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Eustachian tube dysfunction

FUNCTIONS OF EUSTACHIAN TUBE. Eustachian tube usually remains closed. It opens during swallowing, yawning and sneezing.  It plays a key role in middle ear function. It provides ventilation, protection and drainage of the middle ear. Eustachian tube dysfunction

  1. It acts as a ventilatory channel, regulates equilibrium between middle ear pressure and atmospheric pressure. 
  2. It protects middle ear against reflux of nasopharyngeal secretions, sound pressure and organisms from the pharynx.
  3. It drains (clearance of) middle ear secretions toward the nasopharynx by the mucociliary system.

Ventilation. Hearing is optimal when air pressure on both sides of the tympanic membrane is relatively the same. So any change in air pressure on either side will affect hearing. Normally eustachian tube remains passively closed. Intermittent and periodic active opening of the tube during such actions as swallowing, yawning, or sneezing, thereby regulates the equalization of the middle ear and atmospheric pressures. Due to anatomical differences, the tubal function is also not so good in infants and young children and thus leads to increased incidence of otitis media. Eustachian tube dysfunction Eustachian tube dysfunction Eustachian tube dysfunction Eustachian tube dysfunction

Effect of Posture and Seasonal Variation. Posture has been demonstrated to affect ET function; In supine position during sleep or lying down position, there is increased venous blood flow leading to venous engorgement of ET. This causes reduced tubal opening function. ET function is better in the summer than in the winter and spring.

Protective. ET system maintains a healthy middle ear. The Eustachian tube remains closed and does not allow entry of abnormal high sound pressures (e.g. forceful nose blowing), nasopharyngeal secretions due to reflux and noxious agents from the nasopharynx and thereby it protects the middle ear. This protective function is lost if the tube is small in length (as in young children), wider in diameter (patulous tube), or there is a perforation in the tympanic membrane.

Clearance. The mucous membrane of the middle ear is continuous with that of the nasopharynx via the tube and is characterized as respiratory epithelium (ciliated columnar cells). The cilia beat towards nasopharynx and facilitate the clearance of secretions and debris by its mucociliary action.

CAUSES OF EUSTACHIAN TUBE OBSTRUCTION

  • Upper respiratory infection (viral or bacterial)
  • Allergic rhinitis
  • Nasopharyngeal acid reflux
  • Deviated nasal septum/ Sinusitis/ Nasal polyps
  • Hypertrophic adenoids/ Nasopharyngeal tumour/mass 
  • Cleft palate/ Submucous cleft palate/ Down syndrome
  • Granulomatous diseases/ cystic fibrosis/ Samter’s triad/ Kartagener syndrome.

METHODS OF CLINICAL EXAMINATION OF EUSTACHIAN TUBE

In addition to the otoscopic examination, an examination of the nasopharynx and middle ear can tell us about the basic underlying pathology at both ends of the ET system. The examination can be done in the following ways.

  • Posterior rhinoscopy. Indirect mirror examination of the nasopharyngeal end of the ET system.
  • Otoscopic examination of the tympanic membrane, its position, colour, degree of translucency, and mobility.
  • Rigid nasal endoscope for the examination of the nasal cavity and nasopharyngeal end of the ET system
  • Flexible nasopharyngoscope. For examination of both ends of ET system.
  • Operating microscope or otoendoscope. For examination of the tympanic end of the ET system through the pre-existing perforation. The microscope may also reveal retraction pockets or fluid in the middle ear
  • Eustachian tube endoscopy or middle ear endoscopy can be done with very fine flexible endoscopes. 

EUSTACHIAN TUBE FUNCTION TESTS

Besides otoscopic examination using the pneumatic attachment to assess middle ear pressure, other tests that can assess the pressure regulation (ventilation) function of the ET system. The classic methods of Valsalva, Politzer, and Toynbee for assessing the ET are still in use today.

