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EUSTACHIAN TUBE DYSFUNCTION
obstructive ETD. Patulous ETD is more likely to have a structural cause with loss of so
tissue, and it is associated with acute weight loss in one-third of cases. Other associations
include pregnancy, allergy, haemodialysis, neurological disorders, and local radiotherapy,
although in one-third or more of cases no cause is identied.
Assessment and Diagnosis
ETD provides a diagnostic challenge, as the presenting symptoms are non-specic and
similar to many otological conditions, as well as temporomandibular joint disorders, and
even chronic rhinosinusitis. It is important to note that autophony can be caused by other
disorders, such as superior canal dehiscence. Furthermore, patient symptoms correlate
poorly with the underlying ET function and should not be used in isolation when deciding
on management.
1
Symptom severity may be quantied through the use of one of the disease-specic questionnaires, the Cambridge ETD Assessment (CETDA) or the ETD questionnaire (ETDQ-7).
While useful in tracking changes in symptoms and as outcome measures, these tools have
very low specicity and therefore a limited role in diagnosis. A subgroup of patients with
patulous ETD that provides a particular diagnostic challenge are those with a closed ET but
low ET opening pressure. ese individuals tend to sni regularly to generate a negative ME
pressure, stiening an atelectatic tympanic membrane to improve hearing and symptoms
of autophony and aural fullness. is habit can generate a negative ME pressure, leading to
misdiagnosis if tympanometry alone is used to diagnose ETD.
Examination should focus on the assessment of ET function using tests that measure ET
opening and ME pressure equalisation.
ET opening can be assessed with the patient sitting during Valsalva or Toynbee (swallowing with a pinched nose and closed mouth) manoeuvres by watching the tympanic
membrane for deection, which is seen in 80–85% of healthy individuals. If patulous ETD
is suspected, the tympanic membrane is observed as the patient breathes to look for synchronous deection. If no movement is seen, the patient is asked to occlude the contralateral nostril and breathe forcefully. If still negative, the patient should be asked to exercise
(jog on the spot or climb a staircase) prior to examination as intermittent patulous ETD
may be provoked.
Ty mpanometry provide s a useful ind icator of ET funct ion. An ME pressure below –50 d aPa
suggests obstructive ETD with a specicity close to 100%, but sensitivity of only 50%.1
is relies on excluding patulous ETD and sni-induced negative ME pressure, which
may be suggested by the history or a high compliance. It should also be noted that ME
pressure should be measured before asking the patient to perform Valsalva or Toynbee.
Continuous recording of tympanic impedance (long time base or reex-decay tympanometer settings) detects synchronous movement of the tympanic membrane with breathing
in patulous ETD.
Although not widely available, specialist tests such as tubomanometry and sonotubometry
have been shown to have good sensitivity and specicity for ETD, providing a quantitative
assessment of ET opening. Table 8.1 summarises the methods of ET function assessment.
Treatment of Obstructive ETD
e majority of patients with obstructive ETD do not require treatment following reassurance. Most treatments for obstructive ETD (summarised in Table 8.2) lack an evidence base,
including nasal steroids.2 Tympanostomy tubes provide short-term relief in patients with a
predominance of symptoms on baro-challenge, but other symptoms may fail to improve.
Surgery with laser ablation of the mucosa and submucosa around the nasopharyngeal ET
ostium has been shown to improve symptoms and ET function at least in the short term, but
most recent work has focussed on balloon dilation of the ET (BDET).
48 e Ear
EUSTACHIAN TUBE DYSFUNCTION
Table 8.1 Methods of assessing ET function to investigate obstructive or patulous ETD
Method of assessment Indicator of ET function
• Tympanometry ME pressure in relation to ambient pressure
at rest
• Patient-reported ME pressure change
• TM movement on otoscopy
ME pressure changes on ET opening with
Valsalva, Toynbee, or heavy breathing
• Continuous tympanic impedance
monitoring
• Ear canal pressure monitoring (TTAG)
• Nine-step equilibration test (intact TM)
• Forced-response test (perforated TM)
• Tubomanometry (a sealed nosepiece for
pressure delivery and ear canal pressure
sensor)
• Sonotubometry (a speaker held at the
nostril and microphone within an ear
canal probe)
ME pressure equalisation after applied
external canal pressure
ME pressure changes on ET opening with an
induced high nasopharyngeal pressure
synchronised with swallowing
Degree of sound transmission along the ET
with opening during swallowing or heavy
breathing
• Rigid or exible endoscopy Extent of ET movement on swallowing and
atrophy or swelling of ET soft tissues
Note: ET, Eustachian tube; ME, middle ear; TM, tympanic membrane; TTAG, tubo-tympano-aerodynamic-
graphy.
