Eustachian Tube Function and Dysfunction:

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The eustachian tube is an 3-4 cm tubular structure which links two of the major areas of interest in our specialty, the nose and the ear. Dysfunction of the eustachian tube causes many common symptoms that present to our clinics, and may have important management implications. This presentation will consists of a review of the history, anatomy and physiology of the eustachian tube, and the role of the eustachian tube in clinical situations.

The first description of the eustachian tube is attributed to Alcmaceon of Sparta in 400 BC. It was his belief that the eustachian tube allowed goats to breath through their ears as well as their noses.

In 1562, Bartolomeus Eustachius, the Chair of Anatomy in Rome, published the first detailed description in his thesis Epistola de Auditus organis, accurately describing the structure, course, and relations eustachian tube.

Antonio Valsalva, Professor of Anatomy at Bologna, applied the name "Eustachian Tube" to the pharyngotympanic tube, which was described by Eustachius.

In 1724, around the time of Valsalva, Edme-Gilles Guyot, a postmaster at Versailles, described the technique of eustachian tube catheterization. He succeeded in relieving his own deafness by passing a curved pewter tube through his mouth into the opening.

Since that time many noted otolaryngologists, including Drs. Politzer, Bezold, and Bluestone, have contributed significantly to our understanding of the intricacies of eustachian tube anatomy and function, and management of the various disorders that it is embroiled in.

Understanding the development and anatomy of the eustachian tube provides insight into its role in several pathologic processes.The eustachian tube develops as a persistence of the first pharyngeal pouch. At 10 weeks post conception only the epithelial lining of the lumen has differentiated. Between the 10th and 12th weeks post conception the levator veli palatini and tensor veli palatini muscles develop. At 14 weeks the tensor tympani muscle becomes apparent, cartilage differentiation begins and rugae begin to develop within the tube.

The tube increases in length from 1 mm at 10 weeks post conception to 13 mm at birth. Also, the angle between the eustachian tube and the skull base is 10 degrees at birth.

This is in contrast to the adult length of 35 mm and angle of 45 degrees in adults. Vertical development of the skull, and increases in the angle of the skull base, allow the eustachian tube to reach its adult length and angle by age 7.

In the adult, the eustachian tube can be visualized as two truncated cones attached at their narrowed ends. It runs from the middle ear to the nasopharynx and is approximately 31-38 mm in length. Its lumen is roughly triangular and has average diameter of 2-3 mm. The lumen is lined by ciliated psuedostratified, columnar epithelium, which sweeps material from the middle ear to the nasopharynx. Mucous glands predominate near the pharyngeal orifice, and there is a gradual change to a mixture of goblet, columnar, and ciliated cells as the middle ear is approached.

The eustachian tube is composed of an osseous and a cartilaginous portion. The osseous eustachian tube or protympanum measures 11 to 14 mm and extends from the anterior and medial portion of the petrous temporal bone. Its orifice is oval shaped, measures 5 x 2 mm and is located above the floor of the middle ear space. When healthly, the osseous portion of the eustachian tube is always patent. The cartilaginous portion measures 20-25 mm and opens into the nasopharynx approximately 10 mm above the plane of the hard palate. The cartilage protrudes into the nasopharynx, and the protruding portion is known as the torus tubarius. The fossa of Rosenmuller is this area in the nasopharynx superior to the torus tubaris.

The cartilaginous portion is composed of one main piece of cartilage and can be accompanied by several accessory cartilages. Its composition and elasticity is similar to that found in the pinna and nose. It is attached at the sphenoid sulcus on the base of skull superiorly and its anteriomedial end is attached to a small tubercle on the posterior edge of the medial pterygoid plate.

The blood supply to the eustachian tube is from branches of the internal maxillary artery, ascending pharyngeal artery, and the ascending palatine artery. Sensory and motor innervation of the eustachian tube is provided by a branch from the otic ganglion, sphenopalatine nerve, and the pharyngeal plexus, predominately through branches of the glossopharyngeal nerve. Sympathetic branches reach the eustachian tube from the sphenopalatine ganglion, otic ganglion, glossopharyngeal nerve, petrosal nerves, and the carticotympanic nerve. Parasympathetic innervation is from the tympanic branch of the glossopharyngeal nerve. The multiple nerves innervating the eustachian tube, may be a source for referred pain to other anatomic regions of the head and neck.

