the eustachian tube

The eustachian tubeUpdate on anatomy, development,

and function

Greg R. Licameli, MD, FACSDepartment of Otolaryngology and Communications Disorders,

Childrens Hospital, 300 Longwood Ave., Boston, MA 02115, USA

The eustachian tube (ET) is part of a system of connected structures

including the nose, nasopharynx, middle ear, and mastoid. The ET is not

a simple tube but a complex structure, lined with respiratory mucosa, com-posed of bone and cartilage, and surrounded by soft tissue and muscle. ET

dysfunction has been implicated in the cause of acute and chronic otitis

media, the development of tympanic membrane retraction pockets and ate-

lectasis, and cholesteatoma. The study of the anatomy and dynamic func-

tion of this area is important in understanding the diseases and disorders

that affect the middle ear and mastoid.

Anatomy

The ET extends from an opening on the anterior wall of the middle ear to

an opening in the nasopharynx just posterior to the inferior nasal concha

and lateral to the adenoid pad. The lateral third of the tube is comprised

of bone, whereas the anteromedial portion is composed of cartilage and

connective tissue [1]. The narrowest portion of the tube is the isthmus. The

term ‘‘junctional portion’’ was introduced by Sando and refers to the over-

lapping region of bone and cartilage [2].The bony canal is surrounded superiorly by several important structures.

A thin lamina of bone separates the ET from the canal in which the tensor

tympani originates. Inferiorly, it is adjacent to the jugular fossa and, medi-

ally, it abuts the carotid canal. The cartilaginous portion of the ET is pri-

marily composed of a sheet of cartilage that forms the medial wall,

continuing superiorly to form a portion of the lateral wall. Fibroconnective

Otolaryngol Clin N Am

35 (2002) 803–809

E-mail address: [email protected] (G.R. Licameli).

0030-6665/02/$ - see front matter � 2002, Elsevier Science (USA). All rights reserved.

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tissue completes the remainder of the lateral wall. In addition, several acces-

sory cartilages may be found around the pharyngeal orifice, theorized to

help facilitate movement of the tube [1]. The ET lumen is lined with respi-ratory epithelium that is made up of ciliated and nonciliated cells, goblet

cells, and basal cells [3]. The highest density of ciliated and goblet cells is

around the pharyngeal opening and along the inferior aspect of the tube [4].

Physiology

Four muscles are associated with the ET function: the tensor veli palatini,

levator veli palatini, salpingopharyngeus, and tensor tympani. At rest, the

ET is passively closed and is opened by swallowing, yawning, or sneezing.

The primary dilatator is by the tensor villi palatini with perhaps some con-

tribution from the levator veli palatini. The tensor veli palatini is composed

of two bundles of muscle fibers. The lateral bundle arises from the scaphoidfossa and greater wing of the sphenoid superior to the ET cartilage. This

muscle descends inferiorly to wrap around the hamulus of the medial pter-

ygoid and finally insert into the palatal aponeurosis and posterior edge of

the hard palate. The medial bundle arises medially from the lateral lamina

of the cartilaginous portion of the ET, joining the lateral bundle to pass

around the hamulus to its insertion. The medial bundle, lacking in osseous

origin, is considered to be continuous with the tendon of the tensor tympani

muscle. The medial bundle also lies adjacent to the lateral membranous wallof the ET and is called the dilator tubae muscle [1,5–7].

The levator veli palatini muscle arises from the inferior aspect of the pet-

rous portion of the temporal bone. It descends inferiorly and medial to the

ET between the salpingopharyngeus and tensor veli palatini muscle to insert

into the soft palate aponeurosis. The levator veli palatini spread outs and

interdigitates with muscle fibers from the contralateral levator [1]. It is felt

that this muscle at its origin has very loose connective tissue attachments

to the cartilaginous ET and in its anterior two thirds portion is separatedby connective and fatty tissue [8]. The levator veli muscle likely aids in dilata-

tion of the ET in its pharyngeal portion by elevating the cartilage medially [9].

The salpingopharyngeal muscle arises from the medial and inferior aspect

of the cartilaginous ET and inserts, along with part of the palatopharyngeal

muscle, into the wall of the pharynx. In cadaver studies, this muscle was

poorly formed in the majority of specimens [1]. These fibers do not seem

to have a significant physiologic role in tubal function.

Function

The ET has three basic functions [10]. Regulation of middle ear pres-sure with respect to atmosphere pressure, clearance of middle ear secretions,

andprotectionof themiddle ear fromsoundandaccumulationofnasopharyn-

804 G.R. Licameli / Otolaryngol Clin N Am 35 (2002) 803–809

geal secretions are coordinated in part by the anatomic factors outlined

above.

