Key points

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Introduction

The Eustachian tube (ET) is a dynamic structure that has long plagued both physicians and patients alike. It has traditionally been classified as a part of the auditory system, in part, due to its importance in regulating middle ear pressures but also because manifestations of ET dysfunction (ETD) tend to be otologic in nature. Recent investigations have found that a large majority of ET derangements occur in the nasopharyngeal portion of ET and are more rhinologic in nature. This unique dichotomy has led to speculation and confusion regarding the function and physiology of the ET since was first mentioned by Aristotle in the fourth century BC. It was not until the advent of fiberoptic endoscopy in the late twentieth century that the dynamic nature of the ET was first postulated. It is now clear that the ET functions to regulate middle ear pressure with respect to atmosphere pressure, facilitate clearance of middle ear secretions, and protect the middle ear from sound and accumulation of nasopharyngeal secretions. Although the function and nature of the ET has remained elusive until recently, the anatomy of the ET is much more concrete. The composition of the tube itself was first described by Bartolomeus Eustachius in 1562, and muscular attachments were further defined by Antonio Valsalva in 1704. The adult ET has a reported length of 31 mm to 38 mm, of which approximately the medial two-thirds is lined with fibrocartilage and the lateral osseous one-third is within the temporal bone. Three-dimensional modeling has demonstrated an hourglass–like central constriction, referred to as the isthmus, near the junction of these segments. The cartilaginous portion is obliquely angled approximately 45°, and is composed of anterior and posterior laminae. The anterior lamina provides an insertion for the tensor veli palatine muscle approximately 12 to 20 mm deep to the pharyngeal orifice, resulting in a dynamic valvelike region. The constriction of the tensor veli palatine initiates a coordinated sequence in concert with the other peritubal muscles, which leads to the valvelike opening and closing of the ET. This process occurs in 4 distinct phases lasting less than half a second. The abnormal closure of this valve is believed to be the underlying factor in ETD.

Despite a definitive anatomic description of the ET, its elusive nature combined with its remote location in the nasopharynx, has resulted in a lack of objective diagnostic tools and therapeutic treatments. Recent advances in both endoscopic techniques and diagnostic tools have brought a renewed interest restoring the function of ET via therapeutic interventions. The past 2 decades have seen a renewed interest in the surgical management of the ET disorders fueled by the adaptation of modern rhinologic techniques related to traditional ET procedures. As the understanding of both the dynamic and anatomic nature of the ET has increased, so have the options for management. The current surgical treatments available for dilatory dysfunction have expanded from the traditional adenoidectomy and myringotomy with tube placement to include laser and microdebrider Eustachian tuboplasty, as well as balloon dilation of the ET. The surgical corrections for patulous dysfunction have evolved to include, injection of calcium hydroxyapatite, shim placement, and soft tissue augmentation. The purpose of this article is to give an updated review for the evaluation and diagnosis of a dysfunctional ET, as well as describe the current surgical interventions available for the treatment ETD.