Diagnosis of ETD
Clinical history and
examination
Suggestive of
Obstructive ETD
Clinical history and
examination
Suggestive of
Patulous ETD
a
b
Yes
Yes, tympanometr y not
possible e.g. perforation
Yes
Tympanometry
ME pressure
<-50daPa
Yes
No
c
Valsalva AND Toynbee
Ear drum deflection
(Sonotubometry/
Tubomanometry
if available)
Continuous impedance
Breathing-synchronous
(± with provocation)
or TTAG
fluctuation
d
No
e
No
Yes
Otoscopic signs OR
intermittent/
induced symptoms?
No No
f
Yes
Obstructive ETD
Yes
Possible ETD
ETD Unlikely
Investigate
alternate diagnoses
Patulous ETD
g
Figure 8.2 Diagnostic owchart for Eustachian tube dysfunction (modied from Smith et al.
20181).(a,b) Clinical assessment may not be diagnostic of ETD, but remains a means to identify
patients for investigation. (c) Effort should be made during assessment of the clinical history to
identify habitual snifng, as a negative middle ear pressure in these individuals may not indicate
obstructive ETD, and further testing should be undertaken. (d) Valsalva and Toynbee represent
simple tests of ET opening available to any clinician, though more sophisticated tests of ET opening such as sonotubometry and tubomanometry may provide higher accuracy and repeatability.
(e) Tubo-tympano-aerodynamic-graphy (TTAG) is an alternate method recommended if a tympanic
membrane perforation is present. (f) A simple provocation test for use in clinic is asking the patient
to exercise prior to testing. (g) This group could contain healthy patients, or those with patulous
or obstructive ETD. ET function may vary over a relatively short time period. Tests may be repeated
on a separate occasion to improve sensitivity in patients with variable ET function. Patients with
baro-challenge-induced obstructive ETD may present here with normal test results in the absence
of signicant pressure change.
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EUSTACHIAN TUBE DYSFUNCTION
Table 8.2 Management of obstructive ETD
Management of obstructive ETD
Medical/Conservative
• Topical nasal steroids
• Antihistamines
• Management of acid reux
Surgical
• Tympanostomy tubes
• Laser removal of mucosa and submucosa ± cartilage scoring
• Microdebrider removal of tissue at the ostium
• Balloon dilation (transnasal or transtympanic)
BDET uses a high-pressure balloon passed into the ET to dilate the tube and improve opening.
e balloon is typically inserted with an introducer via a nasal approach, guided using a 30°
endoscope, although transtympanic approaches have been described. Improvement in patient
symptoms, tympanometry results, ability to Valsalva, and some objective measures of ET function have been repor ted up to 24 months, but long-term data are lacking. BDET has been used less
in children, but some reports suggest it has a role in the management of otitis media w ith eusion.
ere is no widespread consensus on patient selection criteria for BDET. Several groups
have published criteria, which stress the importance of careful pre-operative diagnosis, and
suggest on the basis of current evidence that BDET may provide benet to patients with
chronic symptoms, serous otitis media, and baro-challenge-induced discomfort. e benet
of BDET as an adjunct to ME surgery has not been determined.