  1. Valsalva Test. It evaluates patency of the eustachian tube by assessing the effect of high positive nasopharyngeal pressure on the ET system. To create positive pressure in the nasopharynx, patient pinches his nose between the thumb and index finger, takes a deep breath, closes his mouth and expires air forcefully and tries to blow air into the middle ear through the eustachian tube. If the air enters into the middle ear, bulging of the tympanic membrane can be seen by otoscope or the microscope due to increased positive pressure in the middle ear, indicating normal tubal function. A hissing sound can be heard with the help of a stethoscope if there is tympanic membrane perforation. A crackling sound is produced if the discharge is also present in the middle ear. Unfortunately, Valsalva’s test results are not reliable as only 65% of persons can successfully perform this test. However, Valsalva can also be advised as a part of treatment when effusion or high negative pressure is present within the middle ear. This test should not be done if there is an atrophic tympanic membrane (as it is weak and thin) can rupture or patient is having URI where infection can be pushed into the middle ear causing otitis media.
  2. Politzer Test. The principle is this test is the same as Valsalva, which is to create positive air pressure in the nasopharynx and transmit it into the middle ear through the eustachian tube. Instead of using forceful expiration in this test, a Politzer’s bag is introduced into the patient’s nostril on one side and another nostril is closed, and the bag compressed while at the same time the patient swallows to close the velopharyngeal port (he can be given sips of water) or says the letter “K”. Significance of the test results is the same as with Valsalva’s test. This test is done in children who are unable to perform the Valsalva test. The test is also used therapeutically to ventilate the middle ear.
  3. Catheterization. In this test, we use a curved metallic eustachian tube catheter to insufflate air in the eustachian tube opening present on the lateral wall of the nasopharynx. 

How to reach the ET opening during catheterisation. First, anaesthetize nose by packing it with 4% xylocaine or by a topical spray of lignocaine. The eustachian tube catheter is then introduced in the nasal cavity and it is moved in a forward direction until it reaches the nasopharynx. The catheter is rotated in 90° medial direction and pulled a little back to engage the posterior free part of the nasal septum. Then rotate the catheter in 180° lateral direction so that its tip reaches the eustachian tube opening. Now a Politzer’s bag is connected to the outer opening of the catheter and air is pushed. Air entry into the middle ear is verified by an auscultation tube, indicating tubal patency.

Complications:

  • Injury to eustachian tube opening can cause nasal bleed and scarring can develop later.
  • The entry of infection from the nasopharynx into the middle ear causing otitis media.
  • Perforation in the atrophic tympanic membrane (as it is weak and thin).

4. Toynbee’s Test. Normally, a negative pressure develops in the middle ear if we swallow with nose closed. in this test, we ask the patient to swallow with his nose pinched manually by himself. It will take out the air from the middle ear and causes inward movement of the tympanic membrane, indicating tubal patency, which can be seen by the examiner with an otoscope or with a microscope. While the above three tests use a positive pressure, Toynbee’s manoeuvre uses negative pressure. Even though it is a rather crude test, the results are more informative, than the Valsalva manoeuvre or Politizer’s tests.

5. Tympanometry. Tympanometry can be used to assess eustachian tube function and confirm the integrity of the auditory system. Eustachian tube dysfunction plays a dominant role in the pathogenesis of suppurative and non-suppurative otitis media. The prognosis and treatment of both types of otitis media are  dependent upon the eustachian tube function. The test is done in an intact tympanic membrane. The impedance audiometer is programmed to measure the middle ear pressure in three conditions (a) the middle ear pressure at the beginning of the test (resting pressure), (ii) after swallowing (with the nose pinched and mouth closed) and (iii) after performing valsalva.

Inference 

  • Normal ET function: Middle ear pressure is same as atmospheric pressure at rest, during swallowing or Valsalva.
  • Impaired ET function: Pressure becomes negative during swallowing. It does not become positive on Valsalva or vice versa.
  • Grossly impaired ET function. Pressure does not change at all in either of the situations.

6. Sonotubometry. It is a non-invasive technique and provides information on active tubal opening. A tone is delivered via a probe to the nose.  Sound is then measured in the external auditory canal and fluctuations during swallowing are recorded. If the tone is heard louder it indicates patent tubal system. The duration for which the tube remains open can also be noted. The accessory sounds produced during swallowing interfere with the test results.

TESTS FOR EUSTACHIAN TUBE MUCOCILIARY CLEARANCE AND DRAINAGE.

These tests can only be done where there is pre-existing perforation of there are the tympanic membrane. Different substances can be introduced into the middle ear and time taken by them to reach the nasopharynx is noted. This indicates the clearance/ drainage function of the eustachian tube. The following substances can be used:

  • Saccharine solution drops – time taken to have a sweet taste in the mouth is noted.
  • Methylene blue dye – time taken by the dye to stain the pharyngeal secretions is noted. 
  • Antibiotic/steroid ear drops – time taken to have its bad taste in the mouth is noted.

EUSTACHIAN TUBE DYSFUNCTION (ETD)

It is described as impairment of ET function which leads to a variety of symptoms and physical findings. It is divided into acute or chronic:

Acute ETD. It can occur during nasal congestion due to a common cold or allergic rhinitis, for example, and is generally transient. 

