Eustachian tube dysfunction diagnosis and treatment

EUSTACHIAN TUBE
DYSFUNCTION- DIAGNOSIS AND
TREATMENT

ANATOMY
• The eustachian tube is a dynamic conduit between the middle ear
and the nasopharynx.
• The eustachian tube in the normal adult measures approximately 31
to 38 mm in length.
• The eustachian tube performs the functions of :
1. Aeration and drainage of middle ear space
2. Protects the middle ear from the reflux of sound and material from
the nasopharynx

ANATOMY
• The eustachian tube contains a physiological valve that is closed in the
passive resting position and is dilated open by active muscular exertion.
• The direction of mucociliary clearance within the eustachian tube flows
from the ear to the nasopharyngeal orifice.
• the proximal one-third is a bony funnel –shaped extension of the middle
ear, which becomes narrowest at the isthmus. The bony portion is lined by
thin layer of cuboidal respiratory epithelium and is a fixed conduit.

ANATOMY
• The distal 2/3rd of the eustachian tube is the pharyngeal portion and
is composed of cartilaginous skeleton.
• The lumen is lined by columnar, taller and more ciliated respiratory
epithelium.
• The cartilaginous part is normally closed in the resting state due to
apposition of the mucosal walls.
• The closure occurs over a variable distance(5-10mm) and is a few
mm.s distal to the isthmus where the cartilaginous part becomes
flexible. This portion of the ET that intermittently dilates to an open
position is termed the “valve”.

ANATOMY
• There are four peritubular muscles attached to the pharyngeal portion
which are capable of a wide range of movements:
1. The levator veli palatini(LVP)
2. The salpingopharyngeus
3. the tensor tympani
4. The Tensor veli palatini(TVP)- principal dilator of the tubal lumen.
• Contraction of the LVP raises the soft palate and medially rotates the
medial cartilaginous lamina. Contraction of the TVP tenses the
anterolateral membranous wall to dilate the tubal valve into an open
position.

PHYSIOLOGY OF TUBAL DILATION
• INVOLUNTARY DILATION OF THE ET TUBE OCCURS THROUGHOUT THE
DAY THROUGH A SWALLOW OR A YAWN.
• INTERMITTENT BRIEF TUBAL DILATION IS THE PRINCIPAL MECHANISM
FOR EQUILIBRATION OF MIDDLE EAR PRESSURE WITH THE AMBIENT
ATMOSPHERE.
• BAROMETRIC AND CHEMICAL RECEPTORSWITHIN THE MIDDLE EAR
PROVIDE AUTONOMIC NERVOUS SYSTEM FEEDBACK TO INFLUENCE
THE FREQUENCY OF INVOLUNTARY TUBAL OPENING.
• 1.4TIMES PER MINUTE DURING DAYTIME; SUBSTANTIALLY REDUCED
DURING SLEEP.

• Muscular contractions initiate rotational movements of the cartilaginous
framework and create tension with effacement and lateral rounding of the
anterolateral wall to produce active dilation of the lumen.
• During swallowing, the muscles that dilate the eustachian tube are activated; As
the soft palate is elevated and seals the nasopharynx, the TVP isometrically
contracts and pulls on the lateral lamina and the connective tissue lateral to the
tube.
• With lateral movement of the lateral lamina, owing to the hinge action between
the laminae where the elastin fibers are in abundance, it becomes more circular
in cross section

• The medial lamella remains relatively rigid, and the sequence of
muscular contraction allows for concerted tubal opening and flow of
gas.
• mechanisms that can initiate tubal opening include yawning,
sneezing, and, in some patients, forced pressurization by swallowing
with a closed glottis (Toynbee maneuver) or with insufflations of air
(politzerization)

• four steps in tubal opening:
(1) palatal elevation with medial movement of the lateral pharyngeal wall
and medial rotation of the medial lamina (initiation of opening of the
distal cartilaginous tube presumably by the LVP),
(2) lateral movement of the lateral wall with dilation of the orifice laterally
and vertically,
(3) propagation of dilation of the tubal lumen from distal to proximal by the
TVP/DT, and
(4) opening of the proximal cartilaginous tube adjacent to the junctional
region with formation of a round to crescent-shaped lumen.