Treatment of Patulous ETD
As with obstructive ETD, the evidence supporting treatments for patulous ETD is oen limited to small case series. Techniques are summarised in Table 8.3. As many symptoms are
believed to be due to tympanic membrane movement, mass loading of the membrane has
been used as a treatment, and this may also explain the benecial eect of tympanostomy
tubes. Before embarking on surgery, many surgeons place Blu-Tack or cream on the tympanic membrane in clinic to assess its eect on symptoms. Increasing evidence suggests good
and sustained results from use of a silicone (Kobayashi) plug or wax-lled catheter inserted
into the ET via either a tympanic or nasal approach. While bulking agents injected around
Table 8.3 Management of patulous ETD
Management of patulous ETD
Medical/Conservative
• Cessation of nasal steroids or decongestants
• Increased weight
• Nasal saline spray
• Nasally applied salicylic or boric acid powder, or dilute hydrochloric acid
Surgical
• Tympanostomy tubes
• Mass loading of the tympanic membrane:
• Paper patches applied to the tympanic membrane
• KTP laser resurfacing of the tympanic membrane
• Cartilage tympanoplasty
• Occlusion of the Eustachian tube lumen:
• Intraluminal occlusion with a silicone plug or blocked catheter
• Injection of bulking agent (Teon, silicone, calcium hydroxyapatite)
• Cartilage grafting (harvested from nasal septum)
50 e Ear
ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION IN ADULTS
the nasopharyngeal ET orice appear to be successful in improving symptoms, the longterm results are poor and some patients need multiple injections.
KEY POINTS
• The ET opening is mediated by intermittent active or passive opening.
• ET disorders are common, with patulous and obstructive dysfunction at either end of a
spectrum of ET function.
• Presenting symptoms and signs are non-specic.
• Tests of ET function are required to distinguish patulous from obstructive dysfunction.
• BDET is increasingly used to treat obstructive ETD, with a body of evidence to suggest
improvements to patient symptoms and objective outcomes.
• Uncertainty remains in relation to patient selection for BDET and long-term outcomes.
• Patulous ETD may be treated by several methods to obstruct the ET lumen or reduce
tympanic membrane movement.
Further Reading
1. Smith ME, Takwoingi Y, Deeks J, et al. Eustachian tube dysfunction: a diagnostic
accuracy study and proposed diagnostic pathway. PLoS One 2018; 13:e0206946.
2. Norman G, Llewellyn A, Harden M, et al. Systematic review of the limited evidence
base for treatments of Eustachian tube dysfunction: a health technology assessment.
Clin Otolaryngol 2014; 39:6–21.
9. ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION IN ADULTS
Acute Otitis Media
Denition
e term otitis media describes inammation of the middle ear space. ‘Acute’ otitis media
indicates a time frame of inammation resolution within 12 weeks. Clearly, timely diagnosis is required to manage such conditions, and thus in practice the term acute otitis media
(AOM) is used to describe an acute infection of the middle ear space. Clinical dierentiation of AOM from an initial presentation of otitis media with eusion (OME) is important,
as overtreatment of OME with antibiotics in primary or secondary care is common.
Incidence
AOM occurs most commonly in children; however, it is seen in adults – a large international
multicentre primary care study recorded that 16% of patients with AOM were aged >15 years.
In a study of U.S. veterans, the incidence of AOM in adults leading to a presentation at a
veterans’ medical centre was 2.6/1000/yr.
Aetiology
Much of our understanding of the aetiology of AOM is based on its clinical presentation in
children. AOM is thought to be caused by a combination of Eustachian tube anatomy, disordered Eustachian tube function, immune status, and infective organisms.
Eustachian tube dysfunction (ETD) may be caused by a viral upper respiratory tract infect ion
(URTI) which may also cause infection within the middle ear cle. ETD can also be associated with smoking. Immune function is most relevant in patients with immunodeciency.
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ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION IN ADULTS
People with human immunodeciency virus (HIV) have an incidence of AOM four times
higher than age-matched controls, and around 50% of patients with common variable
immunodeciency have had AOM episodes. e higher incidence of AOM in children is
thought to be due to anatomical dierences of the Eustachian tube (it is shorter and more
horizontal) and their less mature immune system.
Bacteria are identied in the vast majority of middle ear aspirates, with the most common
organisms identied as Streptococcus pneumoniae, Haemophilus inuenzae, and Moraxella
catarrhalis. ere is an increasing recognition of polymicrobial disease – with both bacterial
and viral pathogens found in approximately 66% of cases. e most common viruses identied are rhinovirus and respiratory syncytial virus.
Diagnosis
History
e charac teristic symptoms of AOM are ota lgia, hearing loss, and systemic upset. Secondary
symptoms include balance disturbance, general malaise, pyrexia, and headache. Otorrhoea
may occur with tympanic membrane perforation, which typically resolves the otalgia and
systemic illness – such cases may need to be dierentiated from bullous myringitis.
