eustachian tube function

Otolaryngol Clin N Am

39 (2006) 1221–1235

Eustachian Tube Functionand the Middle Ear

John W. Seibert, MDa,Christopher J. Danner, MDb,*

aDepartment of Otolaryngology, Washington University School of Medicine,

St. Louis, MO, USAbOtology/Neurotology/Skull Base Surgery, Tampa Bay Hearing and Balance Center,

Tampa Bay, FL USA

The eustachian tube (ET) has three physiologic functions. These are (1)pressure regulation, (2) protection of the middle ear from pathogens/foreignmaterial in the nasopharynx, and (3) clearance of the middle ear space [1].

It is well known that eustachian tube dysfunction (ETD) is linked tochronic secretory otitis media [2]. Other more invasive diseases can also oc-cur with ETD. When the tubal mechanism fails, either in passive or activefunction, a series of events can occur in the middle ear space that variesfrom a mild retraction to fulminate cholesteatoma.

History

The first modern-era researcher of the ET was Bartolomeus Eustachius.He was a 16th century anatomist who taught at the Collegia della Sapienzain Italy. Eustachius, for whom the ET is named, studied several areas in thehuman body including the ET [3]. Further work was done by AntonioValsalva, (1666-1723). Valsalva was a Professor of Anatomy at Bolognaand is most recognized for his middle ear insufflating maneuver that bearshis name. Valsalva is credited with naming the auditory tube, the eustachiantube, and describing its function [4].

Adam Politzer is probably best known for his contribution to otologyand probably considered the greatest otologist of the 19th century. One ofhis legacies was a hand-held air bag that allowed insufflation of the middle

* Corresponding author.

E-mail address: [email protected] (C.J. Danner).

0030-6665/06/$ - see front matter � 2006 Elsevier Inc. All rights reserved.

doi:10.1016/j.otc.2006.08.011 oto.theclinics.com

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1222 SEIBERT & DANNER

ear space or politzerization, as the inventor termed it. Further therapies de-veloped by Politzer included a primitive middle ear ventilation tube [5].

Embryonic development

The development of the eustachian tube and middle ear occurs as an outpouching of the pharynx that forms the tubotympanum and the pneumatizedtemporal bone. [6] The cartilaginous portion of the eustachian tube undergoesthe majority of the growth seen in utero. [1] During development the ET pro-vides a continuous sheet of epithelial cells to create the middle ear lining. [7]One difference between the middle ear mucosa and the ET mucosa is thatthe epithelium of the ET differentiates into respiratory epithelium (pseudos-tratified ciliated columnar), whereas the middle ear epithelium does not.However, more posteriorly in the middle ear, away from the ET orifice,some simple nonciliated cuboidal epithelium is present [8]. This distinctionfound in ET mucosa provides a more effective, inherent protective compo-nent. Unique characteristics of the ET include the presence of more mucuscells and accessory glands when compared with the middle ear mucosa [9].

Compared with adults, the position of the infant ET is 10� from theFrankfort horizontal plane. This angle is different in adults whose tube ispositioned at a 45� [1]. Among other differences in adult and pediatricETs, a less angled ET in the pediatric population has been thought to beresponsible for the increased incidence of middle ear pathology. However,some researchers have found that active muscle function, rather than passiveclearance and impedance of the ET, is responsible for the decreased diseasestate seen in adults [10,11].

A smaller or partially obstructed ET does not necessarily correlate withthe risk of disease or even active disease. Using an in vivo model, Sadeand coworkers [12] in 2004 found that narrowing of the ET alone did notprohibit natural gas flow into the middle ear space with a swallowingmaneuver. Although the narrowed ET was open for a brief period, thiswas sufficient to overcome a negative pressure.

Anatomy

The length of the ET has been reported to be between 31 and 38 mm [13].The normal orientation of the ET is downward, anterior, and with a medialrotation. With this positioning, the ET creates an angle of about 45� and 30�

to 40� with the sagittal and horizontal planes, respectively [9].The ET is made up of bone, cartilage, and fibrous tissue. The bony

component is approximately 12 mm in length, whereas the cartilaginousis about 24 mm in length. This longer portion is described as a triangularplate of elastic fibrocartilage. The base of the tube forms the torus tubarius,which is posterior to the nasopharyngeal opening the eustachian tube [9].