Chronic ETD. Symptoms lasting for more than 3 months consecutively is considered chronic. Chronic ETD can be due to

  • Obstruction of the  Eustachian tube.
  • Patulous (branching) Eustachian tube.

Obstruction of the Eustachian tube. Eustachian tube obstruction can be mechanical, functional or both. 

Mechanical obstruction. It can result from

  1. Intrinsic (obstruction of the lumen of the tube) can be due to inflammation secondary to infection (viral, bacterial) or allergy.
  2. Extrinsic can be the result of compression caused by a tumour or adenoid mass. 

Functional obstruction. One of the most common types of ET dysfunction is when the lumen of the cartilaginous portion of the tube fails to open during swallowing activity. This may be due to

  1. Persistent collapse of the ET due to increased tubal compliance (e.g., lack of stiffness or the tube is too floppy) 
  2. An inefficient active opening mechanismdue to poor function of tensor veli palatini (cleft palate).
  3. Both defects coexist  

Treatment. Cleft palate repair, adenoidectomy, elimination of nasal and nasopharyngeal inflammation, treatment of nasopharyngeal tumours may be associated with improvement in ET function

Patulous eustachian tube (PET)

In this condition, the eustachian tube is hyper-patent. Symptoms include autophony (patients hears his own’s voice), breath synchronous tinnitus (patient hear its own’s breath sounds), aural fullness, and hearing loss which may lead to a huge impact in the quality of life. Due to its undue patency, the protective function of ET system is lost. Pressure changes and unwanted secretions from the nasopharynx gain easy access into the middle ear to such an extent that the tympanic membrane moves synchronously with breathing. This is not always present but is diagnostic when seen.

PET disorders may occur in two types: 

  1. PET type, in which the lumen remains anatomically open, even at rest. 
  2. Semi-patulous Eustachian tube type is a less severe form. Here, the tube lumen is anatomically closed at rest but, due to low tubal resistance to air pressure, it opens easily during physical activity.

Mostly it is idiopathic but it is found in patients following bariatric surgery, acute weight loss, pregnancy especially third trimester, or multiple sclerosis.

Treatment.

  1. Counselling.
  2. An acute condition is generally self-limiting. No treatment required. 
  3. In chronic cases, weight gain, oral administration of saturated solution of potassium iodide, oestrogen nasal drops has been used to induce swelling of the ET opening. Myringotomy and grommet insertion may sometimes alleviate symptoms. Other options are augmentation of the tympanic membrane with cartilage and cauterization of the tubes.

EFFECTS OF ACUTE AND CHRONIC ET DYSFUNCTION/ BLOCKAGE

ET dysfunction is most commonly involved in the pathogenesis of middle ear disease. Acute otitis media, otitis media with effusion, chronic suppurative otitis media are the most frequent middle-ear diseases. Air (composed of oxygen, carbon dioxide, nitrogen and water vapour), normally fills the middle ear and mastoid. When the tube gets blocked either due to anatomical obstruction or a functional obstruction, resorption of air from the middle ear. This results in negative pressure in the middle ear and retraction of the tympanic membrane. If the negative pressure is still further increased, it causes “locking” of the tube with a collection of transudate and later exudate and even haemorrhage.

Symptoms are otalgia, hearing loss, autophony, popping sensation, crackling tinnitus and disequilibrium or may be contributing to vertigo.

Signs. In most cases, the tympanic membrane is retracted, dull in appearance with an abnormal light reflex, congestion may be present, transudate behind the tympanic membrane, giving it an amber colour and sometimes a fluid level may be seen with conductive hearing loss. 

In severe cases (e.g. barotrauma due to scuba diving, air flight etc): Tympanic membrane is strikingly retracted, congested and sometimes it is found ruptured. Air bubbles or haemorrhagic effusion may be seen in the middle ear. 

Effects of acute and chronic tubal blockage.

Acute Chronic
Eustachian tube blockage

Resorption of air from the middle ear

Development of negative pressure in the middle ear

Retraction of the tympanic membrane

Transudate in ME/haemorrhage (acute OME) 
Eustachian tube blockage/dysfunction

OME (thin watery or mucoid discharge)

Atelectatic ear/perforation

Retraction pocket/cholesteatoma

Erosion of the incudostapedial joint 

DISORDERS RELATED TO EUSTACHIAN TUBE DYSFUNCTION

(i) Adenoids hypertrophy and Eustachian Tube Function. In the paediatric population, the adenoids hypertrophy is the most common cause of ET dysfunction. It hinders aeration of the middle ear by

  1. Mechanical obstruction of the nasopharyngeal orifice of the Eustachian tube.
  2. Acts as a Bacterial reservoir 
  3. Mast cells of the adenoid tissue release inflammatory mediators which cause tubal blockage.