There are four muscles associated with the eustachian tube. These include the tensor veli palatini, levator veli palatini, salpingopharyngeus, and the tensor tympani.

The tensor veli palatini is composed of two distinct bundles of muscle fibers mediolateral to the tube. The lateral bundle takes its origin from the scaphoid fossa, and the lateral osseous ridge of the sulcus tubae for the course of the eustachian tube. It descends anteriorly and lateral and inferiorly, to converge in a tendon which passes around the hamulus and inserts on the posterior border of the horizontal process of the palatine bone and into the palatine aponeurosis of the velum.

The medial most portion of the tensor veli palatini originates on the lateral membranous wall of the eustachian tube and blends with the lateral bundle of the tensor veli palatini. This medial portion of the tensor veli palatini, referred to as the dilator tubae muscle, is probably responsible for active dilation of the eustachian tube by inferolateral displacement of the membranous wall.

The levator veli palatini arises from the inferior aspect of the petrous apex, passes inferomedially, paralleling the tubal cartilage, and attaches to the dorsal surface of the soft palate. It is thought to assist in active dilation and provide support.

The salpingopharyngeus arises from the medial and inferior portion of the eustachian tube and descends posterior and inferior to blend with the palatopharyngeus muscle. Its physiologic function is undefined.

The tensor tympani muscle arises from fibers common to the tensor veli palatini. The tendon of the tensor tympani rounds the cochleaform process and inserts into the manubrium of the malleus. It is not thought to play a role in eustachian tube function.

The normal eustachian tube is functionally collapsed at rest, with slight negative pressure present in the middle ear. It opens during swallowing, sneezing, and yawning. The eustachian tube is thought to close through passive reapproximation of the tubal walls by extrinsic forces and recoil of the elastic fibers.

The eustachian tube has three functions: ventilation, drainage, and protection. When the eustachian tube is patent it allows ventilation of the middle ear and equalization of middle ear and atmospheric pressure. It also allows the middle ear to clear unwanted secretions. By staying physiologically obstructed, it protects the middle ear from nasopharyngeal secretions and sound.

Conditions interfering with normal eustachian tube function cover the pathologic spectrum from benign to malignant. Resultant middle ear complications can be the primary condition that the clinician needs to address, may be a sign of something more serious, or may have implications that will affect the outcome of surgical interventions.

Bluestone has classified eustachian tube disorders into obstructive disorders, and disorders of abnormal patency.

Obstructive disorders can be mechanical or functional. Mechanical obstruction can be intrinsic due to intraluminal factors such as mucosal inflammation due to allergy or infection, or extrinsic obstruction resulting in compromise of the lumen. Extrinsic obstruction can be physiologic such as when the patient is supine, or may be caused by a mass lesion such as a neoplasm or an adenoidal mass.

Functional obstruction results from persistent collapse of the eustachian tube due to increased tubal compliance, an abnormal opening mechanism, or both. Functional obstruction is more common in infants and young children, and in many cases can be related to normal or abnormal developmental factors.

There are many methods for evaluating the condition of the eustachian tube, which reflect its deep location and complex physiology.

During the physical examination, otoscopy, pneumatic otoscopy, indirect nasopharyngoscopy, and endoscopy of the nasopharynx can provide clues to the condition of the eustachian tube.

Several maneuvers can be easily performed in clinic that may indicate patency of the eustachian tube. These include the Valsalva test, the Toynbee test, the Politzer test, and eustachian tube catheterization.

The Valsalva test is performed by visual inspection of the tympanic membrane while the eustachian tube and middle ear are inflated by a forced expiration with the mouth closed and the nose occluded by the thumb and forefinger. The test is positive when an intact tympanic membrane is observed moving, or by air heard through a perforated TM. A positive valsalva test only indicates an anatomically patent and probably distensible eustachian tube.

