Clinical Evaluation and Management of the Eustachian Tube

Introduction

The eustachian tube is an ostium that connects the nasopharynx to the middle ear cavity and contains a dynamic valve. In adults its length measures between 31 and 38 mm, the anteromedial two-thirds of which contains a cartilaginous skeleton and the posterolateral one-third is surrounded by bone. Closure of the eustachian tube occurs beginning from a few millimeters distal (i.e. toward the nasopharynx) to the bony-cartilaginous junction and extending over a variable length generally within a centimeter of the nasopharyngeal orifice. The portion of the lumen that opens and closes is considered the functional valve. At rest, the valve remains closed and is opened by the actions of associated muscles.

The eustachian tube has three primary functions that include: (1) ventilating and equalizing pressure in the middle ear space, (2) draining secretions from the middle ear by gravity and mucociliary clearance, and (3) protecting the middle ear from sounds and reflux of pathogens and secretions from the nasopharynx. The eustachian tube is dynamic, with some of its functions requiring that it properly open, and others requiring that it remain closed. Its improper function can happen on either end of this spectrum, opening too frequently or not frequently enough. Obstructive eustachian tube dysfunction occurs when the eustachian tube valve does not open adequately (either sufficiently often or sufficiently open) to serve the functions of middle ear ventilation or clearance of secretions. Patulous eustachian tube dysfunction occurs when the eustachian tube opens too persistently, resulting in failure to protect the middle ear from nasopharyngeal reflux of sound and nasopharyngeal material. For reasons that are not yet understood, obstructive dysfunction may transition to patulous dysfunction and some patients can even fluctuate back and forth along this spectrum, sometimes having obstructive dysfunction and at other times patulous dysfunction. This oscillation between disease states contributes to a significant challenge in diagnosing and managing patients with eustachian tube dysfunction.

The diagnosis of an improperly functioning eustachian tube is often inferred based upon either the symptoms reported by patients or upon the findings a clinician observes on otoscopy. Patients can report symptoms of aural fullness or pressure, otalgia, with or without decreased hearing, but these symptoms can overlap with other diagnoses. Despite the challenges in diagnosis, eustachian tube dysfunction is commonly diagnosed and is thought to be a leading cause of otitis media. Annually, approximately 4 million children and adults visit their physicians and are diagnosed with eustachian tube dysfunction. This chapter will review the clinical evaluation and management of patients with diseases affecting the functions of the eustachian tube.

Eustachian Tube Function Tests

Diagnostic evaluation of the eustachian tube has a rich history. French anatomist Joseph DuVerney (1648–1730) and Italian anatomist Antonio Valsalva (1666–1732) first postulated that aerating the middle ear and clearing secretions were functions of the eustachian tube. They also speculated that proper function of the eustachian tube was important for hearing. At the time, few successful treatments of hearing loss were available. Physicians began performing catheterization of the eustachian tube in the early 18th century for both diagnostic purposes and for treatment. These procedures involved delivering air or fluids to the eustachian tube via a catheter blindly inserted into its lumen. The procedures were technically difficult to perform without direct visualization and eventually fell into disfavor as a result of fatal complications.

Several more recent tests have been developed with the intent of measuring eustachian tube function. These tests typically involve applying pressure (either positive or negative) at the external auditory canal or nasopharynx. The tests have not gained widespread use, in large part due to the poor reliability and lack of correlation with clinical outcomes. The tests will be briefly reviewed here:

Forced response test —In the forced response test a patient with a patent ventilation tube in the tympanic membrane or a tympanic membrane perforation has a specialized tympanometry probe combined with an air pump placed in the ear canal. Increasing pressure is applied via the pump at the ear canal and middle ear until the eustachian tube is forced to open, providing an opening pressure. Resistance of the system can also be measured during swallowing.

Inflation-deflation test —The inflation-deflation test uses a tympanometry probe placed in the ear canal to record pressure changes while the patient swallows. Both the forced response tests and inflation-deflation tests have been used previously to evaluate eustachian tube function in children before tympanoplasty.

Tubomanometry —Tubomanometry measures pressure at the level of the external auditory canal during maneuvers like swallowing, while pressure is applied at the nasopharynx. The patient will swallow with the mouth closed and the nose sealed with a probe that causes gradually increasing pressure in the nasopharynx. The pressure at which the eustachian tube opens can result in an abrupt change in the ear canal pressure and is interpreted as the opening pressure.

Sonotubometry —This is a test in which a sound probe is used to play a tone inside the nasal cavity, while a microphone is placed in the external auditory canal to detect a change in amplitude of the sound when the eustachian tube is opened.

