Otolaryngol Clin N Am

39 (2006) 1221–1235

Eustachian Tube Function

and the Middle Ear
John W. Seibert, MDa,
Christopher J. Danner, MDb,*
a
Department of Otolaryngology, Washington University School of Medicine,
St. Louis, MO, USA
b
Otology/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/foreign
material in the nasopharynx, and (3) clearance of the middle ear space [1].
It is well known that eustachian tube dysfunction (ETD) is linked to
chronic secretory otitis media [2]. Other more invasive diseases can also oc-
cur 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.

History
The first modern-era researcher of the ET was Bartolomeus Eustachius.
He was a 16th century anatomist who taught at the Collegia della Sapienza
in Italy. Eustachius, for whom the ET is named, studied several areas in the
human body including the ET [3]. Further work was done by Antonio
Valsalva, (1666-1723). Valsalva was a Professor of Anatomy at Bologna
and is most recognized for his middle ear insufflating maneuver that bears
his name. Valsalva is credited with naming the auditory tube, the eustachian
tube, and describing its function [4].
Adam Politzer is probably best known for his contribution to otology
and probably considered the greatest otologist of the 19th century. One of
his legacies was a hand-held air bag that allowed insufflation of the middle

* Corresponding author.
E-mail address: cdanner@tampabayhearing.com (C.J. Danner).

0030-6665/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.otc.2006.08.011 oto.theclinics.com
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 out
pouching of the pharynx that forms the tubotympanum and the pneumatized
temporal bone. [6] The cartilaginous portion of the eustachian tube undergoes
the 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 that
the 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 distinction
found in ET mucosa provides a more effective, inherent protective compo-
nent. Unique characteristics of the ET include the presence of more mucus
cells and accessory glands when compared with the middle ear mucosa [9].
Compared with adults, the position of the infant ET is 10 from the
Frankfort horizontal plane. This angle is different in adults whose tube is
positioned at a 45 [1]. Among other differences in adult and pediatric
ETs, a less angled ET in the pediatric population has been thought to be
responsible for the increased incidence of middle ear pathology. However,
some researchers have found that active muscle function, rather than passive
clearance and impedance of the ET, is responsible for the decreased disease
state seen in adults [10,11].
A smaller or partially obstructed ET does not necessarily correlate with
the risk of disease or even active disease. Using an in vivo model, Sade
and coworkers [12] in 2004 found that narrowing of the ET alone did not
prohibit natural gas flow into the middle ear space with a swallowing
maneuver. Although the narrowed ET was open for a brief period, this
was 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 medial
rotation. 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 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 [9].
Blood supply to the ET and its supporting structures originates from the
deep auricular branches of the internal maxillary artery, ascending
 ET FUNCTION AND THE MIDDLE EAR 1223

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 the
tympanic 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 veli
palatini. 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 base
of the medial pterygoid plate on the scaphoid fossa. The second is from the
spina angularis of the sphenoid, and the third is from the lateral wall of the
cartilaginous eustachian tube. The TVP muscle descends and inserts on
a tendon at the pterygoid hamulus [9,15].
Levator veli palatini is a thicker muscle compared with the TVP and lies
lateral to the choanae. Its origin is from two anatomic sites. The first is the
inferior surface of the apex of the petrous part of temporal bone. The second
origin is the medial lamina of the cartilage of the ET. The muscle extends
above the superior pharyngeal constrictor merging with the opposite levator
muscle at midline [9,15].
Salpingopharyngeus originates from the inferior portion of the ET
extending downward joining the pharyngopalatinus muscle and assists
with 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 greater
wing of the sphenoid. The third is attachments to the bony canal in which
the muscle travels. The tensor tympani insertion is at the manubrium of
the malleus [9,15].

Function and dysfunction of ET

Normally, the ET stays closed and opens when necessary to equalize
pressure. Other functions include clearance of middle ear fluid while at
the same time preventing nasopharyngeal secretions refluxing into the mid-
dle ear space.
Ghadiali and coworkers [16] looked at the physiologic function of the ET
and found that the ET opening was highly sensitive to the applied muscle
1224 SEIBERT & DANNER

forces and relatively insensitive to cartilage elastic properties. In their anal-

ysis of the muscle forces (tensor and levator veli palatini) and soft tissue
elastic properties, luminal dilation of the ET was caused by muscle contraction
causing medial-superior rotation of the medial lamina, which in turn caused
a 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 sequence
of 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, and
subsequent adhesive otitis media [17]. Although otologic surgery generally
has been successful in clearing cholesteatomas, those patients with nonfunc-
tioning or marginally functioning ETs traditionally have had less successful
results. Reoccurrence rates in pediatric patients have been linked to poor ET
function [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 have
equal pressure between the middle and lateral sides of the tympanic mem-
brane, some patients will prefer a negative pressure in their ear. Bunne
and 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 negative
middle ear pressure