The Politzer test is performed by visual inspection of the tympanic membrane while compressing one naris into which the end of a rubber tube attached to an air bag has been inserted while the opposite naris is compressed with digital pressure. The patient is asked to repeat the letter K or to swallow while air is injected into the nasal cavity. When positive, the overpressure that develops in the nasopharynx is transmitted to the middle ear, and only indicates an anatomically patent ET tube.

Both the Politzer and Valsalva test may be beneficial as a temporary treatment of effusion or high negative middle ear pressure.

The Toynbee Test is performed by visual inspection of the tympanic membrane while the patient swallows with their nose manually occluded. This 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 eustachian tube function. This is in contrast to the Politzer and Valsalva tests which only test patency. The results of this maneuver can often be equivocal, since several studies have shown that a significant portion of normal adults and children can not open their eustachian tubes with this maneuver, and patients with patulous eustachian tube often can not maintain a negative pressure within their middle ears.

Eustachian tube catheterization can be performed, and also can indicate eustachian tube patency.

Radiographic evaluation includes computed tomography, and magnetic resonance imaging. The use of contrast materials to evaluate patency has been described in the past, but is infrequently used today.

There are several more complex methods of evaluating eustachian tube function that have been described and most involve the use of manometry, sonometry, of tympanometry. Besides tympanometry most of these tests require complex equipment, and are mainly used in a research setting.

Here are a small sample of the clinical scenarios where eustachian tube dysfunction is important:

Obstruction may result in persistent high negative middle-ear pressure. If pressure equalization does not occur, atelectasis of the tympanic membrane-middle ear, sterile otitis media with effusion, or both can occur. If the negative pressure is overcome, it can aspirate secretions from the nasopharynx resulting in an acute otitis media.

Serous otitis media with effusion can result from either inadequate ventilation of the middle ear or from reflux of unwanted nasopharyngeal secretions into the middle ear. Both types of eustachian tube dysfunction can result in otitis media, abnormal patency and obstruction.

This is common in children and infants probably due to the configuration of their eustachian tube, shorter length, and lower efficiency of their tensor veli palantini.

While serous otitis media is something that many of us treat on a daily basis, Dr. Gacek of Syracuse reminds us, in an article entitled "A Differential Diagnosis of Unilateral Serous Otitis Media", of the potentially serious nature of this condition. Clinicians need to maintain a high index of suspicion, particularly in adults, in unilateral cases, and in persistent or recurrent cases. From Dr. Gacek's article, it is important to remember:

Dr. Gacek reinforces the importance of a thorough head and neck examination including the nasopharynx, CT scan of the head including the neck, and myringotomy as the minimal workup in any pediatric or adult patient with unilateral recurrent or persistent serous otitis media without an obvious explanation for eustachian tube obstruction.

He also emphasizes that in pediatric patients, the eustachian tube lumen and nasopharynx are the anatomic locations most frequently responsible, but congenital CSF leaks should be suspected in patients with a history of meningitis, or if the fluid after myringotomy resembles CSF.

Patients with nasopharyngeal carcinoma frequently have complications that relate to their eustachian tube. The frequently present with serous otitis media. Also, high-dose radiation therapy, the treatment for nasopharyngeal carcinoma, causes edema, vasodilation, mucosal damage, and fibrosis of the eustachian tube and middle ear resulting in damage to the middle ear contents and poor middle ear ventilation.

While it seems intuitive that serous otitis media with effusion in patients with nasopharyngeal carcinoma would be caused by mechanical obstruction of the pharyngeal orifice of the eustachian tube, several studies question whether nasopharyngeal tumors, actually obstruct the lumen of the eustachian tube, and instead propose that eustachian tube dysfunction and resulting otitis media with effusion is caused by infiltration of the tensor veli palatini muscle.

