despite medical therapy' above.)

Patulous Eustachian tube dysfunction treatment

-All patients with patulous ET dysfunction should maintain adequate hydration.

For those who have been empirically treated with decongestants or nasal steroid therapy, these should be discontinued as they are not generally effective and may worsen symptoms. Treatment should be directed at the underlying cause (allergies, LPR, temporomandibular disorders [TMD], anxiety, neuromuscular disorders); appropriate therapy can improve tube function and reduce or eliminate symptoms. (See 'Initial management for all patients' above.)

-For patients with more severe symptoms, or persistent symptoms lasting beyond six weeks that do not improve with adequate hydration or treatment of the underlying condition, we suggest treatment with intranasal saline drops rather than other therapies (Grade 2C). Saline causes local mucosal irritation, inflammation, edema, and increased secretions, thus helping "close" the patulous ET lumen. (See 'Additional medical management for patients with persistent symptoms' above and 'Intranasal saline drops' above.)

-Surgical management is reserved for patients with severe patulous symptoms who do not respond to medical management (eg, adequate hydration, treatment of the underlying etiology, intranasal saline). Surgical options include tympanostomy tubes, ET shim placement, ET augmentation, ET reconstruction, and, as a final option if all other treatments fail, ET obliteration. (See 'Surgery for severe, persistent symptoms' above.)

When to refer – Referral to an otolaryngologist is indicated for persistent ET dysfunction without an identifiable underlying cause; hearing loss; troublesome or persistent otalgia; lack of improvement or worsening symptoms despite appropriate medical treatment; cholesteatoma; recurrent otitis media; TM perforation that is symptomatic or persistent; persistent unilateral otitis media with effusion (OME, which may indicate a concerning underlying etiology such as malignancy). (See 'When to refer to a specialist' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Bassem Hanna, MD, who contributed to an earlier version of this topic review.

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Topic 14608 Version 47.0

References

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