Introduction

The Eustachian tube (ET) is a dynamic structure that has long plagued both physicians and patients alike. It has traditionally been classified as a part of the auditory system, in part, due to its importance in regulating middle ear pressures but also because manifestations of ET dysfunction (ETD) tend to be otologic in nature. Recent investigations have found that a large majority of ET derangements occur in the nasopharyngeal portion of ET and are more rhinologic in nature. This unique dichotomy has led to speculation and confusion regarding the function and physiology of the ET since was first mentioned by Aristotle in the fourth century BC. It was not until the advent of fiberoptic endoscopy in the late twentieth century that the dynamic nature of the ET was first postulated. It is now clear that the ET functions to regulate middle ear pressure with respect to atmosphere pressure, facilitate clearance of middle ear secretions, and protect the middle ear from sound and accumulation of nasopharyngeal secretions. Although the function and nature of the ET has remained elusive until recently, the anatomy of the ET is much more concrete. The composition of the tube itself was first described by Bartolomeus Eustachius in 1562, and muscular attachments were further defined by Antonio Valsalva in 1704. The adult ET has a reported length of 31 mm to 38 mm, of which approximately the medial two-thirds is lined with fibrocartilage and the lateral osseous one-third is within the temporal bone. Three-dimensional modeling has demonstrated an hourglass–like central constriction, referred to as the isthmus, near the junction of these segments. The cartilaginous portion is obliquely angled approximately 45°, and is composed of anterior and posterior laminae. The anterior lamina provides an insertion for the tensor veli palatine muscle approximately 12 to 20 mm deep to the pharyngeal orifice, resulting in a dynamic valvelike region. The constriction of the tensor veli palatine initiates a coordinated sequence in concert with the other peritubal muscles, which leads to the valvelike opening and closing of the ET. This process occurs in 4 distinct phases lasting less than half a second. The abnormal closure of this valve is believed to be the underlying factor in ETD.

Despite a definitive anatomic description of the ET, its elusive nature combined with its remote location in the nasopharynx, has resulted in a lack of objective diagnostic tools and therapeutic treatments. Recent advances in both endoscopic techniques and diagnostic tools have brought a renewed interest restoring the function of ET via therapeutic interventions. The past 2 decades have seen a renewed interest in the surgical management of the ET disorders fueled by the adaptation of modern rhinologic techniques related to traditional ET procedures. As the understanding of both the dynamic and anatomic nature of the ET has increased, so have the options for management. The current surgical treatments available for dilatory dysfunction have expanded from the traditional adenoidectomy and myringotomy with tube placement to include laser and microdebrider Eustachian tuboplasty, as well as balloon dilation of the ET. The surgical corrections for patulous dysfunction have evolved to include, injection of calcium hydroxyapatite, shim placement, and soft tissue augmentation. The purpose of this article is to give an updated review for the evaluation and diagnosis of a dysfunctional ET, as well as describe the current surgical interventions available for the treatment ETD.

Content/Discussion

ETD is defined by symptoms and signs of pressure dysregulation in the middle ear, and until recently there were many varied definitions of what this meant clinically. A recent consensus statement has clarified and standardized the definition. It divides ETD into 3 subtypes: baro-challenge-induced, dilatory, and patulous dysfunction. Dilatory dysfunction can be further broken down as follows: functional obstruction, dynamic dysfunction (muscular failure), and anatomic obstruction Baro-challenge dysfunction is elicited or exacerbated by changes in altitude or barometric pressure. Dilatory dysfunction of the ET is characterized as aural fullness that is usually associated with some degree of hearing loss or tinnitus. When it becomes more severe, otalgia followed by otitis media and the complications of otitis, such as atelectasis, retraction pockets, or even cholesteatoma. Dilatory dysfunction has been estimated to affect up to 30% to 80% of children at some point during their childhood. Despite the maturation of the ET, and the aggressive medical and surgical management of underlying pathologies, ETD continues to plague approximately 1% of the population throughout their adult lives. In 1997, Kujawaski ushered in the modern era of surgical treatment of the ET by describing the first tuboplasty. He approached the ET both transoral as well as transnasal to obliterate both mucosa and cartilage from the posterior cushion using a laser. Ten years later, Metson described a rhinologic-based version of this procedure that used a microdebrider through an exclusively transnasal approach. In 2010, Ockerman published his study exploring the value in using sinus balloons as a potential surgical intervention for the treatment of ETD.

