Diagnosis and Management of the Patulous Eustachian Tube

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Chapter 7 Diagnosis and Management of the Patulous Eustachian Tube

image Videos corresponding to this chapter are available online at www.expertconsult.com.

A patient with a patulous or abnormally patent eustachian tube (ET) can experience symptoms that lead him or her to seek medical advice and possibly undergo surgery. This condition can be overlooked or mistakenly thought of as not having sufficient bearing on a patient’s quality of life to warrant efforts for its identification and correction. The ET has a pivotal role in the maintenance of proper volume and pressure homeostasis of the middle ear cleft, in expelling middle ear secretions, and in protecting the middle ear from reflux of sound and material from the pharynx.1 Dysfunction of the ET may be divided into two groups: dilatory dysfunction with failure to open the valve of the ET adequately, and patulous dysfunction with failure to close the valve adequately. This chapter addresses the diagnosis and treatment of an excessively open ET.

ANATOMY AND PATHOPHYSIOLOGY OF THE PATULOUS EUSTACHIAN TUBE

The ET is an organ composed of a skeleton made of cartilage and bone and associated muscles, fat, connective and lymphoid tissues, nerves, and blood supply.2 The normal ET is maintained at a closed resting position, and opens by voluntary and nonvoluntary maneuvers, such as swallowing; yawning; and deliberate manipulations of the palate, pharynx, muscles of mastication, and mandible. The tube may also open passively by changes in ambient air pressure or by forcing passage of air, such as with a Politzer maneuver.

As mentioned, tubal opening can be a by-product of movements initiated for other purposes (e.g., swallowing), but it can also be triggered by direct reflex stimuli. Gas is exchanged between the middle ear space, surrounding mucosa, and blood vessels. There is a net absorption of gas into the circulation; when the ET is closed, this causes an increasingly negative pressure beyond that of the normal resting pressure of the middle ear. The absorption rates of the constituents of air differ with nitrogen being the predominant gas, but having relatively slow absorption compared with oxygen and carbon dioxide. Therefore, the gas composition varies over time after each dilation of the ET. It is thought that deviation from the set-points of pressure and gas composition may be detected by a combination of baroreceptors and chemoreceptors that initiate the opening of the ET to convey air into the middle ear and re-establish homeostasis.3

Active opening of the ET usually lasts about 400 ms. It is the result of a coordinated effort of four muscles, the most important of which is the tensor veli palatini (TVP), laterally dilating the anterolateral membranous wall.1,4,5 Although the opening mechanism of the ET has been studied extensively, closing of the ET has received less attention. The part of the ET that is normally closed at rest and open on dilation is referred to as the valve. The valve constitutes the approximately 5 mm long segment of apposing mucosal surfaces within the middle of the cartilaginous portion of the ET.6 Closure of the ET is thought to be the result of the following factors: recoiling memory properties of the cartilaginous ET, relaxing bulk of the TVP muscle, and pressure of neighboring paraluminal tissue. The closed lumen is likely maintained by all of these factors, and aided by the surface tension of the apposed wet mucosal surfaces.

Transnasal endoscopy and surgery of patulous ETs has revealed that the underlying pathology is a longitudinal concave defect in the anterolateral wall of the valve (Fig. 7-1). This wall normally has a convex bulge into the lumen of the ET in the relaxed position. The defect represents a lack of tissue volume that can be a deficiency of the lateral cartilaginous lamina, Ostmann’s fat, TVP muscle bulk, submucosa, or mucosa. Examples of these deficiencies, either isolated or in combination, are seen in clinical cases. Temporary or permanent obliteration of the defect, even with some mucus, immediately relieves patients’ symptoms.

The cartilaginous canal is anchored to the basisphenoid bone in its lateral side. The medial cartilaginous lamina is mobile, principally by action of the levator veli palatini muscle. Superiorly, the medial and much smaller lateral cartilaginous laminae come together to form a junction rich in elastin fibers that contributes to the springlike quality of the cartilage. The recoiling qualities of the cartilaginous canal play an important role in ET closure.

Because the cartilaginous backbone of the ET is open in its medial-anterior aspect, the lumen patency also depends on the pressure of the abutting soft tissues. The relaxed paratubal muscles (mainly the TVP) and Ostmann’s fat pad contribute to lumen closure. Glandular tissue and the size of Ostmann’s fat pad were found to be smaller in patients with a patulous ET compared with normal controls as measured by computed tomography (CT) scans.7 The mucosal and submucosal tissue layers increase in thickness as they are relieved of tension with muscle relaxation, and are in themselves a factor in closure of the valve. A report of fluctuating patulous symptoms in hemodialysis patients describing relief of symptoms during fluid retention and exacerbation after excretion showed the close connection between periluminal mass and symptoms of patulous ET.8

ETIOLOGY AND CLINICAL PRESENTATION

An overly patent ET allows for the free passage of air and the sound it carries from the nasopharynx to the middle ear, creating a pathologic acoustic and pressure environment. The most prominent symptoms of a patulous ET are aural fullness and autophony of a patient’s own breathing noises and voice. Symptoms are mostly related to free passage of air and sound, but not reflux of material. Symptoms compatible with patulous ET have been described since the second half of the 19th century. The constellation of symptoms compatible with those seen in patients with patulous ET was reported by Jago in 1858,9 who later described his personal experience with the condition. Schwartze recognized the connection between the patulous ET and excursions of the tympanic membrane with respiration. Zollner and Shaumbaugh emphasized the important symptom of autophony in a series of patients with patulous tubes (as reported by Bluestone and Magit10).