Blood supply to the ET and its supporting structures originates from thedeep auricular branches of the internal maxillary artery, ascending

1223ET FUNCTION AND THE MIDDLE EAR

pharyngeal artery, and the ascending palatine artery [14]. Sensory and mo-tor innervation of the ET is supplied by a branch from the otic ganglion,sphenopalatine nerve, and the pharyngeal plexus from branches of the glos-sopharyngeal nerve. Sympathetic branches innervate the ET from the sphe-nopalatine ganglion, otic ganglion, glossopharyngeal nerve, petrosal nerves,and the carticotympanic nerve. Parasympathetic innervation is from thetympanic branch of the glossopharyngeal nerve [1,14].

Muscles of the ET

Four muscles are associated with the ET, which through a complex inter-action, assist with equilibrating middle ear pressure. These muscles are: (1)tensor veli palatine, (2) levator veli palatine, (3) salpingopharyngeus, and (4)tensor tympani.

The tensor veli palatini (TVP) is a thin muscle lateral to the levator velipalatini. The medial portion of this muscle is the primary dilator of the ET.The origin of the muscle arises from three locations. One origin is at the baseof the medial pterygoid plate on the scaphoid fossa. The second is from thespina angularis of the sphenoid, and the third is from the lateral wall of thecartilaginous eustachian tube. The TVP muscle descends and inserts ona tendon at the pterygoid hamulus [9,15].

Levator veli palatini is a thicker muscle compared with the TVP and lieslateral to the choanae. Its origin is from two anatomic sites. The first is theinferior surface of the apex of the petrous part of temporal bone. The secondorigin is the medial lamina of the cartilage of the ET. The muscle extendsabove the superior pharyngeal constrictor merging with the opposite levatormuscle at midline [9,15].

Salpingopharyngeus originates from the inferior portion of the ETextending downward joining the pharyngopalatinus muscle and assistswith elevation of the pharynx and opening of the ET with deglutition [9,15].

Tensor tympani is a large muscle encased in a bony canal above the os-seous portion of the ET. The tensor tympani origin involves three locations.The first is the cartilaginous portion of the ET, and the second is the greaterwing of the sphenoid. The third is attachments to the bony canal in whichthe muscle travels. The tensor tympani insertion is at the manubrium ofthe malleus [9,15].

Function and dysfunction of ET

Normally, the ET stays closed and opens when necessary to equalizepressure. Other functions include clearance of middle ear fluid while atthe same time preventing nasopharyngeal secretions refluxing into the mid-dle ear space.

Ghadiali and coworkers [16] looked at the physiologic function of the ETand found that the ET opening was highly sensitive to the applied muscle


forces and relatively insensitive to cartilage elastic properties. In their anal-ysis of the muscle forces (tensor and levator veli palatini) and soft tissueelastic properties, luminal dilation of theETwas caused bymuscle contractioncausing medial-superior rotation of the medial lamina, which in turn causeda deformation of fatty tissue surrounding the ET (Ostmann’s fat pad) [16].

Bluestone and colleagues [17] reported on the progression to cholestea-toma describing how acquired cholesteatoma can develop. This sequenceof pathogenesis (Fig. 1) involved functional failure of the ET, leading to in-creased negative middle ear pressure, atelectasis of the tympanic membrane,formation of a retraction pocket in attic or posterior-superior quadrant, andsubsequent adhesive otitis media [17]. Although otologic surgery generallyhas been successful in clearing cholesteatomas, those patients with nonfunc-tioning or marginally functioning ETs traditionally have had less successfulresults. Reoccurrence rates in pediatric patients have been linked to poor ETfunction [18]. ET dysfunction has also been shown to adversely affect post-operative hearing results in children [19].

Although the normal physiologic state of the middle ear is to haveequal pressure between the middle and lateral sides of the tympanic mem-brane, some patients will prefer a negative pressure in their ear. Bunneand coworkers [20] in 1999 found that these patients complained of hyper-acusis and autophony with the tympanic membrane in the normal position.Two groups with retracted tympanic membranes and sound disturbances

Functional failure of the ET

Increased negativemiddle ear pressure

Atelectasis of thetympanic membrane

Retraction pocket in atticor posterior-superior

quadrant

Adhesive otitis media

Fig. 1. Pathway of acquired cholesteatoma. (From Bluestone CD, Cantekin EI, Beery QC, et al.