• To be fully opened, the dilatory muscles must overcome the intraluminal
surface tension.
• Surfactant protein B, has been identified in the secretory granules of
surface cells lining the eustachian tube.
• The surface tension in the normal eustachian tube is typically 58 mN/m,
but is elevated in serous and mucoid otitis media.
• Tubal surface tension is under control of the autonomic nervous system,
and increased parasympathetic transmission has been shown to impair
tubal opening.

• Mucus of the tube is composed of a thick, more superficial, gel phase and a
thin sol phase. The cilia move in the sol phase with their tips contacting the
overlying gel phase, propelling the mucous blanket.
• Surfactant potentiates the movement of the gel over the sol phase.
• Fluid and secretions in the middle ear are cleared by a combination of muscular
pumping action associated with the tubal closing process and mucociliary
activity.
• Reflux of nasopharyngeal secretions into the middle ear is prevented by the
closed position of the resting pharyngeal eustachian tube and by the trapped
volume of gas in the middle ear and mastoid bone which creates a “gas
cushion”

EUSTACHIAN TUBE DYSFUNCTION
• Eustachian tube dysfunction is defined as inadequate dilatory function causing
secondary ear pathology.
• Failure to dilate for an extended period of time can lead to pathologically
severe negative pressure and result in tympanic membrane retraction,
atelectasis and otitis media with effusion.
• It may result from anatomical obstruction or physiologic failure(dynamic
dysfunction) which may be due to various causes, broadly classified as
1. Hereditary factors
2. Mucosal inflammation with functional obstruction or failure of dilation.
3. Muscular problems causing dilatory dynamic dysfunction.
4. True anatomical obstruction due to neoplasms or other mass lesions.

BAROTRAUMA:
• Under nonphysiologic pressure changes, such as ascent or descent in an airplane,
hyperbaric oxygen treatment, or diving in water, the function of the eustachian tube
is stressed.
• During descent, if the tube is not frequently opened, it may “lock” from increasing
negative pressure in the middle ear. This can induce barotrauma with resulting
middle ear effusion, with the possibility of hemorrhage (hemotympanum), tympanic
membrane rupture, and perilymph fistula.
• Delayed barotrauma may occur in a diver who descends using pure oxygen because
this would be principally concentrated in the middle ear.
• On ascent, the oxygen diffuses into the circulation more rapidly than it can be
replaced by inhaled nitrogen, setting up a middle ear gas deficit and negative
pressure.

• In adults with eustachian tube dysfunction, the most common
pathologic finding is mucosal and submucosal edema of the lateral
wall resulting in inadequate lateral excursion and decreased ability to
dilate the tube.
• Other observed pathologies include:
1. inadequate or abnormal muscular movements and
2. disorganization or absence of the typical dilatory wave.
Among muscular weakness, reduced TVP muscle action with decreased
excursion of anterolateral wall is most commonly observed.

INCREASED SUSCEPTIBILITY IN INFANTS:
• Anatomic changes relevant to pressure equalization and middle ear
protection occur with aging and likely account for a difference in
susceptibility to otitis media.
• The ability to equilibrate negative middle ear pressure is less efficient in
children. The shorter length of the tube, its more horizontal orientation, and
relative compliance of the cartilaginous portion allow it to be forced open by
nasopharyngeal pressure.
• The shallower alignment of the tube counteracts gravitational forces and
theoretically makes mucociliary clearance less efficient.
• An infant feeding in the supine position is susceptible to nasopharyngeal
pooling and retrograde flow

• Other important influences on tubal function and susceptibility to otitis
media have been identified:
• adenoidal hypertrophy,
• allergy,
• sinonasal disease,
• craniofacial anomalies such as cleft palate and Down syndrome,
• neoplasm
• extraesophageal reflux, and
• genetic predisposition.

1. DUE TO ADENOID HYPERTROPHY:
• Hypertrophic adenoids may extrinsically compress the
nasopharyngeal orifice of the tube, and may act as a bacterial
reservoir in cases of chronic infection.
• Patients with a large adenoid pad and shallow nasopharynx are
predisposed to middle ear effusion and negative middle ear pressure.
• Adenoidectomy has been shown to improve manometric measures
of eustachian tube function and diminish the need for myringotomies
in children.

