Dr. Alok Banka

ENT Surgeon
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Eustachian tube dysfunction


The length of the ET varies between 31 and 38 mm . The normal orientation of the ET is downward, anterior, and with a medial rotation. With this positioning, the ET creates an angle of about 45 and 30 to 40 with the sagittal and horizontal planes, respectively . The ET is made up of bone, cartilage, and fibrous tissue. The bony component is approximately 12 mm in length, whereas the cartilaginous is about 24 mm in length. This longer portion is described as a triangular plate of elastic fibrocartilage. The base of the tube forms the torus tubarius, which is posterior to the nasopharyngeal opening the eustachian tube .

Function and dysfunction of ET

The eustachian tube (ET) has three physiologic functions. These are

(1) pressure regulation,

(2)protection of the middle ear from pathogens/foreign material in the nasopharynx, and

(3) clearance of the middle ear space .

Normally, the ET stays closed and opens when necessary to equalize pressure.

It is well known that eustachian tube dysfunction (ETD) is linked to chronic secretory otitis media . Other more invasive diseases can also occur with ETD. When the tubal mechanism fails, either in passive or active function, a series of events can occur in the middle ear space that varies from a mild retraction to fulminate cholesteatoma.

Although the normal physiologic state of the middle ear is to have equal pressure between the middle and lateral sides of the tympanic membrane, some patients will prefer a negative pressure in their ear. Bunne and coworkers in 1999 found that these patients complained of hyperacusis and autophony with the tympanic membrane in the normal position.

Functional failure of the ET

Increased negative middle ear pressure

Atelectasis of the tympanic membrane

Retraction pocket in attic or posterior-superior quadrant

Adhesive otitis media

Etiology of ETD

Multiple causes of ET dysfunction exist. This varied differential includes infectious, allergic, mechanical (obstructive), environmental exposure, genetic, reflux, congenital, and iatrogenic causes.

Chronic sinusitis

Stoikes and Dutton [22] found that postoperatively, patients who had undergone ESS had relief of their otologic symptoms related to ETD.

Allergic rhinitis

Known to cause ETD, allergic rhinitis and viral infections interact to enhance physiologic response in the middle ear and ET.

Adenoid hypertrophy

It is well known that adenoid enlargement can obstruct the nasopharyngeal opening of the ET, but it can also impair mucociliary clearance from the tube by means of nonciliated metaplastic epithelium and fibrosis of connective tissue associated with adjacent adenoid tissue .

Tobacco smoke

Two studies published by Agius and coworkers , confirmed that there was a decrease in ciliary beat frequency of the mucosa of the ET.


White and coworkers determined that exposure to gastric contents in the nasopharynx caused a significant ET dysfunction in an animal model. Their experiment found that middle ear pressure regulation and mucociliary clearance of middle ear contents were disabled.

Cleft palate

The incidence of ETD has been quoted as high as 79% in patients with cleft palate and cleft lip/palate.


Treatment of nasopharyngeal malignancies with external beam radiation has detrimental effects on the surrounding structures, especially the ET. Multiple investigators have found patients with early and late middle ear pathologies secondary to iatrogenic ET injury.

Reduced mastoid air cell system

The presence of a mastoid air cell system has been reported as an important criterion postoperatively to act as a pressure buffering system. However, this function is dependent on having healthy mastoid mucosa.

Evaluation of the ET

Assessment can be started initially by taking a thorough history. A typical ETD patient will complain of fullness or clogging of the ears, pain or discomfort, hearing loss, tinnitus, and dizziness. Most concerning to these patients is when these symptoms cannot be relieved by swallowing, yawning, or chewing. Physical examination Using pneumatic otoscopy, an examiner can evaluate the mobility of the tympanic membrane. Stiffness or middle ear effusions are suggestive of ETD. Indirect nasopharyngoscopy, using a small dental mirror, represents another manner to visually inspect the posterior nasopharynx and proximal opening of the ET. Pathology such as adenoid hypertrophy or mucosal edema can be seen. It is well known that a rigid or flexible nasal endoscope allows the examiner to visualize the nasopharyngeal opening of the ET. Usually 30or 70 rigid Hopkins rod endoscopes provide the best visualization. 0.8-mm flexible fiberscopes is used to evaluate beyond the isthmus of the ET and even into the middle ear cleft . objective and subjective assessments helpful in studying ETD. A tympanogram plots a measure of how energy is transmitted through the middle ear. When pressures between the middle ear space and the ear canal are equal, a normal or ‘‘type A’’ tympanogram is recorded. Abnormal admittance in the form of a retraction or stiffness will result in a plotted graph know as a ‘‘type C’’ or ‘‘type B’’ tympanogram, respectively . Other subjective testing includes the Valsalva test, which involves patients holding their nose and blowing out with a closed mouth. The Toynbee test is a similar maneuver. In this test, patients hold their nose and swallow. While patients swallow, the examiner can visually inspect the tympanic membrane and evaluate for movement. This exercise generates a positive pressure within the nasopharynx, followed by a negative pressure phase and is considered positive when there is an alteration in middle-ear pressure as assessed by pneumatic otoscopy before and after the maneuver. Negative middle ear pressure or temporary negative middle ear pressure followed by return to ambient pressure after the Toynbee test usually is indicative of normal ET function. In the Politzer test, one of the patient’s nostrils is occluded with a rubber balloon as the examiner pinches the other nostril tightly. The patient elevates the palate by swallowing or phonating. The examiner then forces air into the closed nasal cavity from Politzer’s bag. Air can be heard going into the middle space with an auscultation device. The examiner can also visually compare the tympanic membrane before and after the procedure to determine its relative patency . A final testing mechanism is sonotubometery. In this procedure, a sound source is applied to the nostril as a microphone in the external auditory canal records the transmitted sound. Sound levels are measured as the ET opens and closes. The advantage of this diagnostic test is the ability to evaluate the ET with or without an intact membrane under physiologic conditions.

Medical treatment of ET dysfunction

Decongestant-antihistamine combination with or without steroid is the preferred mode of treatment.

Surgical treatment of ET dysfunction

Insertion of pressure equalization tubes (PET) had been the mainstay surgical treatment of ETD. Although the pressure difference between the middle ear and the external auditory canal is resolved immediately with this procedure, little effect can be seen the ET itself. Adenoidectomy for ETD is done in children with obstructive adenoids of the nasopharynx.


Cholesteatoma is the most worrisome complication for patients with chronic ET dysfunction. Other possible sequelae include retraction, effusion, and atelectasis. Each of these pathologies can be associated with conductive hearing loss of varying degrees.

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