As more physicians contemplate the surgical correction of dilatory and baro-challenge dysfunction, it is important to have a good understanding of patulous dysfunction, as it can result from overcorrection of dilatory dysfunction as well as mimic dilatory dysfunction to the less-experienced clinician. Patients with patulous dysfunction also present with aural fullness and potentially otalgia, but they most often relate a history of autophony, both to voice and to respiratory sounds. Patients with patulous ET may state that their symptoms are better in the supine position, during upper respiratory tract infections, and worse with exercise, public speaking, singing, or caffeine ingestion. Myringotomy and tympanostomy tube placement can alleviate aural fullness and tympanic membrane excursions, but is often ineffective for autophony. A recent systemic review of the published literature by Hussein and colleagues described several transnasal surgical options now being used, including shim placement, augmentation with injectable filler, or autologous tissue.

The treatment of ETD is further confounded by its multifactorial pathophysiology. One study, looking at the possible causes of dilatory dysfunction, found that mucosal edema involving the ET orifice was present in 83% of patients and 74% of patients were noted to have decreased anterolateral wall motion that was attributed to inflammation. Poe reports the most common cause of dilatory dysfunction is mucosal inflammation within the cartilaginous ET, most often secondary to allergic rhinitis, chronic rhinosinusitis, laryngopharyngeal reflux, and smoke exposure. It has also been observed in patients with systemic mucosal disorders, such as granulomatous disease, cystic fibrosis, Sampter triad, and Kartagener syndrome. Patulous dysfunction on the other hand has most often been associated with recent and significant weight loss; however, more recent studies have shown rheumatologic, or other chronic disease conditions, stress, and oral contraceptives to be more likely causes. Identifying and treating these underlying pathologies before invasive therapies will both improve outcomes and avoid unnecessary interventions.

Anatomic abnormalities can also play a role in ET disorders, especially when it is found to be unilateral. For instance, residual adenoid tissue or significant scarring after adenoidectomy has been associated with limitation of tubal opening, and cartilaginous abnormalities of the posteromedial wall have been found to cause obstruction leading to dilatory dysfunction. It is important to mention that if the obstruction is isolated to the inferior portion of the ET it can prop open the superior portion of the tube causing patulous dysfunction. Nasal anatomy may also indirectly contribute to ETD. A study by McNicoll showed in a prospective controlled trial that septoplasty corrected 94% ETD in submariners with septal deviation. These findings indicate nasal airflow may play a significant role in disorders of the ET.

It is the experience of the authors that successful treatment and management of ET disorders is directly related to the accuracy in identifying the pathogenesis related to both the patient’s symptoms and the causative factors. This requires a detailed past medical history and physical examination in conjunction with several validated symptom scores and function tests. Obtaining the past medical history needs to be targeted at identifying both underlying causative factors, the timing of symptoms related to certain potential triggers, such as changes in barometric pressure and altitude, as well as the worsening of sinonasal congestion and gastroesophageal reflux disease. The physical examination begins with bilateral otomicroscopy. Patients with active dilatory dysfunction often exhibit tympanic membrane retraction or effusion, but it is important to remember that although retraction pockets in the posterior superior quadrant or attic may have originated from ETD, they may persist or progress because of unrelated inflammatory mechanisms. Nonfixed retraction or atelectasis, or middle ear effusions indicate active dilatory dysfunction, whereas medial and lateral excursions of the tympanic membrane with ipsilateral nasal breathing indicate active patulous dysfunction. If the patient is suspected of having patulous dysfunction by history, having the patient exercise for several minutes before otoscopy may provoke symptoms, if not present initially.

Endoscopic examination of the upper respiratory tract and ET should be performed to evaluate for evidence of inflammatory or granulomatous disease. To optimize the view of the ET orifice during opening and closing, the endoscope should be brought to the tubal orifice and directed 45° laterally and superiorly to the nasal floor. This can be accomplished by rotating a fiberoptic endoscope into position either from the ipsilateral or contralateral nasal cavity. The ET orifice is located just posterior to the inferior turbinate. The torus tubarius or “posterior cushion” contains the mobile medial cartilaginous lamina marking the anterior aspect of the ET. The most common findings seen in dilatory dysfunction include mucosal inflammation, hypertrophy, excessive mucus, hyperemia, and cobble-stoning, although patients with patulous dysfunction often exhibit a concave defect in the anterolateral wall leading to insufficient closure of the lumen as opposed to the normal convex bulge.