2. DUE TO ALLERGY
Four mechanisms involved in tubal dysfunction due to allergy:
(1) targeting of middle ear mucosa in an allergic reaction,
(2) eustachian tube obstruction by mucosal edema,
(3) inflammatory obstruction of the nose and nasopharynx, and
(4) insufflation or reflux of allergic nasopharyngeal secretions into the
middle ear.

IN CLEFT PALATE:
• In a patient with cleft palate, persistence of eustachian tube dysfunction and
susceptibility to otitis media are related to anomalies in the course and
insertion of the TVP and the shape and development of the cartilaginous
tube.
• Anomalies include a poorly developed lateral lamina that does not describe
the typical “S” shape with the lateral tubal wall and an abnormal attachment
of the TVP to this lamina.
• patients with cleft palate, 96% have middle ear disease, and nearly 50%
require more than one set of myringotomy tubes

4. NEOPLASM:
• In patients with neoplasms of the nasopharynx, eustachian tube
function can be disturbed by occlusion of the nasopharyngeal orifice
of the tube and, more commonly, by direct invasion of malignant cells
into the paratubal muscles causing functional obstruction

Assessing Function of the Eustachian Tube:
• tubal function tests are of two types:
1. tests that measure passage of air through the tube, and
2. tests that measure active muscular opening of the tube.
Tympanometry is an adjunct measure that determines the flow of acoustic
energy through the middle ear system (immitance testing) and indirectly
measures eustachian tube function by determining the relative middle ear
pressure.

Assessing Function of the Eustachian Tube
• Tests that measure airflow through the tube include:
Inflation and Deflation tests.
The Politzer test involves placement of a rubber reservoir with a nasal tip into
the nostril while occluding the contralateral nostril.
When the patient swallows or phonates, with elevation of the palate, air is
forced into the nasal cavity.
In the Valsalva test, the patient pinches the nose and attempts to exhale with a
closed mouth forcing air into the tube.
The Toynbee test is performed similarly, but involves a swallow
while the nose is occluded.

Assessing Function of the Eustachian Tube
• The forced opening test may be performed in a patient with a
perforated tympanic membrane and involves placement of positive
pressure in the external canal.
• The pressure is recorded continuously, and the pressure is increased
until a sudden decrease occurs when the tube opens (“opening
pressure”). In healthy ears, a slight positive pressure remains (“closing
pressure”).
• This test may also be performed with the patient swallowing (forced
response test) with the resistance to airflow through the tube measured
during the resting condition (passive resistance) and at the moment of
swallowing (active resistance).

EUSTACHIAN TUBE ENDOSCOPY
• Topical spray anaesthetic and decongestant, lidocaine 4% mixed with equal
parts of phenylephrineHCl 0.5% solution is applied to both nasal cavities.
• The endoscopes that are used are usually either a 4-mm-diameter steerable
flexible fiberoptic nasopharyngoscope EMF-P3 (Olympus, Tokyo, Japan) or a
4-mmdiameter, 30-degree view angle, Hopkins Rod rigid sinus surgery
endoscope.
• The endoscopes are used with a charge-coupled device (CCD) camera in
place, and images are viewed on a video monitor

• Endoscopes are introduced into the nasal cavity and advanced up to
the nasopharyngeal orifice of the eustachian tube, just posterior to the
inferior turbinate and identified by the torus tubaris.
• The 30-degree rigid endoscope is introduced with the view angle
looking directly laterally and passed along the nasal floor, following the
inferior turbinate until reaching the nasopharyngeal orifice and
eustachian tube.
• Once at the orifice, the endoscope is rotated slightly to look superiorly
toward the long axis of the eustachian tube.

• The patient is asked to vocalize “K-K-K” repeatedly to isolate the action of
the levator veli palatine (LVP) from the tensor veli palatini (TVP).
• The “Ks” stimulate palatal elevation and posteromedial rotation of the
medial cartilaginous lamina and posteromedial wall of the eustachian tube.
• Swallows are done to induce normal physiologic tubal dilations, and forced
yawns are performed to cause maximal sustained dilation.
• The procedure is repeated from the contralateral eustachian tube orifice.
• Lastly, a fiberoptic endoscope is passed through the nasal cavity into the
hypopharynx to inspect the larynx for any evidence of laryngopharyngeal
reflux (LPR) of gastric contents

• Normal dilation and opening were observed to have four consistent
sequential phases during a normal swallow:
1. The soft palate elevates with simultaneous medial rotation of the
posteromedial wall. The lateral pharyngeal wall also medializes,
causing transient constriction of the nasopharyngeal orifice despite
the medial rotation of the eustachian tube medial wall.
2. The palate remains elevated, and the posteromedial wall remains
medially rotated as the lateral pharyngeal wall displaces laterally to
begin the dilation of the nasopharyngeal orifice.