Regulation of middle ear pressure is primarily caused by contraction of

the tensor veli palatini during swallowing or yawning. This allows openingof the ET and passive exchange of air between the middle ear and the naso-

pharynx. Airflow is intermittent, lasting approximately 0.2 seconds once

every 1–2 minutes and occurs in both directions, based on the pressure dif-

ferences between the middle ear and the atmosphere [11]. During the major-

ity of the time, the pharyngeal opening of the ET remains closed.

Negative middle ear pressure is common to many disease processes

involving the middle ear such as chronic otitis media, the promotion of

retraction pockets, and atelectasis of the tympanic membrane. The mostcommon explanation is that the ET fails to open, either from physical or

physiologic obstruction. Physical obstruction at the pharyngeal orifice can

arise from adenoid hypertrophy, tumor, or fibrosis. Obstruction at the mid-

dle ear opening can come from hypertrophied middle ear mucosa, cholestea-

toma, or rarely, tumor. Physical obstruction is usually caused by the

hypertrophy of the mucosa lining the tube and secondary to infectious eti-

ologies, although allergic factors have also been implicated.

Physiologic obstruction arises from the failure of the muscles involved toopen the ET, a theory supported by several studies showing that young chil-

dren commonly have difficulties with active opening [10,12]. Nearly all

patients with unrepaired cleft palates have difficulties with middle ear effu-

sion, caused in part by abnormal development of the tensor levi palatini and

levator veli palatini. Repair of their palates is associated with improved ET

function [13]. In a study that underscored the function of the tensor veli

palatini, Casselbrant et al paralyzed this muscle in monkeys by injecting bot-

ulinum toxic, which resulted in negative middle ear pressure and effusion[14]. Other anatomic variations between the child and adults, such as the

length and angulation of the ET and the compliance and density of the tubal

cartilage and elastin, have been implicated [15].

A second factor important in the regulation of middle ear pressure is

based on gas exchange in the middle ear and mastoid. Regulation of gas

exchange between the middle ear and the middle ear mucosa circulation is

not well understood. Tissue diffusion of gases is dependent on the thickness

of the middle ear mucosa, the rate of perfusion of the mucosa, the perme-ability of the blood vessels, and the partial pressure of gas in the middle ear

and blood. The fact that middle ear gasses are more similar to venous blood

than atmospheric air suggests that this regulation is critical in understanding

middle ear dynamics. Experiments looking at gas exchange have shown that

inflamed middle ear mucosa transports gases more rapidly that healthy

mucosa. The regulation of this process is felt to be multifactorial [11].

Furthermore, the presence of air in the mastoid acts as a buffer for the

middle ear. A well-pneumatized mastoid has the capacity to offset anymiddle ear pressure changes more than a contracted, poorly pneumatized

805G.R. Licameli / Otolaryngol Clin N Am 35 (2002) 803–809

mastoid. Underdeveloped or poorly pneumatized mastoids are common in

children with chronic otitis media, patients with retracted tympanic mem-

branes, and those with cholesteatoma.The second function of the ET is the clearance of secretions. Clearance of

secretions has been found to be an active process based on the mucociliary

lining of the tube. The movement of material from the middle ear into the

nasopharynx has been shown to occur in both human and animal models.

Embryologically, the ET forms by an invagination of the nasopharyngeal

mucosa, with the structure of the epithelium and submucosal layer similar

to other parts of the respiratory tract [16]. A variety of irritant factors, such

as environmental pollutants, bacterial and viral infection, and irradiationaffect the function of this epithelium. Studies have shown that ciliated cells

and goblet cells are more populated along the floor of the ET and increase in

density from the tympanic to the nasopharyngeal opening. The activity of

these cells has been shown to move secretions actively out of the middle ear

[17]. Sando et al also found more mucosal folds along the floor of the ET

which led them to theorize that the floor was more important for secretion

clearance, and that the roof of the ET was involved in the ventilation of the

middle ear [18].The third function of the ET is protection of the middle ear. A closed ET

pharyngeal orifice protects the middle ear from sounds generated in the res-

piratory tract and from secretions entering from the nasopharynx. The pres-

ence of an intact middle ear and mastoid, which provides a ‘‘cushion’’ of air

behind the tube, also aids in preventing secretions from entering the ET ori-

fice. Though closure of the ET orifice is largely passive, dysfunction of the

process of active dilation can also cause difficulties.

Several anatomical features of the ET have been shown to contribute tothe mechanical protection of the ET. Though opening of the ET is largely an

active process based on the contraction of the tensor veli palatini, closure is

passive. In the midportion of the ET, elastin is present between the medial

and lateral lamina [15]. Sando et al has hypothesized that this allows the lat-

eral lamina to close the roof of the ET after contraction of this muscle [19].