Function of the eustachian tube related to surgical management of acquired aural cholesteato-

ma in children. Laryngoscope 1978;88(7 Pt 1):1155-64; with permission.)


were evaluated. There was the expected group, 45%, that complainedthat sound was too weak or muffled. Hearing results improved with valsalvafor these patients. However, a larger group had loud sound sensitivity andintermittent autophony after swallowing or valsalva. This group was thoughtto represent patients with poor tubal function in which the ET stays openand fails to protect the ear from these loud noises [20]. These patients werealso at risk for the development of retraction pockets and atelectasis fromchronic sniffing, which was done to achieve a more comfortable state.

Continuous opening of the ET is described as patulous. Patients with thisdisorder complain about autophony or hearing their own breathing or echo-like vocalizations. Causes can include hormonal changes (decreased estro-gen levels), rapid weight loss, or chronic middle ear dysfunction.

Etiology of ETD

Multiple causes of ET dysfunction exist. This varied differential includesinfectious, allergic, mechanical (obstructive), environmental exposure, ge-netic, reflux, congenital, and iatrogenic causes. Although not a completelist, some of the more common etiologies will be explored.

Viral upper respiratory tract infection

Doyle and coworkers [21] confirmed that not only was the ET affected byviral upper respiratory tract infections (URIs), but also that healthy ETfunction decreased the risk of complications resulting from URI.

Chronic sinusitis

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

Allergic rhinitis

Known to cause ETD [23,24], allergic rhinitis and viral infections interactto enhance physiologic response in the middle ear and ET [25].

Adenoid hypertrophy

It is well known that adenoid enlargement can obstruct the nasopharyn-geal opening of the ET, but it can also impair mucociliary clearance fromthe tube by means of nonciliated metaplastic epithelium and fibrosis of con-nective tissue associated with adjacent adenoid tissue [26].

Tobacco smoke

Two studies published by Agius and coworkers [27,28], confirmed thatthere was a decrease in ciliary beat frequency of the mucosa of the ET in


smokers compared with nonsmokers. This finding, however, has beentempered by work by Coggins and colleagues [29] and Antonelli and co-workers [30] who found passive tobacco smoke in the animal model tohave little effect on otitis media. According to Dubin and coworkers [31],passive smoke does affect the ET function, but may play only part ofa role in causing middle ear disease.

Reflux

White and coworkers [32] determined that exposure to gastric contentsin the nasopharynx caused a significant ET dysfunction in an animalmodel. Their experiment found that middle ear pressure regulation andmucociliary clearance of middle ear contents were disabled. Heavner andcoauthors [33] in 2001 had previously published similar results in ananimal model.

Cleft palate

Previous research has found that children with a cleft palate have an in-creased risk of middle ear pathology [34]. The incidence of ETD has beenquoted as high as 79% in patients with cleft palate and cleft lip/palate asfound by Goldman and coworkers [35]. Interestingly, in their cohort, only2 of 110 patients had acquired cholesteatoma.

Arnold and coworkers found patients with bilateral cleft palate to havea nearly horizontal course of the ET, possibly worsening symptoms. Al-though TVP muscle had a bony attachment on either side, the levator velipalatini muscle also showed an abnormal course. This finding led the inves-tigators to conclude that, during contraction, an aberrant obstruction of theET may result.

Unfortunately, some cleft patients continue to have ETD postoperativelyand as they growth into adulthood. One third of the adults in a 2006 studyby Gudziol and Mann [36] with cleft lip and palate had persistent ETD.

Radiation

Treatment of nasopharyngeal malignancies with external beam radiationhas detrimental effects on the surrounding structures, especially the ET.Multiple investigators have found patients with early and late middle ear pa-thologies secondary to iatrogenic ET injury [37–39].

Reduced mastoid air cell system

The presence of a mastoid air cell system has been reported as an impor-tant criterion postoperatively to act as a pressure buffering system. How-ever, this function is dependent on having healthy mastoid mucosa [40].


Nitrous oxide

A study by Teixeira and coworkers [41] in 2005 found that approximatelyone half of patients who received 50% nitrous oxide under general anesthe-sia, had Type C tympanograms postoperatively, compared with a Type Atympanogram preoperatively. This change in middle ear pressure is likelysecondary to absorption of nitrous oxide, leaving a decrease in gaseous vol-ume in the middle ear space.

