Surgical Management of Obstructive ET Dysfunction

Dennis S. Poe, MD, PhD, and Ralph B. Metson, MD

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Today, surgery on the Eustachian tube (ET) can be performed with safety and efficacy for the treatment of obstructive and patulous ET dysfunction (ETD). Until recently, the management of chronic otitis media with effusion or retraction of the tympanic membrane with negative middle ear pressure has been largely limited to the placement of tympanostomy tubes. However, there are adverse effects from tubes, and they do not correct pathology within the ET. Past attempts to widen the isthmus and bony portion of the ET all met with failure to produce lasting benefit, and complications included injuries to the middle and inner ear and scarring of the ET.¹ Deaths from injection of Teflon into the internal carotid artery during treatment for patulous ET resulted in the condemnation of surgery on the ET for decades.²

Research subsequently revealed the most common pathology seen in chronic obstructive ETD was inflammatory disease within the cartilaginous ET, leading to a change in the concept of ET function.^3-6 The cartilaginous portion of the ET works as a functional valve6 that must open periodically to aerate the middle ear as the middle ear gas exchange continually absorbs gases.^7,8 Failure of adequate opening results in obstructive ETD (OETD) with the consequence of excessively negative pressure within the middle ear that can lead to otitis media, fixed retraction pockets, and cholesteatoma. Failure of competent closure of the “valve” is the cause of patulous ETD (PETD) with autophony of voice and breath sounds. 

Procedures to remove a portion of diseased mucosa and submucosa from within the lumen of the cartilaginous ET using laser^1,9 or microdebrider¹⁰ have demonstrated moderate success in improving OETD. More recently, balloon dilation of the ET (BDET) has yielded higher success rates with more consistency than the previous methods.^11-13 A small human study showed that balloon dilation stripped off diseased surface epithelium, while leaving the basal layer intact, and crushed the submucosal inflammation and adenoid-like lymphoid follicles. Postoperative histology demonstrated restoration of healthy pseudocolumnar epithelium and replacement of inflammatory tissue with thin scar.¹⁴ Similar findings were obtained in a recent study using a rat model.¹⁵ The mechanism of effect of the balloon may be in reduction of inflammation and adenoid-like tissue, similar to having performed an adenoidectomy within the valve of the ET. 

Clinically significant improvement in measures of ET function following BDET has been consistently reported in approximately 70% to 80% of patients.^16-19  Outcomes have included tympanogram, otoscopic exam, ability to perform a Valsalva or modified Valsalva maneuver, various ET function scores, and a patient-reported outcomes symptom score, Eustachian Tube Dysfunction Questionnaire (ETDQ-7). Studies with mean follow-up of two or more years have all shown durability of success,^13,20-22 which may be due to the histological effects of the procedure. Long-term success with BDET is optimized by maintaining good control of underlying medical causes of inflammation within the ET and with careful patient selection. 

Differential Diagnosis 

The differential diagnosis of aural fullness is broad and includes OETD, PETD, temporomandibular disorder (TMD), inner ear conditions (including otic capsule dehiscence syndrome, endolymphatic hydrops, sensorineural hearing loss), and otologic migraine²³ (Figure 1). The lack of a unified test for ET function presents challenges to surgeons in identifying appropriate candidates for treatment. The hallmark of OETD is negative pressure in the ear that can be observed with pneumatic otoscopy and measured with tympanometry. Retraction of the tympanic membrane is characteristic, and there may be middle ear effusion. Fixed retraction pockets remain adherent and may progress to cholesteatoma due to upregulated inflammatory mediators,^24,25 even in the absence of OETD. Patients who have mild OETD such that they only experience difficulty aerating their ears when subjected to rapid changes in pressure, such as with flights or diving (barochallenge), may not exhibit negative pressure in the middle ear when examined, and their history is critical for the diagnosis. 

Figure 1. Differential diagnosis of aural fullness.

Click here for larger image.

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PETD is characterized by complaints of autophony of voice, breathing, and often of pulse. When active, excursions of the tympanic membrane may be seen on otoscopy or measured on a tympanogram (reflex decay mode) while patients perform ipsilateral nasal breathing (contralateral nostril and mouth closed, deep and mildly rapid breathing as if for auscultating the lungs). Patients who present with significant negative pressure, but are frequently sniffing, usually have PETD, but it may be easily misdiagnosed and underreported due to the clinical findings resembling OETD. PETD may be present with TM retraction, middle ear effusion, and even cholesteatoma.²⁶ All patients presenting with symptoms and signs that resemble OETD should be asked about autophony and sniffing as PETD is very common.^27,28 

Aural fullness with normal otoscopy and tympanograms and in the absence of evidence of negative middle ear pressure, barochallenge, or autophony have a condition other than obstructive or patulous ETD. TMD is very common and usually involves muscle tension or spasms in the muscles of mastication, but a subset may also have joint dysfunction (TMJ). Bimanual intra- and extra-oral examination of the masseter and pterygoid space muscles can reveal hypertrophy and tenderness when symptoms are active. Otologic migraine may be suspected if there is a history of potential migraine triggers and an absence of the above findings. Inner ear causes are less common, and they may be differentiated by their specific symptoms, signs, and findings. 