Obstructive Eustachian Tube Dysfunction

Obstructive dysfunction occurs when there is failure of the eustachian tube lumen to open sufficiently to serve its functions. The result is inadequate ventilation of the middle ear cleft and inadequate clearance of material. A constant gas exchange normally occurs in the middle ear and mastoid due to diffusion across a gradient. As oxygen, CO ₂ , and nitrogen equilibrate with the venous blood, which has lower partial pressures of these gases, the pressure in the middle ear space becomes progressively lower than ambient atmospheric pressure as long as the eustachian tube remains closed ( Fig. 131.1 ). Brief dilations of the eustachian tube lumen that occur as a result of actions of the levator and tensor veli palatini muscles during swallowing or yawning allow equilibration of middle ear pressure with ambient pressure. If the eustachian tube is obstructed, negative pressure progressively develops in the middle ear until it may become sufficiently severe that tissue transudates fill the vacuum, creating a middle ear effusion. The resultant retracted tympanic membrane or effusion can be observed on pneumatic otoscopy by insufflation of the tympanic membrane with negative pressure or measured as a type B or type C curve using tympanometry. The hallmark of obstructive eustachian tube dysfunction is evidence of negative pressure persisting within the middle ear.

Inspection of the tympanic membrane without insufflation is not adequate by itself to diagnose obstructive eustachian tube dysfunction. It has been shown that static findings of the tympanic membrane do not correlate with the presence or severity of obstructive or patulous dysfunction . Therefore inspection alone, even with otomicroscopy, can be misleading. Although otitis media with effusion can be caused by obstructive eustachian tube dysfunction, it may also be caused by inflammatory conditions and is not necessarily indicative of eustachian tube pathology. Examination of the lumen of the eustachian tube for pathology by endoscopy may be indicated. Tympanic membrane retractions, too, are not always indicative of current eustachian tube dysfunction. A retraction may initially have been caused by obstructive eustachian tube dysfunction; however, once the tympanic membrane contacts middle ear mucosa (e.g., incus or under the scutum), there is upregulation of inflammatory mediators such as fibroblast stimulating and epithelial spreading factors that induce adhesions and progression of a retraction pocket through a separate biological process. The presence of a fixed, adherent retraction pocket, even if progressive, may have been initiated by obstructive dysfunction, but progression may continue through a biological process that is independent of the current functional status of the eustachian tube. Obstructive dysfunction can usually be recognized by mobility of a retracted tympanic membrane on pneumatic insufflation and the severity of the tubal pathology can be assessed by endoscopic examination of the lumen.

Some individuals have obstructive eustachian tube dysfunction that is intermittent or occurring only during rapid or significant ambient pressure challenges, such as when traveling on an airplane or scuba diving. In the normal situation, individuals can swallow, yawn, or perform a Valsalva maneuver to restore equilibration of pressure between the middle ear and the environment, thereby relieving symptoms. However, in some with baro-challenge –induced obstructive eustachian tube dysfunction, symptoms of aural fullness, decreased hearing, and otalgia may not be readily relieved and may persist for several days. In extreme examples, the pressures can be transmitted to the inner ear, causing damage such as hearing loss or vestibular dysfunction, or can result in a hemotympanum or tympanic membrane perforation. Obstructive eustachian tube dysfunction that occurs only when baro-challenged usually represents a lesser degree of pathology along the spectrum of tubal disease than patients who have chronic negative pressure or effusion.

Concomitant disorders that are suspected of being potentially causal of chronic obstructive eustachian tube dysfunction include allergic disease, reflux of stomach contents (laryngopharyngeal reflux), hypertrophy of the adenoid tissue or adenoid-like tissue in the tubal tonsil and tubal lumen, rhinosinusitis, primary mucosal diseases such as Samter's (aspirin sensitivity, nasal polyps, asthma) triad, or immunodeficiency. Environmental exposure to irritants such as tobacco smoke can contribute to obstructive eustachian tube dysfunction. Less commonly, there can be extrinsic anatomic obstruction from neoplasms such as nasopharyngeal carcinoma or submucosal lymphoma.

In the bony eustachian tube, the epithelial lining is smooth and tightly adherent to the periosteum. In the cartilaginous portion of the eustachian tube the walls contain thicker tissue with lymphoid follicles and ciliated columnar epithelium. The glandular tissue located on the medial aspect of the torus tubarius is called the tubal tonsil of Gerlach, and it can become enlarged in inflammatory conditions. These lymphoid follicles extend deep into the cartilaginous eustachian tube. A common finding on exam in patients with obstructive eustachian tube dysfunction is edema of the mucosa and submucosa near the eustachian tube valve and cobblestone-like lymphoid hyperplasia. Swelling and inflammation of the tissues at the tubal orifice and within the lumen may contribute to obstructive dysfunction, making it more difficult to open. In addition, bulky tubal tonsil tissue may restrict opening of the eustachian tube during swallows by compressing the torus tubarius toward the lumen, especially when combined with hypertrophied adenoid tissue contacting the medial aspect of the torus tubarius.