ET, mastoid, and cholesteatoma

The status of the mastoid has been found to affect the progression of cho-lesteatomas. In some instances, this factor was more important than thepresence of poor ET function. Hasebe and coworkers [42] in 2001 comparedthree groups with varying degrees of tympanic membrane retraction. Thisgrouping included patients with a severe attic retraction pocket, patientswith cholesteatoma but could be treated conservatively, and patients withcholesteatoma but needing surgery. All three groups had ETD, but no sig-nificant difference in the function of the ET was found among the threegroups. Progression of the cholesteatoma appeared to be related more tothe ventilatory condition of the mastoid rather than the ET function. Thisobservation was based on less aeration seen in the surgery group comparedwith the nonsurgical group [42].

When the ET fails to equalize pressure, a negative pressure in the middleear space occurs. The mastoid is seen by many researchers as a buffer zonefor the middle ear and tympanic membrane allowing some equalization ofthis abnormal pressure. Cinamon and Sade [43] developed a model to eval-uate how pressure homeostasis of the middle ear can be maintained. Theyfound that the worst "model" for adapting to these changes was a middleear space with a small mastoid. The investigators proposed that this ana-tomic finding may lead to patients developing compensatory bufferingmechanisms, such as retraction or fluid accumulation, which reduced middleear volume [43].

Retraction pockets are well known to result from ETD. Wolfman andChole [44] in 1986 found cauterized ETs of the Mongolian gerbil resultedin a progressive retraction in 75% of the animal in a 16-week period.

Examining the retracted tympanic membrane, Paparella and coworkers[45] described epithelial and subepithelial changes such as keratin accumu-lation, papillary growth, mucosal adhesion, irregular epithelium, and bonedestruction. Although reasonable theories exist to describe why cholesteato-mas occur, it is not entirely known what allows retraction pockets to evolveinto cholesteatomas (Fig. 2).

Cholesteatomas are known to arise more commonly in the pars flaccida.The reason for this may be that there is poorer aeration in this area, espe-cially in the area of the tympanic isthmus. Kobayashi and colleagues [46]


in 1994 compared computed tomography scans of 53 patients with retrac-tions in the pars flaccida, including those with cholesteatoma. Their resultsfound little association with this blockage and progression ofa cholesteatoma.

Evaluation of the ET

Assessment can be started initially by taking a thorough history. A typ-ical ETD patient will complain of fullness or clogging of the ears, pain ordiscomfort, hearing loss, tinnitus, and dizziness. Most concerning to thesepatients is when these symptoms cannot be relieved by swallowing, yawning,or chewing.

Physical examination

Using pneumatic otoscopy, an examiner can evaluate the mobility of thetympanic membrane. Stiffness or middle ear effusions are suggestive ofETD. Indirect nasopharyngoscopy, using a small dental mirror, representsanother manner to visually inspect the posterior nasopharynx and proximalopening of the ET. Pathology such as adenoid hypertrophy or mucosaledema can be seen.

It is well known that a rigid or flexible nasal endoscope allows the exam-iner to visualize the nasopharyngeal opening of the ET. Usually 30� or 70�

rigid Hopkins rod endoscopes provide the best visualization. Other re-searchers have advocated using 0.8-mm flexible fiberscopes to evaluatebeyond the isthmus of the ET and even into the middle ear cleft [47,48].

Pars Flaccida

Retraction with debris

Pars Tensa Retraction

Robert W. Seibert, MD

Fig. 2. Retracted tympanic membrane caused by ETD. (Courtesy of Robert W. Seibert, MD,

Little Rock, AK.)


ET testing

Some researchers have reported that tests for evaluating ET function arenot reliable [49]. However, most agree that there are objective and subjectiveassessments helpful in studying ETD.

A tympanogram plots a measure of how energy is transmitted throughthe middle ear. When pressures between the middle ear space and the earcanal are equal, a normal or ‘‘type A’’ tympanogram is recorded. Abnormaladmittance in the form of a retraction or stiffness will result in a plottedgraph know as a ‘‘type C’’ or ‘‘type B’’ tympanogram, respectively [50].