Atelectasis of the
tympanic membrane

Retraction pocket in attic

or 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.)
 ET FUNCTION AND THE MIDDLE EAR 1225

were evaluated. There was the expected group, 45%, that complained
that sound was too weak or muffled. Hearing results improved with valsalva
for these patients. However, a larger group had loud sound sensitivity and
intermittent autophony after swallowing or valsalva. This group was thought
to represent patients with poor tubal function in which the ET stays open
and fails to protect the ear from these loud noises [20]. These patients were
also at risk for the development of retraction pockets and atelectasis from
chronic sniffing, which was done to achieve a more comfortable state.
Continuous opening of the ET is described as patulous. Patients with this
disorder 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 includes
infectious, allergic, mechanical (obstructive), environmental exposure, ge-
netic, reflux, congenital, and iatrogenic causes. Although not a complete
list, 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 by
viral upper respiratory tract infections (URIs), but also that healthy ET
function 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 interact
to 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 from
the 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 that
there was a decrease in ciliary beat frequency of the mucosa of the ET in
1226 SEIBERT & DANNER

smokers compared with nonsmokers. This finding, however, has been

tempered by work by Coggins and colleagues [29] and Antonelli and co-
workers [30] who found passive tobacco smoke in the animal model to
have little effect on otitis media. According to Dubin and coworkers [31],
passive smoke does affect the ET function, but may play only part of
a role in causing middle ear disease.

Reflux
White and coworkers [32] 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. Heavner and
coauthors [33] in 2001 had previously published similar results in an
animal 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 been
quoted as high as 79% in patients with cleft palate and cleft lip/palate as
found by Goldman and coworkers [35]. Interestingly, in their cohort, only
2 of 110 patients had acquired cholesteatoma.
Arnold and coworkers found patients with bilateral cleft palate to have
a nearly horizontal course of the ET, possibly worsening symptoms. Al-
though TVP muscle had a bony attachment on either side, the levator veli
palatini muscle also showed an abnormal course. This finding led the inves-
tigators to conclude that, during contraction, an aberrant obstruction of the
ET may result.
Unfortunately, some cleft patients continue to have ETD postoperatively
and as they growth into adulthood. One third of the adults in a 2006 study
by Gudziol and Mann [36] with cleft lip and palate had persistent ETD.

Radiation
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 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].
 ET FUNCTION AND THE MIDDLE EAR 1227

Nitrous oxide
A study by Teixeira and coworkers [41] in 2005 found that approximately
one half of patients who received 50% nitrous oxide under general anesthe-
sia, had Type C tympanograms postoperatively, compared with a Type A
tympanogram preoperatively. This change in middle ear pressure is likely
secondary 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 the
presence of poor ET function. Hasebe and coworkers [42] in 2001 compared
three groups with varying degrees of tympanic membrane retraction. This
grouping included patients with a severe attic retraction pocket, patients
with cholesteatoma but could be treated conservatively, and patients with
cholesteatoma but needing surgery. All three groups had ETD, but no sig-
nificant difference in the function of the ET was found among the three
groups. Progression of the cholesteatoma appeared to be related more to
the ventilatory condition of the mastoid rather than the ET function. This
observation was based on less aeration seen in the surgery group compared
with the nonsurgical group [42].
When the ET fails to equalize pressure, a negative pressure in the middle
ear space occurs. The mastoid is seen by many researchers as a buffer zone
for the middle ear and tympanic membrane allowing some equalization of
this abnormal pressure. Cinamon and Sade [43] developed a model to eval-
uate how pressure homeostasis of the middle ear can be maintained. They
found that the worst "model" for adapting to these changes was a middle
ear space with a small mastoid. The investigators proposed that this ana-
tomic finding may lead to patients developing compensatory buffering
mechanisms, such as retraction or fluid accumulation, which reduced middle
ear volume [43].
Retraction pockets are well known to result from ETD. Wolfman and
Chole [44] in 1986 found cauterized ETs of the Mongolian gerbil resulted
in 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 bone
destruction. Although reasonable theories exist to describe why cholesteato-
mas occur, it is not entirely known what allows retraction pockets to evolve
into 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]
1228 SEIBERT & DANNER

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.)

in 1994 compared computed tomography scans of 53 patients with retrac-

tions in the pars flaccida, including those with cholesteatoma. Their results
found little association with this blockage and progression of
a 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 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 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 evaluate
beyond the isthmus of the ET and even into the middle ear cleft [47,48].
 ET FUNCTION AND THE MIDDLE EAR 1229