As clinicians are beginning to understand the pathophysiology behind ET disorders, there have been many studies looking at both the efficacy and safety of surgical procedures aimed at treating the ET. Several meta-analyses have concluded that although surgical management of the ET has been shown to be relatively safe and patients report significant benefit, there is not enough objective evidence to determine the actual effectiveness and indications of these procedures. This has been attributed, in part, to the lack of validated diagnostic tools and applicable function tests. A large number of tests related to ET function have been created, but unfortunately the clinical relevance of these tests has remained unclear. Compounding this, little to no recognized standards exist regarding evaluation protocols, thus making the current data that have been generated difficult to compare. In 2012, McCoul and colleagues attempted to address this deficiency with the introduction of the eustachian tube dysfunction questionnaire (ETDQ-7), a validated Quality-of-Life Questionnaire, which has been shown to statistically correlate with clinical and objective improvement. It is important to note that although the ETDQ-7 is sensitive and specific in identifying patients with a dysfunctional ET, it is ineffective in differentiating between patulous and dilatory dysfunction. In 2013, Doyle and colleagues performed a randomized controlled trial that identified 4 ET function test parameters (Valsalva, ET opening pressure, dilatory efficiency, and percentage of positive pressure equilibrated) that when looked at together correctly identified patients with ETD with a sensitivity of 95% and a specificity of 83%. Interestingly, the tests evaluating the opening efficiency of the ET where statistically relevant; however, tests evaluating structural properties were not. Impedance tympanometry is the most objective and sensitive test to evaluate patients with patulous dysfunction, as it shows fluctuations in tympanic membrane compliance with ipsilateral nasal breathing while the patient is symptomatic. It is important to note that although this test is essential to differentiate between dilatory and patulous dysfunction especially with a positive ETDQ-7, it cannot be used in patients with a pressure equalization tube or tympanic membrane perforation. Together these tests are beginning to provide researchers and clinicians with objective and validated metrics that can help evaluate the effectiveness of specific treatments of ETD, and there are now several ongoing prospective randomized trials using these tools to better understand the role specific treatments play in management of ETD.

One of the reasons clinically relevant diagnostic tests have not evolved earlier is due to the paucity of proven treatment options. In fact, current medical management of dilatory ETD is directed at treating the underlying pathology, as there is no Food and Drug Administration–approved therapy indicated for ETD. A placebo-controlled randomized double-blinded trial evaluated intranasal Triamcinolone spray over 6 weeks in patients with otitis media with effusion or negative middle ear pressure failed to show any statistical difference. Medical therapies have been slightly more successful in patients with patulous dysfunction, and they are aimed at thickening peritubal mucosa, reestablishing a competent valve. Medications that stimulate mucus production or tissue inflammation, such as a saturated solution of potassium iodine drops mixed with water or juice taken 3 times, have been used with varied results. Hydrochloric acid–based topical nasal drops, boric acid, silver nitrate, salicylic acid powder, and phenol are all irritants that been used to create mucosal inflammation and increase mucus production. Hormones such as Premarin and Depo-Estradiol estrogens may be used to cause mucosal hypertrophy and provide relief of symptoms for undetermined durations. Although weight loss has been thought to lead to patulous dysfunction, weight gain as treatment for aural symptoms is generally discouraged. When medical management is insufficient to control symptoms secondary to either dilatory or patulous dysfunction, and causes a significant decrease in quality of life, surgical intervention should be considered.