Other subjective testing includes the Valsalva test, which involves patientsholding their nose and blowing out with a closed mouth. The Toynbee test isa similar maneuver. In this test, patients hold their nose and swallow. Whilepatients swallow, the examiner can visually inspect the tympanic membraneand evaluate for movement. This exercise generates a positive pressurewithin the nasopharynx, followed by a negative pressure phase and isconsidered positive when there is an alteration in middle-ear pressure asassessed by pneumatic otoscopy before and after the maneuver. Negativemiddle ear pressure or temporary negative middle ear pressure followedby return to ambient pressure after the Toynbee test usually is indicativeof normal ET function [51].

In the Politzer test, one of the patient’s nostrils is occluded with a rubberballoon as the examiner pinches the other nostril tightly. The patient ele-vates the palate by swallowing or phonating. The examiner then forces airinto the closed nasal cavity from Politzer’s bag. Air can be heard goinginto the middle space with an auscultation device. The examiner can alsovisually compare the tympanic membrane before and after the procedureto determine its relative patency [52].

A final testing mechanism is sonotubometery. In this procedure, a soundsource is applied to the nostril as a microphone in the external auditorycanal records the transmitted sound. Sound levels are measured as the ETopens and closes. The advantage of this diagnostic test is the ability to eval-uate the ET with or without an intact membrane under physiologic condi-tions [53].

Medical treatment of ET dysfunction

A review of the literature finds that there is no clear consensus on oral/topical medications for the treatment of ETD. Some of the more pertinentstudies are mentioned. van Heerbeek and coworkers [54] studied outcomesof using pseudoephedrine in children already treated with pressure equaliza-tion tubes. Their findings showed there was no significant effect on ETfunction in children who used this topical decongestant.

In a double-blind, placebo-controlled, crossover study, Cantekin andcolleagues [55] in 1980 found that children without an upper respiratorytract infection had a lower closing pressure of the ET after taking


a decongestant-antihistamine combination compared with their controlgroup. In the presence of normal mucosa, this study confirmed that someeffect on the performance of the ET was possible.

Dexamethasone has shown promising results. Silverstein and coworkers[56] in 2003 published their findings in a small group of chronic ETD pa-tients that benefited from direct treatment of the ET with dexamethasone.This application, however, required that a pressure equalization tube beplaced first and that the medication be applied transtympanically. Shapiroand colleagues [57] in 1982 showed increased benefit in achieving normalmiddle ear pressure and tympanic membrane mobility with aerosolizednasal dexamethasone. This positive result was tempered by a concern raisedon cortisol levels, which were lowered in two of the study patients.

This early success of steroids on ETD laid a foundation on which otherstudies using less potent treatments could be built. Tracy and coauthors [58]found that intranasal beclomethasone may be a useful adjunct to prophylac-tic antibiotic treatment of chronic middle ear effusion. The investigators re-ported that patients had a more rapid improvement in the first 8 weekscompared with the antibiotic-alone treatment arm. Although this studydoes not address the functional status of the ET itself, one can inferimprovement with the resolution of the effusion.

A later study by Karlidag and coworkers [59] in 2002, failed to duplicatethe results. These researchers found no statistical difference in the nasal ste-roid treatment group compared with the antibiotic alone group. However,both groups were more effective than the control (no treatment). The inves-tigators blamed the lack of significance on the sample size. A previous studyby Ruohola and colleagues [60] in 2000 may weaken this hypothesis. Thislarger study evaluated 210 children. Those patients who received intranasalsteroids had no statistical difference in the development of acute otitis mediacompared with the placebo group. Again, although ET physiologic statuswas not measured directly, failure to treat the targeted anatomy can beattributed to a poor-functioning ET.

Surgical treatment of ET dysfunction

Insertion of pressure equalization tubes (PET) had been the mainstay sur-gical treatment of ETD. Although the pressure difference between the mid-dle ear and the external auditory canal is resolved immediately with thisprocedure, little effect can be seen the ET itself. Several investigators havefound that active tubal function does not change after PET insertion and re-mains at the same poor level postoperatively [61,62]. However, van Heer-beek [61] and coworkers did identify changes to the ET seen in the formof passive tubal function. These patients had a significant increase openingpressure compared with preoperative measurements.