3. The TVP begins to contract, causing dilation of the lumen to propagate
from the nasopharyngeal orifice toward the bony isthmus. The dilation
occurs by displacement of the anterolateral tubal wall laterally and away
from the already contracted and medially rotated posteromedial wall.
Tubal opening occurs as the functional valve of the cartilaginous tube
dilates into a roughly rounded aperture.
4. Closure of the tube begins with closure of the valve area and
propagates proximally toward the nasopharyngeal orifice. This distal to
proximal closure has been hypothesized to have a pumping action that
may protect against reflux.

DIFFERENTIAL DIAGNOSIS FOR CHRONIC
EUSTACHIAN TUBE DYSFUNCTION.
• ALLERGIC DISEASE
• LARYNGO-PHARYNGEAL REFLUX
• HYPERTROPHIED ADENOID CONTACTING POSTERIOR CUSHIONS
• CHRONIC SINUSITIS
• PNEUMONIA OR CHRONIC PULMONARY DISEASE
• PRIMARY MUCOSAL DISEASE:
1. Immune deficiency/suppression
2. Samter’s triad(asthma, aspirin sensitivity, nasal polyps)
3. Wegener’s or other granulomatous disease.
• NEOPLASMS

MANAGEMENT OF ETD
MEDICAL TREATMENT:
• Tubal dysfunction is predominantly due to mucosal inflammation and
can be managed in most cases with medical treatment.
• The identification of underlying etiology is critical for success of
treatment.
• LPR should be treated with dietary management, daily or twice daily PPI
and H2blockers at bedtime.
• In cases of allergy, avoidance of allergens, oral 2nd generation
antihistamines, leukotriene inhibitors, nasal antihistamines or mast cell
stabilisers, nasal steroid sprays and immunotherapy should be
considered.

MANAGEMENT OF ETD
• Functional obstruction due to hypertrophied adenoid tissue contacting
the posterior cushion can be excised/curetted.
• Recurrent infections due to nasal or sinus disease must be treated with
appropriate antibiotics; immunodeficency or primary mucosal disorders
must be treated with accordingly.
• Chronic fullness in ear associated with a normal appearing tympanic
membrane, absence of any retraction or effusion and a normal
tympanogram should be evaluated for Minor’s syndrome (semicircular
canal dehiscence), TMJ disorder, and endolymphatic hydrops.

MANAGEMENT OF TUBAL DYSFUNCTION
Surgical management:
• Persistent tubal dysfunction with OME or atelectasis can be successfully
managed in most cases with tympanostomy tubes.
• In patients with recurring effusion and atelectasis, Eustachian
tuboplasty has been used to ablate mucosa and submucosa from within
the tubal lumen on the posterolateral wall to widen the lumen and
facilitate the dilatory process.
• Healing occurs with fibrosis and mucosa along the posterior cushion
and posterior wall is thinner and with reduced inflammation.

INDICATIONS FOR SURGERY:
• Patients who have had maximal medical therapy for their underlying
pathology, yet have irreversible mucosal disease and persistent
atelectasis, difficulty with airplane flights, or intermittent/persistent
OME despite tympanostomy tubes are candidates for surgery

CONTRAINDICATIONS:
• Primary middle ear disease, not secondary to tubal dysfunction
• Patients undergoing radiation therapy for nasopharyngeal carcinoma.
• Extensive nasal or nasopharyngeal mucosal disease due to an
underlying, uncontrolled inflammatory process.

EUSTACHIAN TUBOPLASTY
• Eustachian tuboplasty is a nasal or transoral endoscopic outpatient
procedure requiring general anesthesia.
• A laser or microdebrider is used to strip away hypertrophic mucosa
and cartilage on the posterior eustachian tube cushion and into an
area called the valve to clear obstruction.
• Patients who undergo eustachian tuboplasty generally experience
very few significant complications postoperatively.