In most cases it is important to obtain a computed tomography (CT) scan before committing to a surgical intervention. The images are helpful for defining the length and diameter of the ET as well as evaluating for internal carotid artery (ICA) dehiscence. However, in a retrospective review, Schoder demonstrated that preoperative high-resolution CT scan of the temporal bone does not seem to be suitable to predict intraoperative or postoperative difficulties of balloon dilation of the ET. Nevertheless, for inexperienced surgeons, or to further investigate unclear pathology such as superior canal dehiscence, CT scans of the temporal bone may beneficial in understanding the relation between ICA and the ET as well as identifying potential obstructing pathology, such as cartilaginous anomalies, or tumors.

Modern endoscopic Eustachian tuboplasty was first introduced less than 20 years ago and remains a satisfactory surgical option to treat pathologies located in the proximal portions of the nasopharyngeal ET orifice and can be efficiently combined with adenoidectomy or sinus surgery. The goal of this procedure is to remove inflamed soft tissue from the luminal side of the posterior cushion and postero-medial wall. This surgical debulking removes inflamed and hypertrophied mucosa facilitating regrowth of healthy tissue, which is thought to both widen the lumen and permit more efficient dilatory action of the tensor veli palatini muscle. Several studies have looked at this procedure with success rates ranging from 36% to 92%. Tissue removal can be accomplished with either a laser or microdebrider and begins at the nasopharyngeal edge of the posterior cushion and extends up to the valve region. Within the valve region, resection of submucosal soft tissue is performed as necessary, but the mucosa is spared to prevent synechiae formation. An unusually prominent bulge of cartilage into the lumen can also be resected if necessary. It is important always to be oriented to the location of both the anterolateral wall and ICA and avoid damaging either structure.

Although there is still a place for traditional tuboplasty, endoscopic balloon dilation of the cartilaginous ET has emerged over the past 5 years as the treatment of choice due to its high reported success rates ranging from 64% to 97%, and low risk profile and incidence complications of approximately 3%. A significant advantage of balloon dilation is that it targets dilatory dysfunction at both the mucosal and muscular levels. Ilkka demonstrated histologic evidence that the balloon causes both shear and crush injury the epithelium, but spares the basal layer allowing for rapid healing. The balloon also crushes lymphocytes and lymphoid follicles within the submucosa leading to the formation of a fibrous scar. This combination significantly reduces the overall inflammatory burden and may provide lasting clinical improvement in both ET dilation and ventilation. Muscle “tightness” or shortening has been shown to be due to an increase in tension and significantly limits range of motion. This increase in tension has been shown to be secondary to postural adaptation and/or scarring secondary to inflammatory process. The diameter of the ET ranges from 0.6 to 3.0 mm at the isthmus and 20.0 to 30.0 mm at the nasopharyngeal orifice. A fully dilated balloon usually has a diameter of 6 mm, causing significant stretch on peritubal musculature. The effect of this can be evaluated at looking at Hoffman reflexes (H-reflex) on electromyography. The H-reflex is a measurement of the muscle’s level of excitability, and lower H-reflexes are associated with decreased excitability. Interestingly, H-reflexes have been found to be depressed with a precontraction stretch and the resultant decreased excitability of the muscle may allow the muscle to relax despite increased stimuli. This leads to a refractory period after contraction known as “autogenic inhibition,” where muscle relaxes due to neuro-reflexive mechanisms, thus increasing muscle length. Both of the proposed mechanisms of action of balloon dilation have been shown to take place primarily in the cartilaginous portion of the ET. This is important to note because not only do attempts to dilate the bony portion of the ET risk the ICA, which runs in close proximity to the osseous ET, but also limits the effectiveness of the balloon by restricting expansion and pressure on the cartilaginous ET. Multiple recent studies demonstrate that balloon dilation of the cartilaginous ET lumen is feasible, safe, and provides therapeutic benefit. Reported complications of balloon dilation of the ET include minor tears of the mucosal lumen, epistaxis, exacerbation of tinnitus, and subcutaneous emphysema, all of which resolved spontaneously. Transnasal dilation of the cartilaginous ET is carried out using a 30 or 45° endoscope. Traditionally an angled guide catheter is used to introduce the 6 × 16-mm sinuplasty balloon into the nasopharyngeal orifice of the ET. It is useful to gently retract the posterior cushion medially to allow a view of the ET valve, providing guidance while advancing the balloon superiorly. The balloon catheter should be advanced until the 31-mm yellow mark is even with the medial edge of the anterior cushion or the catheter encounters resistance at the bony-cartilaginous isthmus. Inflation of the balloon has been described from either 10 or 12 atm for various time intervals; however, sustaining the dilation at 12 atm for 2 minutes is becoming the standard practice. Transnasal endoscopic ET dilation as performed by the authors is demonstrated in [CR] . There are several reports that deinflation followed by reinflation for 1 minute may be useful if there is a significant burden of disease. Extreme caution should be used when performing balloon dilation on patients who appear to have dehiscence of the carotid canal due to the possible although unlikely risk of inserting the balloon into the bony canal.