With regard to patients after radiation, a study by Hsu, et al, in 1995, showed that 95% of 38 eustachian tubes were patent prior to radiotherapy, 34% where patent at 6 months after radiotherapy, and 60% were patent at 5 years after radiotherapy using the passive opening test. They also showed decreased dynamic function and clearance at six months after radiotherapy and improved at 5 years. They attributed these findings to inflammation caused by radiation rather than tumor obstruction. Electromyographic evaluation of the tensor veli palatini in patients with nasopharyngeal carcinoma status post radiation indicated neurogenic paralysis.

These authors have also found that in patients treated with ventilation tube insertion for post-irradiation OME tend to develop a chronic draining ear, and deterioration of hearing. They suggest myringotomy, avoidance of ventilating tubes, and frequent local treatment of infections of the nose, sinuses, and nasopharynx to avoid this outcome.

Patulous eustachian tubes often present a frustrating problem for patients and clinicians.The incidence is reported to be between 0.3-6.6% of the general population.

Patients with patulous eustachian tubes complain of aural fullness, humming tinnitus, and autophony. They also may hear their own breath sounds, which is known as tympanophonia. The sound is synchronous with nasal respiration and resolves when the patient is supine or when upper respiratory tract inflammation occurs. The sounds may be aggravated by mastication.

Symptoms are usually absent when the patient is supine or relieved when the patient bends forward with the head between the knees. For this reason, patients should not be examined in a supine position. Physical examination may reveal a tympanic membrane that moves during forced breathing through one nostril, and an amorphic sound may be heard using a diagnostic tube in the patient's ear.

The eustachian tube is usually closed, and closure is maintained by the elasticity of its cartilage, mucosal lining, surrounding muscles and fat. Alteration of any of these anatomic components may cause patulous eustachian tubes.

Conditions associated with patulous eustachian tubes include: radiation therapy, hormonal therapy, pregnancy, nasal decongestants, fatigue, stress, and weight loss.

Patulous eustachian tubes in the most severe form may be patent at all times, whereas a less severe form has been reported, where the tube is anatomically closed at rest, but may open easily during exercises or in association with a decrease in peritubal extracellular fluid.

Many patients can be treated with simple reassurance after a thorough history and physical examination. Treatment or removal of underlying factors may reverse the problem. Such as weight gain by patients who have lost weight.

Many medical regimens have been described including agents which produce intraluminal and extraluminal swelling, including: insufflation of boric acid and salicylate powder as described by Bezold, application of nitric acid and phenol, oral administration of saturated solution of potassium iodide (10 drops in juice TID), premarin nasal spray (25 mg in 30 cc NS).

New medications are currently under investigation including a herbal combination being evaluated in Japan, and a medication reported Dr. DiBartolomeo of Santa Barbara, California that is composed of chlorobutanol, benzyl alcohol, diluted hydrochloric acid, and propylene glycol. In the initial report, complete elimination of symptoms was reported by 8 of 10 patients. This formulation was derived from chlorinated pool water based on the observation that several patients had eustachian tube congestion proportional to the frequency of time they spent in a public pool. In letter to the editor in American Journal of Otology, Dr. DiBartolomeo indicated that the medication was held up with the FDA.

In patients who do not improve with medical therapy and who want further treatment, several surgical interventions have been used including electrocauterization of the eustachian tube orifice, peritubal injection with gelfoam, paraffin, avitene, or teflon paste, transposition of the tensor veli palatini muscle medial to the pterygoid hamulus, myringotomy with ventilation tube placement, and insertion of an indwelling catheter and subsequent ventilation tube placement. Catheter placement is through either an anterior tympanomeatal flap or through a myringotomy.

The close anatomic relationship of the eustachian tube and the carotid artery should be noted by clinicians who plan inject materials into the eustachian tube orifice, as injection of telfon paste into the carotid artery has been reported.

Another clinical situation where proper eustachian tube function is important is in the use of hyperbaric oxygen therapy, particularly in patients who require multiple sessions.

Hyperbaric oxygen therapy involves intermittent inhalation of 100% oxygen under greater than 1 atmosphere of pressure and is being used increasingly in patients with decompression sickness, osteomyelitis, carbon monoxide poisoning, crush injuries, radiation necrosis, and poorly healing wounds. Many of these patients develop otalgia and aural fullness that may be long-standing. Reports in the literature indicate that the incidence of middle ear barotrauma ranges from 5% to 28% of all patients.