ET testing
Some researchers have reported that tests for evaluating ET function are
not reliable [49]. However, most agree that there are 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 [50].
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 [51].
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 ele-
vates 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 [52].
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 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 pertinent
studies are mentioned. van Heerbeek and coworkers [54] studied outcomes
of using pseudoephedrine in children already treated with pressure equaliza-
tion tubes. Their findings showed there was no significant effect on ET
function in children who used this topical decongestant.
In a double-blind, placebo-controlled, crossover study, Cantekin and
colleagues [55] in 1980 found that children without an upper respiratory
tract infection had a lower closing pressure of the ET after taking
1230 SEIBERT & DANNER

a decongestant-antihistamine combination compared with their control

group. In the presence of normal mucosa, this study confirmed that some
effect 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 be
placed first and that the medication be applied transtympanically. Shapiro
and colleagues [57] in 1982 showed increased benefit in achieving normal
middle ear pressure and tympanic membrane mobility with aerosolized
nasal dexamethasone. This positive result was tempered by a concern raised
on cortisol levels, which were lowered in two of the study patients.
This early success of steroids on ETD laid a foundation on which other
studies 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 weeks
compared with the antibiotic-alone treatment arm. Although this study
does not address the functional status of the ET itself, one can infer
improvement with the resolution of the effusion.
A later study by Karlidag and coworkers [59] in 2002, failed to duplicate
the 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 study
by Ruohola and colleagues [60] in 2000 may weaken this hypothesis. This
larger study evaluated 210 children. Those patients who received intranasal
steroids had no statistical difference in the development of acute otitis media
compared with the placebo group. Again, although ET physiologic status
was not measured directly, failure to treat the targeted anatomy can be
attributed 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 this
procedure, little effect can be seen the ET itself. Several investigators have
found 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 form
of passive tubal function. These patients had a significant increase opening
pressure compared with preoperative measurements.
Fuldaer ventilation surgery proposed by Kaftan and Draft [63] in 2000
combined different methods to improve ventilation of the middle ear. The
 ET FUNCTION AND THE MIDDLE EAR 1231

surgeon performed mastoidectomy, posterior tympanotomy, and removal of

the 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 the
nasopharynx (Wright-tube). This aggressive approach showed some success
in preventing disease. Specifically, approximately 26% of those patients with
chronic 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 in
patients with ETD by performing mastoid and epitympanic obliteration
technique alone [64].
Once patients have been determined to have poor mastoid aeration in asso-
ciation the ETD, little can be done to correct these areas surgically. This theory
is based on the fact that patients with poor ET function are more likely to have
retraction pockets and recurrent cholesteatoma. Mastoid obliteration has
shown promising in preventing this recurrent disease owing to malfunctioning
ET by eliminating the potential space for development [64,65].
One of the few procedures to treat proximal dysfunction of the ET is laser
eustachian tuboplasty. This technique, proposed by Kujawski and Poe [66],
provides a means to treat intractable ETD. In this procedure, a CO2 or
a 980-nm diode laser was used to obliterate mucosa and cartilage from
the luminal posterior wall of the ET. A 65.21% success rate at 3 years
was reported with minimal postoperative complications.
Adenoidectomy for ETD remains a controversial topic. Bluestone and
colleagues [67] in 1975 found that children with obstructive adenoids of
the nasopharynx and proximal opening of the ET showed some benefit after
adenoidectomy in active opening and closing of the ET. Other investigators
have 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 investigators
had difficulty determining whether the ETD was the etiology or the se-
quelae of a cholesteatoma, it is known that these sequelae likely increases
the risk of reoccurrence.

Complications
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.
Aside from the complaints of discomfort with ETD, other traumatic events
can occur in these patients in the form of otic barotraumas. Because of their
1232 SEIBERT & DANNER

inability to equalize pressure normally, patients with ETD have an increased

risk of injury to the tympanic membrane when involved in activities such as
descending and ascending in aircraft, scuba diving, and driving in higher ele-
vations. Sade and colleagues [72] in 2003 reported that during a commercial
plane flight, the middle ear has to equalize about 20% of its gas volume
with the ambient pressure. This equalization must take place within 15 to 20
minutes 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-developed
mastoid 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 the
subsequent 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 reoccurrence
of cholesteatoma can be reduced significantly with improved ET function.
Several etiologies exist that can cause ETD, which can lead to a wide
spectrum of middle ear disease from a mild retraction to an invasive choles-
teatoma. However, there are little data to explain why some retractions are
stable, while others progress to cholesteatoma.
Although some findings have suggested that the degree of aeration of the
mastoid 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 had
success in the preventing or treating ETD, whereas surgical treatment has
shown to be more effective in addressing the sequelae rather than the cause
itself.

Acknowledgment
I would like to thank Chris Danner, MD, for inviting me into this project
and 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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