Thus, adenoid hyperplasia results in otitis media with effusion or recurrent acute otitis media. Adenoidectomy is treatment.

(ii) Cleft Palate and Tubal Function. In infants and young children having cleft palate, otitis media is usually present. There is a failure of the tube’s opening mechanism due to aberrations in the para tubal muscles that are normally responsible for Eustachian tube opening. Structural abnormalities associated with cleft palate are:

  1. Presence of high elastin density in torus tubarius, making it difficult to open.
  2. Tensor veli palatini muscle which is a primary opener of the eustachian tube does not insert or insert firmly into the torus tubarius,therefore, lacks the anchorage to effectively open the Eustachian tube.

Otitis media with effusion is common in these patients. Not always surgical repair of the cleft reduce the incidence, many of them still require insertion of grommets for ventilation of middle ear.

(iii) Down Syndrome and Tubal Function. In down syndrome, ET dysfunction occurs due to

  1. Defective muscle tone of tensor veli palatini muscle
  2. Altered shape of nasopharynx.

Both are responsible for failure in preventing reflux and infection from the nasopharynx into the eustachian tube causing repeated otitis media or otitis media with effusion.

(iv) Barotrauma.  Due to eustachian tube dysfunction, there is failure of eustachian tube to equalize pressure between the middle ear and the atmospheric air pressure during sudden pressure changing situations such as rapid descent during air flight, scuba diving or hyperbaric oxygen therapy in pressure chamber. It may result in both middle ear or inner ear barotrauma.

(a) Middle ear barotrauma. It is a nonsuppurative condition occurs due to sudden negative pressure in the middle ear causing redness and retraction of the tympanic membrane, engorgement of vessels, transudation and haemorrhages. In more severe cases middle ear may show fluid accumulation or haemotypanum. It can also result in perforation of the tympanic membrane and ossicular damage.

  Tympanic membrane appearance in middle ear barotrauma 
Grade  Symptoms and signs 
Symptoms, no signs 
Redness and retraction 
Intratympanic membrane haemorrhage 
Gross tympanic membrane haemorrhage 
Haemotympanum 
Perforation 

(b) Inner ear barotrauma. It is usually seen when divers performs a Valsalva manoeuvre in order to equalize the middle ear pressure, there is increase in pressure causing inner ear. If the forced Valsalva opens the Eustachian tube, middle ear pressure increases leading to rupture of the round window membrane or disruption of the stapes footplate. If the Eustachian tube does not open by forced valsalva, there is increase in intracranial pressure which gets transmitted along a patent cochlear duct or the internal auditory meatus, causing disruption of the round window or the stapes footplate. In both situations, perilymph fistula or damage to intracochlear membrane may result in SNHLand balance disturbance.  

Mechanism 

When atmospheric air pressure is high as compared to middle ear pressure, air is not able to enter the middle ear. If the difference gets above the critical level of 90 mm Hg, it causes locking of the eustachian tube. 

Clinical features 

  1. Sensation of a blocked ear 
  2. Severe progressive otalgia
  3. Hearing loss is usually conductive but sensorineural type of loss may also be seen.
  4. Tinnitus 
  5. Vertigo is not common but may occur due to sudden ingress of water into the middle ear may result in caloric vertigo. 
  6. Tympanic membrane appears red and retracted and perforation may be present. 
  7. Middle ear may show accumulation of fluid, haemotypanum and ossicular damage.

Treatment.

Depends upon signs and symptoms present.

  • Type 1: Only symptoms are present, but no (or minimal) signs, no specific treatment is required.
  • Type 2: Both signs and symptoms are present but no perforation in tympanic membrane, conservative treatment is indicated with either decongestant nasal drops or oral nasal decongestant with anti- histaminics. Myringotomy can be done to aspirate the fluid if there is presence of fluid or when symptoms are not improving with conservative management.
  • Type 3: Perforation is present, myringoplasty can be done if perforation does not heal spontaneously.

Prevention.