Clicking and popping sounds are generally associated with PETD and TMD rather than OETD.

When the cause of aural fullness is uncertain, a myringotomy or insertion of a tympanostomy tube will equalize middle ear pressure with ambient air and relieve symptoms due to OETD. When a myringotomy fails to help with symptoms of aural fullness, OETD can be ruled out as the cause.

Endoscopic Examination of the ET

A view deep into the lumen of the ET should be obtained with a view of both the cartilaginous and membranous walls during swallows (normal physiological opening of the valve) and yawns or vocalizing “Ahhhh” (sustained maximal dilatory effort). A dynamic examination of the valve can be obtained with a flexible endoscope (turned 90 degrees so that it can align with the lumen) or with rigid endoscopes (30- or 45-degree view angles are usually needed as zero degree often yields an inadequate view). An assessment is made of the degree of mucosal inflammation and ability to open the valve.

A grading system has been validated:²⁹

1. Normal (Figure 2a and b)
2. Mild: mild inflammation with no visible compromise of opening of the valve
3. Moderate: moderate inflammation with compromise of opening of the valve (Figure 3)
4. Severe: moderate to severe inflammation with inability to open the valve (Figure 4)

Figure 2. 45-degree transnasal endoscopic view of left normal Eustachian tube, inflammation/opening of valve scale Grade 1 (a) resting position and (b) open position.

Figure 3. 45-degree transnasal endoscopic view of left Eustachian tube with moderate inflammation/ compromise of opening of the valve, Grade 3 (a) resting position and (b) open position.

Figure 4. 45-degree transnasal endoscopic view of left Eustachian tube with moderate inflammation/anterior thrusting of the torus tubarius that prevents opening of the valve,
Grade 4 (a) resting position and (b) open position.

Patient Selection for BDET

There is no medical treatment that is indicated for nonspecific OETD,³⁰ but medical management may be appropriate if an underlying etiology can be identified, such as allergic rhinitis, rhinosinusitis, and laryngopharyngeal reflux. In the event that medical management is appropriate, but fails to resolve the symptoms, surgery can be considered. Tympanostomy tubes, microdebrider Eustachian tuboplasty,¹⁰ and BDET are surgical options that can be offered. 

BDET is indicated for chronic OETD (≥3 months duration),³¹ and ideally there should be pathology (usually inflammatory) within the cartilaginous ET seen on office endoscopy.

Patients may have either (a) active evidence of negative middle ear pressure—otitis media with effusion or retraction of the tympanic membrane that insufflates with negative pressure and type B or C tympanogram—or (b) flight or scuba barochallenge consistent history.

A common scenario is a patient who has had symptom relief with a tympanostomy tube but OETD persisted when the tube extruded. If a tube fails to improve symptoms, there is likely a diagnosis other than OETD.

Candidates for BDET generally are barochallenged, may have had otitis media, and are unable to perform a modified Valsalva maneuver (nose and mouth closed, gentle elevation of intranasal pressure with nose blow, simultaneous swallow). 

PETD symptoms have been reported after BDET. To minimize the risk, the duration of the balloon inflation (dilation time) may be reduced from the maximum of two minutes (e.g., 90, 60, or 30 seconds). Patients with chronic allergic rhinitis may be at increased risk.³² The dilation time should be adjusted to be commensurate with the severity of inflammatory pathology seen within the lumen of the ET. For example, mild inflammation (grade 2) may be adequately managed with just 60-90 seconds dilation time.  

Adjunctive procedures may be indicated such as tympanostomy tube, tympanoplasty, adenoidectomy (especially the lateral portion if interfering with movement of the torus tubarius on office endoscopy as in Figure 4), septoplasty, sinus surgery, turbinate reduction, and others if needed to optimize the management of the upper airway and reduce inflammation.

Avoidance of Intraoperative Complications

The lumen of the ET is best seen with a 30- or 45-degree-angled endoscope, although sometimes a zero-degree scope may provide an adequate view of both membranous and cartilaginous walls. The balloon catheter should be introduced tangential to the very thin membranous wall, which curves medially initially before turning toward the ear. The catheter should be inserted slowly and gently, never pushing against resistance. The catheter should be calibrated to avoid possible entry into the bony portion of the ET, which could risk injury to the internal carotid artery or to middle ear structures.^31,33

Postoperative Management

Patients are instructed to avoid nose-blow or Valsalva maneuvers for the first postoperative week to avoid the rare complications of subcutaneous emphysema and pneumomediastinum.³⁴ Humidification with saline products and humidifiers are optional. After one week, it is beneficial to perform a modified Valsalva maneuver at least four times daily until the patient perceives that the insufflation of the middle ear may be occurring spontaneously with swallows and yawns. It takes approximately four to six weeks for the swelling to subside from the balloon dilation.²¹ 

Ongoing management of underlying medical etiologies is important for long-term success. BDET may be thought of as performing an adenoidectomy within the lumen of the ET, and regrowth of adenoid tissue is known to occur with inflammatory conditions such as allergic rhinitis.

With proper patient selection, preoperative treatment of any underlying medical etiology, good surgical technique, balloon dilation time commensurate with degree of pathology, use of adjunctive procedures when indicated, and maintenance of medical control postoperatively, the procedure is expected to provide lasting benefit. 

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