PREOPERATIVE MANAGEMENT:
• Patients are treated with 6 weeks of nasal steroids to treat nasal allergies
that may be contributing to chronic disease and the swelling of the
eustachian tube mucosa.
• Controlling the underlying cause of inflammation helps to increase the
success rate of Eustachian tuboplasty for chronic eustachian tube
dysfunction.
• HRCT of temporal bones and nasopharynx is done to rule out
concomitant disorders of the ear, sinuses, or nasopharynx.
• Preoperative video endoscopy should be routinely done and reviewed
prior to surgery.

PROCEDURE:
• Patient is kept in supine position and maintained under general
anaesthesia with endotracheal intubation.
• A myringotomy with or without temporary tube insertion may be
done to aspirate effusion.
• Patient is draped for nasal endoscopic surgery.
• Nasal decongestion is applied to both nasal cavities.
• A tonsil mouth gag is placed and the mouth is opened moderately

PROCEDURE:
• The Eustachian tube is viewed with a 30-degree, 4mm nasal endoscope,
using a CCD camera attached to the endoscope lens.
• Local infiltration with lidocaine 1% solution with 1:100,00 epinephrine is
done in the nasopharyngeal orifice of the Eustachian tube with a curved
endosinus needle passed through the oral cavity.
• The Eustachian tube orifice may be dilated with a 2mm wide sliver of
Merocel soaked in epinephrine solution and delivered into the tubal
lumen; removed after 5 minutes.
• Mucosal ablation may be carried out using Laser or Microdebrider.

PROCEDURE:
Laser Tuboplasty
• A fiber-delivered diode pumped KTP laser with handpiece manually bent
into a 60-degree arc, is passed through the mouth to perform the tissue
ablation.
• Laser cauterization begins on the mucosa overlying the medial
cartilaginous lamina within the posterior cushion.
• All mucosa and submucosa is ablated down to the exposed cartilage
making a triangular defect that extends along the cartilage proximally up
to the valve.
• No more than 40% of the circumference of the lumen is ablated.

PROCEDURE:
• special care is taken to steer clear of injury to the mucosa on the
anterior cushion to avoid postoperative scarring and stenosis of the
eustachian tube orifice.
• The medial cartilaginous lamina is the most important landmark
which not only leads the surgeon up to the valve but also serve to
protect the internal carotid artery. Therefore care must be taken not
to puncture through the cartilage.
• Cauterisation for haemostasis maybe required occasionally.

Fig.: Preoperative transnasal endoscope
view of right eustachian tube orifice
before eustachian tuboplasty. The valve
mucosa is thickened, especially on the
anterolateral wall adjacent to the
posterior cushion (torus tubaris).Fig.
2. Initial debulking for mucosa and
submucosa is done on the anterolateral
wall with cautery and a KTP laser.Fig.
3. Submucosal debulking is done higher
inside the valve, sparing the mucosa to
avoid cicatrix formation.Fig. 4. Completed
eustachian tuboplasty.

PROCEDURE:
• A pledget of merocel soaked in prednisolone drops is applied to the
surgical defect at the end of the procedure.
• Patient can be discharged home on the same day of surgery and are
restricted to light activities for ten days.
• Saline sprays must be advised at least 3 times a day for 2 weeks.
• Patients with allergic disease must continue nasal steroid sprays for 6
weeks
• Antihistamines are continued.
• Follow up examinations are done after 1, 6, 12, 24 and 36 months.

COMPLICATIONS:
• peritubal adhesions
• intranasal synechia.
• Puncturing of the medial cartilaginous lamina could cause carotid
injury resulting in life-threatening bleeding and brain complications.

BALLOON TUBOPLASTY
• Eustachian tuboplasty by balloon dilation involves the cannulation of
the cartilaginous portion of the ET via the nasopharynx with a balloon
catheter. This catheter is inflated to multiple atmospheres of pressure
(typically 10–12 bar) for a short amount of time and then removed.
• Balloon is intended to dilate the valve region in the distal portion of
ET.
• Balloon should never be advanced through bony isthmus, which is in
close proximity to the carotid artery.

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