Autophony is described by patients as hearing their own voice and breathing noises. A patient’s own voice sounds to them as if they are talking very loudly into a barrel, typically prominent on pronunciation of “M” and “N.” Clinicians can simulate the symptoms by talking and breathing into the diaphragm of their stethoscopes. Because the auditory feedback can be disturbingly loud, there is a wide range of cognitive and emotional responses ranging from asymptomatic to suicidal ideation. Autophony can be disturbing to the extent of leading to depression and the need for psychiatric medication or intervention. The perception of pressure changes in the middle ear with breathing can be loud windlike noise, constant ear blockage or pressure, and the sense of the medial and lateral excursions of the tympanic membrane. When patients forcibly blow their nose, there can be pain from the increased middle ear pressure on the tympanic membrane.

Aural fullness and the sensation of ear blockage can be misdiagnosed as dilatory dysfunction of the ET, especially because the patient usually describes the ear as “blocked.” The differential diagnosis for aural fullness also includes temporomandibular joint or related musculoskeletal dysfunction, Minor’s syndrome of semicircular canal dehiscence, and endolymphatic hydrops (see Fig. 7-3). Because of the typical complaint of “ear blockage,” many patients are initially treated with medications directed against dilatory dysfunction, such as nasal decongestants, steroid topical sprays, and topical or systemic antihistamines, all of which fail to help or even aggravate the symptoms.

Symptoms are mitigated by maneuvers and conditions that support tubal closure by increasing venous congestion in tubal tissues, causing inflammation of the tissues, or restoring some hydration or mucus onto the luminal surfaces. Placing the head in a dependent position (supine or between the legs), pressure on the ipsilateral internal jugular vein, upper respiratory tract infections and allergies, and sniffing inward to “lock” the ET closed by creating negative middle ear pressure all are capable of generating temporary symptom relief in most patients. Symptoms are typically relieved overnight and may start sometime after arising in the morning. They are often initiated by exercise, possibly because of dehydration or epinephrine-like hormones causing nasal decongestion, or by prolonged speaking and singing, possibly from desiccation of the mucosa from air movement.

The etiology for the loss of tissue creating a patulous ET is uncertain. Possibly associated factors such as weight loss and tissue atrophy from chronic disease account for only two thirds of the patients.11 Loss of tissue volume from within the tubal lumen is cited as the most common pathogenesis and most commonly reported with weight loss.12 Shea (personal communication, 2007) noted that one third of patients have a significant weight loss, and one third have some sort of rheumatologic condition. The authors’ experience has been similar.

Simonton13 grouped etiologies according to positive and negative contributing factors. Positive factors were defined as factors actively reducing tissue volume, such as with scarring from previous procedures, inflammation, and radiation.14,15 Negative factors were due to a passive loss of tissue around the pharyngeal orifice, loss of tonic action of the TVP muscle, and conceivably reduced coiling properties of the ET. Hormonal factors include pregnancy,16 high-dose oral contraceptives, and estrogen treatment for prostate cancer. Estrogen can reduce the viscosity of tubal secretions, reduce the elastic properties of the tubal cartilage, and elevate the level of surfactant via a change of prostaglandin levels. All these factors would support opening of the ET. Reflux of gastric contents and allergy were reported to be the cause in 3 of 11 patients in one series.17 Other contributors reported include abuse of nasal decongestants and cocaine, poliomyositis, multiple sclerosis and other neuromuscular disorders, cerebrovascular accidents, craniofacial abnormalities, temporomandibular joint malfunction, and malocclusion. Occasional association between patulous ET and palatal myoclonus has been reported.18 The habit of sniffing or Valsalva’s maneuver can be acquired in patients attempting to aerate their middle ears at times of otitis media, but may ultimately result in a patulous tube.

DIAGNOSIS

The diagnosis is certain when medial and lateral excursion of the tympanic membrane with breathing is observed. Otoscopy should be done with an otoscope or microscope and the patient seated. If the patient does not have autophony at the time of the examination, it may be induced by physical activity. Excursions of the tympanic membrane can be enhanced by closure of the contralateral nostril during nasal breathing.

The improved inspection and manipulation of the nasopharynx brought about with the introduction of endoscopic sinus surgery tools greatly improved the ability to diagnose and correct patulous ET. High-quality endoscopy allows for direct and detailed examination of the ET valve. Done with either a rigid or a flexible endoscope, it may show a concave defect in the anterolateral part of the valve, instead of the normal convexity.19 The defect prevents normal closure of the orifice in the resting position, leaving a slitlike opening in the lumen of the orifice.

Ancillary tests may be of some assistance in the diagnosis of patulous ET. Impedance tympanometry while the patient experiences autophony may reveal fluctuation in tracing in line with tympanic membrane excursion (Fig. 7-2). Tympanometry can also record middle ear negative pressure or hypermobility of the tympanic membrane. Sonotubometry can directly measure ET patency.20,21 During the examination, a sound is emitted in the nasal cavity and is recorded by a microphone located in the external auditory canal of the examined ear. As the ET opens, the sound recorded in the external auditory canal intensifies, and an increase of 5 dB or more is considered to reflect opening of the ET reliably.22 Severity of subjective autophony was found to be correlated with objective measurements of ET function by sonotubometry.23 This test is not available routinely in the clinical setting. It has been suggested more recently to make use of this principle in performing audiometry masked by a nasally presented noise. In subjects with patulous tubes, thresholds of low tones were significantly elevated more than in normal controls because sound presented in the ear was masked by the noise escaping the nasal cavity to the middle ear through the patent ET. The thresholds normalized in most patients after corrective measures were taken.24

Imaging is not routinely used for the diagnosis of patulous ET. Until more recently, CT scanners required a recumbent examinee, a position that commonly results in closure of the patulous tube. The availability of scanners allowing examinations in the seated position has allowed researchers to record patency of the ET in resting and under Valsalva maneuver.25 Imaging-based measurements of a group of patients with patulous ETs were statistically significant compared with normal controls.

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