Muscular dysfunction involving the muscles that open the eustachian tube is a less common cause of eustachian tube dysfunction. As discussed in the previous chapter, two muscles are important for proper function of the eustachian tube valve. The levator veli palatini muscle elevates the palate and medially rotates the torus tubarius. This muscle provides a stable platform by which the relatively weak tensor veli palatini muscle can then contract and open the eustachian tube ( Fig. 131.2 ). The muscles may be inherently weak or underdeveloped, such as in craniofacial anomalies or muscular disease. The most commonly observed abnormality is decreased action of the tensor veli palatini muscle, impairing the excursion of the anterolateral wall. Following repair of a cleft palate, the levator muscle is suspended higher in the process of the reconstruction, but this may cause a functional limitation of tubal opening when the elevated levator muscle contracts, rising high enough to restrict the lumen. There may even be discoordination. The levator muscle has been observed to relax prematurely, eliminating the stable scaffold by which the tensor muscle must contract in order to dilate the lumen. Occasionally, increased active dilatory or chronic persistent excursions of the anterolateral wall may be observed, preventing full closure of the functional valve of the eustachian tube and possibly contributing to patulous eustachian tube dysfunction. The responsible muscles could be the tensor veli palatini muscle or possibly the pterygoid muscles, which have been hypothesized to act as accessory dilators of the eustachian tube.

Eustachian Tube Endoscopy

Attempts had been made to perform endoscopy on the eustachian tube for over a century. With the introduction of improved endoscopic technology in the 1970s and 1980s, there was renewed interest in eustachian tube endoscopy, initially for research to better understand eustachian tube physiology and later in patients with middle ear disease to better understand pathophysiology. Ongoing improvements in camera technology and high definition video have led to even better image resolution and the ability to observe actions of the eustachian tube in slow motion with replay. Widespread availability of this technology has also expanded the opportunities to use endoscopic technology to evaluate for pathology.

Endoscopy of the eustachian tube can be performed in the clinic ( Video 131.1 ). Topical anesthetic and decongestant spray can improve viewing and allow for a more comfortable examination. Although a 0-degree Hopkins rod rigid endoscope is useful for evaluating the nasal passages and the adenoid, an angled view (using 30-degree or 45-degree rigid endoscopes or by aligning a flexible nasopharyngoscope with the longitudinal axis of the lumen) is essential to see the eustachian tube anatomy and assess its valve-like dynamic function. The clinician must see into the lumen of the eustachian tube to inspect for pathology and to judge the quality of opening and closing of the functional valve. The size and geometry of the adenoid tissue impinging on the torus tubarius, the bulk and shape of the tubal tonsil tissue, and the presence of scar bands from prior adenoidectomy should be noted. The fossa of Rosenmuller must always be investigated for masses. Polypoid lymphoid hypertrophy of the torus tubarius or cobblestoning of the mucosa may be observed, even sometimes overlying the eustachian tube orifice.

The dynamic function of the eustachian tube valve should be evaluated with the patient participating. The patient is initially asked to vocalize the “Ka Ka Ka” sound to observe the isolated action of the levator veli palatini muscle as the palate elevates and rotates the torus tubarius medially. Having the patient swallow will allow assessment of normal eustachian tube dilatory efforts. A yawn or vocalizing “Ahh” produce maximal dilatory efforts.

In the normal exam, a series of actions are observed during endoscopy that lead to dilation of the eustachian tube ( Fig. 131.3 ). First, the soft palate elevates with activation of the levator veli palatini muscle, causing the torus tubarius to medially rotate (see Fig. 131.3B ). The lateral pharyngeal wall medializes, which may serve to protect the eustachian tube against reflux during its opening. The lateral pharyngeal wall then relaxes, while the palate remains elevated and the torus tubarius remains medially rotated. The third step involves contraction of the tensor veli palatini muscle in the anterolateral wall of the eustachian tube lumen, causing a dilation of the lumen of the eustachian tube that begins with the nasopharynx and propagates toward the isthmus (see Fig. 131.3C ). Contraction of the tensor veli palatini muscle acts against this scaffold of the elevated and medially rotated torus tubarius. The net result is a visible concave appearance to the anterolateral wall, compared with its usual convex appearance in the resting state (see Fig. 131.3A and B ). The valve then closes proximally, progressing toward the nasopharyngeal orifice. This final action may have a role in expelling secretions from the eustachian tube.

In most cases, the normal dilatory sequence can be observed in real time.

• 1

  Initial contraction of the levator muscle, which sustains the contraction

• 2

  Tensor muscle subsequently contracts to open the valve

• 3

  Relaxation of both muscles to allow closure of the valve

For a more detailed examination for pathology or to carefully assess the actions and timing of the muscular components, the images can be recorded and replayed in slow motion. Although the medial and lateral pterygoid muscles may be involved in the dynamic functions of the eustachian tube, these muscles are not apparent on endoscopy and their impact on eustachian tube function is unclear. A study by Alper et al. provided some validation that these endoscopic findings correlated with simultaneous electromyographic recordings from the levator and tensor muscles and sonotubometry to verify opening of the tubal valve.

The narrowest portion of the eustachian tube, the isthmus, is at the proximal end of the cartilaginous portion, just distal to the bony portion. It measures approximately 1 to mm in width and 2 to 3 mm in height, such that a flexible nasopharyngoscope can be advanced toward the isthmus but cannot pass through. Endoscopic exams have been done with ≤1-mm diameter scopes but with some challenges due to limited optical resolution and obscuration of views as the tip of the endoscope would contact secretions. However, studies using microendoscopy have demonstrated that there has been a patent bony eustachian tube in patients with active otitis media with effusion, suggesting that the location of the pathology is more likely to be in the cartilaginous portion of eustachian tube.

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