In patients with patulous ET, myringotomy and tympanostomy tube placement has been shown to alleviate aural fullness and tympanic membrane excursions but is often ineffective for autophony. Shim placement is a minimally invasive surgical option that can effectively relieve patulous symptoms while preserving ET function in most cases. Patients being considered for shim placement should undergo a preoperative CT scan to ensure that the ICA canal is not dehiscent. We perform shim placement under general anesthesia by using a polypropylene stylet obtained from a disposable 10-French catheter cut to size: 36 to 38 mm in female and 38 to 40 mm for male individuals. The distal centimeter of the catheter is then tapered to the diameter of the isthmus seen on CT reconstructions, usually this is approximately 2 mm. The catheter is then placed transnasally under 45° endoscopic guidance. The shim is first inserted into the end of a 70° curved guide catheter and then advanced with the remaining stylet. The shim is then slowly and atraumatically advanced into the lumen. Retraction of the posterior cushion straightens out the curvature of the ET, allowing for a view deep into the lumen until meeting resistance as it passes through the isthmus, steady firm pressure should then be placed at the end of the shim until it is seated within the lumen of the bony isthmus. The catheter is considered in good position once the distal end is flush with the free margin of the posterior cushion, just inside the anterior cushion. Most catheters remain lodged within the isthmus for years without any perception of its presence by the patient. The shim functions by lying within the concave defect in the valve, filling it sufficiently to restore competency to valve closure, surprisingly this usually occurs without occluding the ET. In the event of premature catheter extrusion, reconstruction of the patulous ET should be considered. Calcium hydroxyapatite paste augmentation of the ET luminal wall was initially reported as a standalone procedure, and resulted in complete or significant improvement in voice autophony 69% of the time; however, due to migration of the paste within the loose tissue planes of the anterolateral wall as well as a mild degree of absorption, symptom relief may be only temporary, thus requiring multiple injections. Because of these limitations, this procedure most often been regulated as a secondary procedure to augment deficient areas after soft tissue augmentation. Soft tissue augmentation was initially described as an anterior lateral cartilage graft designed to reconstruct the deficient cartilaginous canal. It is now this author’s practice to make an incision along the anterior cushion and elevate the mucoperichondrium off the anterior wall of the ET, once the pocket is developed an autologous fat or fascial graft is placed followed by a tapered conchal cartilage graft in an attempt to both augment the anterior lateral wall as well as replicate the soft tissue consistency of a healthy ET. Transnasal endoscopic treatment of patulous ET as performed by the authors is shown in [CR] . If an element of patency to the ET remains, a vertical incision is then made in the posterior canal wall and the mucoperichondrium is elevated and a perichondrial graft is placed in the dissected space to augment the posterior wall and facilitate closure of the valve as demonstrated by the authors in [CR] . Due to the difficulty of placing effective sutures in this area, the remaining perichondrium is placed over the fat and cartilage in an underlay technique and covered with DuraSeal (Confluent Surgical Inc, Waltham, MA).