Following measures should be taken: 

  1. No air travel and diving during or immediately after an upper respiratory infection or allergy.
  2. No use of occlusive earplugs when diving or flying.
  3. Frequent swallowing movements such as sipping drinks, sucking sweets or chewing gum during ascent and descent, help in equalizing pressure.
  4. Avoid sleeping during descent as normal swallowing movements decreases during sleep.
  5. Pressure equalizing manoeuvres like Valsalva and Toynbee can play a major role in preventing barotrauma. 
  6. Look for deviation of the septum, nasal polyposis, sinus infections, allergy for repeated episodes of barotrauma and should be treated.
  7. Local vasoconstrictors and oral anti-histaminic and systemic decongestant, can be advised half an hour before the descent.

Retraction pockets and eustachian tube 

A retraction pocket is a localized area of indrawing (or invagination) of tympanic membrane into the middle ear or attic. The initial cause of retraction pockets is recurrent or chronic negative pressure in the middle ear, due to dysfunction of the eustachian tube. Retraction of the tympanic membrane is commonly seen in both children and adults. 

Common sites of retraction pockets:

  1. Pars flaccida. The pars flaccida is actually thicker than the pars tensa, but it is the weakest part of the TM due to thinner less-organized collagen fibres which are loosely arranged in lamina propria. There is also absence of annulus sulcus, which stabilizes the insertion of the TM to the surrounding bone.
  2. Posterosuperior quadrant of the pars tensa. It has thinner, more sparsely distributed collagen and is highly vascularized and thus more prone to inflammatory reactions, which causes breakdown of collagen skeleton due to secretion of collagenase enzyme. Because of this TM becomes atrophic and susceptible to retraction.

Types of retraction pockets:

  1. Shallow pockets. The extent of pocket is visible on examination. These pockets are usually nonprogressive and self-cleaning pockets.
  2. Deep pockets. The extent of pocket is not visible on examination. It tends to collect squamous keratin debris and becomes a cyst. When infected, these cysts drain and granulation tissue develops around the sac, causing bone erosion and possible complications. 

Classification of retraction.

Stages of retraction of Pars Tensa by Sadé and Berco. 

  • Grade I. Tympanic membrane is retracted but does not contact the incus. There is loss of light reflex.
  • Grade II. Tympanic membrane is retracted on long process of incus.
  • Grade III. Also called middle ear atelectasis. Tympanic membrane comes to lie on the promontory but not adhered. It moves on Valsalva maneuverer or suction tip.
  • Grade IV. Also called adhesive otitis media. Tympanic membrane is adhered to the promontory. It does not moves on Valsalva maneuverer or suction tip.

Stages of retraction of Pars Flaccida by Tos et al. 

  • Grade I. The pars flaccida is dimpled and more retracted than normal but not adherent to the malleus.
  • Grade II. The retraction is adherent to the neck of the malleus.
  • Grade III. Partial erosion of the bony attic wall
  • Grade IV. Definitive Erosion of bony attic wall

Clinical features

There may be persistent ear discharge, hearing loss, and cholesteatoma formation.

Management:

  • Shallow pockets. Observation with periodic microscopic examination and regular suctioning and cleaning of debris or cerumen. Encourage auto inflation and look for contributing factor (adenoid disease, allergy and GERD) for eustachian tube dysfunction. Placement is tympanostomy tube or simple excision of damaged TM can be done if the pocket is progressive.
  • Deep pockets. Demands urgent surgical mastoid exploration under general anaesthesia for correction/repair of the irreversible pathologic processes.

———— End of the chapter ————

Learning resources.

  • Scott-Brown, Textbook of Otorhinolaryngology Head and Neck Surgery.
  • Glasscock-Shambaugh, Textbook of  Surgery of the Ear.
  • Logan Turner, Textbook of Diseases of The Nose, Throat and Ear Head And Neck Surgery.
  • Rob and smith, Textbook of Operative surgery.
  • P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
  • Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
  • Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck surgery.
  • Anirban Biswas, Textbook of Clinical Audio-vestibulometry.
  • W. Arnold, U. Ganzer, Textbook of  Otorhinolaryngology, Head and Neck Surgery.
  • Salah Mansour, Textbook of Comprehensive and Clinical Anatomy of the Middle Ear.
  • Susan Standring, Gray’s Anatomy.
  • Ganong’s Review of Medical Physiology.

Author:

Dr Rahul Bagla

Dr. Rahul Kumar Bagla
MS & Fellow Rhinoplasty & Facial Plastic Surgery.
Associate Professor
GIMS, Greater Noida, India
msrahulbagla@gmail.com

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