Fuldaer ventilation surgery proposed by Kaftan and Draft [63] in 2000combined different methods to improve ventilation of the middle ear. The


surgeon performed mastoidectomy, posterior tympanotomy, and removal ofthe incus and the head of the malleus with an interposition of the incus. Af-ter the tympanic membrane was reconstructed with a cartilage-perichon-drium graft, a tube was placed into the middle ear orifice leading to thenasopharynx (Wright-tube). This aggressive approach showed some successin preventing disease. Specifically, approximately 26% of those patients withchronic ETD who have not responded to previous surgeries required subse-quent revision surgery for recurrent cholesteatoma. However, other investi-gators have gained similar results for preventing recurrent cholesteatoma inpatients with ETD by performing mastoid and epitympanic obliterationtechnique alone [64].

Once patients have been determined to have poormastoid aeration in asso-ciation theETD, little canbe done to correct these areas surgically. This theoryis based on the fact that patients with poor ET function aremore likely to haveretraction pockets and recurrent cholesteatoma. Mastoid obliteration hasshown promising in preventing this recurrent disease owing tomalfunctioningET by eliminating the potential space for development [64,65].

One of the few procedures to treat proximal dysfunction of the ET is lasereustachian tuboplasty. This technique, proposed by Kujawski and Poe [66],provides a means to treat intractable ETD. In this procedure, a CO2 ora 980-nm diode laser was used to obliterate mucosa and cartilage fromthe luminal posterior wall of the ET. A 65.21% success rate at 3 yearswas reported with minimal postoperative complications.

Adenoidectomy for ETD remains a controversial topic. Bluestone andcolleagues [67] in 1975 found that children with obstructive adenoids ofthe nasopharynx and proximal opening of the ET showed some benefit afteradenoidectomy in active opening and closing of the ET. Other investigatorshave found that adenoidectomy did not affect either passive or active open-ing or closing pressures of the ET [68–70].

ETD is a risk after cholesteatoma surgery. Chao and coworkers [71]1996 looked at a 5-year follow-up of postoperative tympanomastoidec-tomy patients. Sixty-six percent of these patients had a retraction pocket,most obviously seen near the scutum defect. Although the investigatorshad difficulty determining whether the ETD was the etiology or the se-quelae of a cholesteatoma, it is known that these sequelae likely increasesthe risk of reoccurrence.

Complications

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

Aside from the complaints of discomfort with ETD, other traumatic eventscan occur in these patients in the form of otic barotraumas. Because of their


inability to equalize pressure normally, patients with ETD have an increasedrisk of injury to the tympanic membrane when involved in activities such asdescending and ascending in aircraft, scuba diving, and driving in higher ele-vations. Sade and colleagues [72] in 2003 reported that during a commercialplane flight, the middle ear has to equalize about 20% of its gas volumewith the ambient pressure. This equalization must take place within 15 to 20minutes of ascent and descent, otherwise otic barotraumas can result. An in-teresting note, chronic ear patients had a smaller mastoid air cell volume.When compared with patients with history of barotraumas, a less-developedmastoid routinely found in chronic ear patients was more protective of injury.Thus, chronic ear patients are at less risk for barotrauma.

Summary

There appears to be a correlation between ET dysfunction and thesubsequent development of a cholesteatoma. Although both a healthy mas-toid and adequate ET function seem to be instrumental in providing aera-tion to the middle ear, the physiologic state of the ET plays a larger role.Postoperative conductive hearing loss and the incidence of reoccurrenceof cholesteatoma can be reduced significantly with improved ET function.

Several etiologies exist that can cause ETD, which can lead to a widespectrum of middle ear disease from a mild retraction to an invasive choles-teatoma. However, there are little data to explain why some retractions arestable, while others progress to cholesteatoma.

Although some findings have suggested that the degree of aeration of themastoid is an important physical finding, the key to interrupting this evolu-tion appears to be treatment of the underlying cause of the negative pres-sure, in this case a poorly functioning ET. Medical intervention has hadsuccess in the preventing or treating ETD, whereas surgical treatment hasshown to be more effective in addressing the sequelae rather than the causeitself.

Acknowledgment

I would like to thank Chris Danner, MD, for inviting me into this projectand his perseverance to teach residents. I would also like to thank my wife,Shannon, and my three children for their continual support.

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eustachian tube function

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