Protection of the floor of the tube may come from the presence of Ost-

mann’s fat pad, which exerts pressure on the orifice when the tensor veli palat-

ini relaxes [20]. On cross sectional analysis, this fat pad is located betweenthe ET and the tensor. The presence of a relatively larger Ostmann’s fat pad

in children versus adults may be a contributing factor for otitis media.

The ET has been shown to be significantly shorter in length in children

< age 5–6 years and in those with cleft palate, Down syndrome, and other

craniofacial syndromes [10]. A shorter tube provides poor protection by

allowing easier access of nasopharyngeal secretions to the middle ear space.

There exists a mechanical system in which the muscles that connect to the

ET coordinate the opening of the ET orifice. With the advent of microfiber-optic endoscopes, the dynamic study of physiologic function is possible. Poe

et al have observed consistent muscle movement patterns in normal subjects


that were absent in patients with ET dysfunction [21]. Four phases were

described during opening: (1) with palate elevation, the medial cartilage

lamina of the ET orifice rotates medially, (2) the lateral wall then moves lat-

erally dilating the ET orifice, (3) the tensor veli palatini dilates the lumen dis-tally, and (4) the isthmus valve opens secondary to dilator tubae muscle

contraction. In patients with ET dysfunction and pathology such as choles-

teatoma, tympanic membrane atelectasis, or otitis media, findings were that

of physical obstruction of the orifice from polyps or edema or dyskinetic

movement of tubal peristalsis.

Kimura first introduced trans-ET endoscopy in 1989, and several articles

have followed evaluating the anatomy in both cadaveric temporal bones

and human subjects. Su examined 18 awake patients under local anesthesiaand was able to pass a microfiberoptic endoscope transtympanically into

the tube to the isthmus region in 505 of patients, evaluating its dynamic mo-

tion [22]. Linstrom et al reported significant narrowing of the isthmus in pa-

tients with chronic ear disease examined at the time of surgery, particularly

those with a history of cholesteatoma [23]. Currently, a limiting factor

for this technique is the fragile nature of these expensive endoscopes, with

outer diameter sizes between 0.5 and 1.6 mm, which are prone to fiber

breakage.The recent use of three-dimensional computer graphics of temporal bone

studies has helped elucidate the function of the ET. Earlier measurements of

tube size and geometry were made with cross-sectional histiologic analysis,

which is subject to tissue processing and sectioning errors. A study by Sudo

et al measured the cross section of the ET lumen throughout its entire

course, identifying the narrowest portion of the ET to reside within the car-

tilaginous portion [24]. Of significance is the finding that the tensor veli pala-

tini muscle inserts into the lateral lamina of the ET in this region, asdescribed in this and previous studies. Suzuki et al noted that the growth

of the cartilaginous portion of the ET produces a marked increase in the vol-

ume of the ET lumen in childhood. They also found a difference in the shape

of the lumen in the cartilaginous portion of the ET between adults and chil-

dren. In children, the ET lumen was uniformly smaller over most of the

length of the cartilaginous tube from the pharyngeal orifice. In contrast with

adults, the cross-sectional area of the lumen decreased gradually to the isth-

mus region [25]. Ishijima et al evaluated the postnatal development of thetube by three-dimensional reconstruction of temporal bones. The length

of the ET in a 3-month-old infant doubles from an average of 21 mm to

37 mm in the adult. Furthermore, the bony and cartilaginous portions of the

ET in a child are aligned in a straight line between the pharyngeal and tym-

panic orifices, whereas in the adult the cartilaginous portion angles inferiorly

and laterally, aiding in protection of the middle ear. The distance between the

pharyngeal and tympanic orifices reached adult dimensions at age 4, while the

length of the ET reached adult dimensions at age 7. Earlier studies suggesteda ratio of the cartilaginous portion to the bony portion of the ET to be 2:1


in infants; however, in this study the ratio was found to be 8:1, with a ratio

in adults of 4:1 [26].

A novel approach to assess the anatomy of the ET and paratubal struc-tures was described by Helweg et al, who used a specially designed endo-

luminal ultrasound to examine this region. It is possible that future

applications of this device could illuminate the real time function of the

ET [27].

Summary

Central to many pathologic conditions affecting the middle ear is the fail-

ure of the ET to perform its functions of regulation of middle ear pressure,

clearance of middle ear secretions, and protection of the middle ear space.

Recent advances in radiologic imaging and fiberoptic endoscopes have

allowed a more detailed description of the structure and function of this

area. Hopefully, with the knowledge gained from advances in this area,

more effective medical treatment options for common otologic problems,such as otitis media, will become available.

References

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the eustachian tube

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