Fernau, et al suggest patients should be taught clearing techniques such as the Valsalva or Politzer maneuver, supplemented with topical and/or systemic decongestants, subjected to slower compression rates, or possibly have ventilation tubes placed.

In a study of 33 patients undergoing hyperbaric oxygen therapy by Fernau, et al. in 1992, 82% of patients developed fullness in their ears, 52% developed serous otitis media, and 21% developed otalgia requiring ventilation tubes. Of 11 patients managed with decongestants,10 patients resolved their effusion and pain and did not require further therapy. 45% of 33 patients had evidence of pre-existing eustachian tube dysfunction using the inflation-deflation test. Of these patients 100% developed aural fullness, 87% developed serous otitis media, and 47% required tympanostomy tubes. Fernau, et al, identified a history of eustachian tube dysfunction as a risk factor for serous otitis media in patients undergoing hyperbaric oxygen therapy.

An article by Presswood, et al, points out that the middle ear complication rate in intubated patients receiving hyperbaric oxygen therapy is 94% compared to 46% of non-intubated patients. (Hemotympanum and otalgia) They state that the use of nasal decongestants in this population is controversial, and probably of no value in patients who are intubated. They recommend ventilation tubes should be placed in their ears prophylactically.

Obviously, there are many more clinical situations that the role of eustachian tube dysfunction is important. Disorders of the eustachian tube present important issues that in diagnosis and management that are faced in daily clinical practice. Despite the large volume of literature on eustachian tube dysfunction, the lack of well-designed prospective studies make the literature difficult to decipher, and these disorders continue to represent some of the most challenging management problems we face as otolaryngologists.

The eustachian tube is an important anatomic structure that ventilates, protects, and drains the middle ear.

During development the eustachian tube lengthens and the angle between it and the skull base increases from 10 degrees in infancy to 45 degrees in adulthood.

Eustachian tube dysfunction can be caused by mechanical obstruction, which may be intrinsic or extrinsic, by functional obstruction, or by the presence of patulous eustachian tubes.

Otitis media with effusion is a common sequalae of eustachian tube dysfunction, but a high index of suspicion must be maintained in adults, in unilateral cases, and in patients with recurrent or persistent disease without an obvious explanation.

A 54-year-old male was referred to the Bobby R. Alford Department of Otorhinolaryngology and Communicative Sciences for evaluation and management of a right patulous eustachian tube. The patient had previously undergone a right myringotomy and ventilation tube placement without resolution of his symptoms.

He complained of right aural pressure and autophony for over one year. The autophony was particularly bothersome while singing. The patient had a history of high pitched noise exposure while in the military, and wears ear protection while at work. He denied headaches, nausea, vomiting, vertigo, otorrhea, otalgia, ear trauma, or ear surgery. He had no history of recent weight loss, and the remainder of his medical history was unremarkable.

Physical examination revealed his left tympanic membrane to be clear, intact, and mobile. The right tympanic membrane had a scar in the anterior inferior quadrant, but was otherwise unremarkable. The right tympanic membrane did not move with swallowing or Valsalva maneuver. There were no masses noted in the nasopharynx. The rest of physical examination was unremarkable.

The patient had an audiogram which was remarkable for symmetric severe sensorineural hearing loss above 2000 hertz bilaterally. He had Type A tympanograms bilaterally.

The patient was reassured of his condition and Premarin nose drops were started, but the patient failed to respond. The patient was given the option of surgical intervention, and has noted an improvement in symptoms 2 weeks status post eustachian tube obliteration and ventilating tube placement.

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©2001-2006 Baylor College of Medicine
Bobby R. Alford Department of Otolaryngology-Head and Neck Surgery
Mail: One Baylor Plaza, NA102, Houston, TX 77030
Phone: 713-798-5906
E-mail: oto@bcm.edu

Last modified: Feb. 13, 2006