Examination
Otoscopy may be challenging as the bulging red tympanic membrane may prove dicult to
focus on until the examiner realises the drum is more lateral than usual, and withdraws the
otoscope slightly to allow the drum to appear in focus. e bulging of the tympanic membrane is the most reliable otoscopic indicator of AOM.
Other signs include perforation and pus in the ear canal. Swelling of the posterior ear canal
is a sign of mastoiditis.
Differential Diagnosis
Bullous myringitis mimics AOM most closely. Otitis externa may have similar symptoms
and abnormal examination. Temporomandibular joint dysfunction may also cause otalgia
with normal examination ndings.
Examination ndings of AOM can be similar to those seen in OME, middle ear paraganglioma, or aberrant middle ear vasculature.
Management
Although most cases will resolve spontaneously and only analgesia/antipyretics are required,
AOM is still the most common cause of antibiotic prescription in the United States. In the
United Kingdom, the National Institute of Health and Care Excellence recommends withholding antibiotic treatment for 3 days in the majority of cases, and reserving antibiotics for
cases that do not improve, for those who are systemically unwell, and for younger children
with bilateral AOM. is is based on evidence showing that antibiotics have limited ecacy
in AOM in all patients, and with particularly limited evidence in the adult population. e
recommended rst-line agent is a 5- to 7-day course of amoxicillin, or a macrolide such as
clarithromycin in penicillin-allergic patients.
e treatment of AOM in the 10% of patients who have perforated their tympanic membrane
but have ongoing symptoms is controversial. Topical ciprooxacin can be used, although
the evidence base for this is largely based on its use in grommet-related otorrhoea. Systemic
antibiotics are more frequently recommended as more pathogenic organisms, such as group
A Streptococcus, are associated with perforation.
Complications of AOM are typically divided into intracranial and extracranial complications. All are rare, although it is interesting to note that adults with AOM are at higher risk
of intracranial complications than adults with chronic otitis media. Extracranial complications include facial palsy, acute mastoiditis, purulent labyrinthitis, and abscesses associated
with structures connected to the temporal bone, such as the sternocleidomastoid, digastric,
52 e Ear
ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION IN ADULTS
or zygoma. Intracranial complications include sigmoid sinus thrombosis, otitic hydrocephalus, subdural empyema, intradural abscesses, Gradenigo’s syndrome (middle ear infection
complicated by petrous apicitis causing cranial nerve VI palsy and retro-orbital pain), and
meningitis. Facial palsy accounts for 30% of these complications, but full recovery occurs
in most cases. Treatment of complications is with antibiotics, drainage of any abscess, and
urgent mastoidectomy to treat the infection source. Many advocate adding anticoagulants in
cases of sigmoid sinus thrombosis.
Recurrent AOM is almost invariably seen in children, but it can occur in adults, and may
be treated by grommet insertion, or rarely antibiotic prophylaxis, with modest ecacy.
Pneumococcal vaccination has also been shown to be eective in preventing episodes of
otitis media in both adults and children.
Proposed treatments for the future include transtympanic or intranasal antibiotics or
bacteriophages, probiotics, vaccination against viral pathogens, and treatment directed at
Haemophilus-associated biolm. ere is limited evidence to support the use of systemic
steroids, although they are not used commonly.
Otitis Media with Effusion in Adults
Denition
OME describes a collection of uid in the middle ear associated with inammation, but not
active infection, of the middle ear cle.
Incidence
In a very large analysis of U.S. ambulatory medical care attendance with OME, adults >20
years accounted for about one-third of patients for about 1.2 million visits per year (this gives
a visit prevalence, and not an incidence). In the United Kingdom, a cross-sectional study
found a point prevalence of all ETD diagnoses of about 1% in adults.
Aetiology
e aetiology of otitis media in adults, and the dierences in its nature with paediatric disease are incompletely understood. Adult OME is a condition that arises from the interaction
of a number of factors, the most important of which are Eustachian tube function and upper
respiratory tract inammation.
Eustachian Tube Function
Objective tests have revealed evidence of abnormal Eustachian tube function in adults
with OME. e signicance of these tests is uncertain. It is nevertheless well recognised that
obstructing lesions in and around the Eustachian tube, such as nasopharyngeal carcinoma,
or skull base tumours such as intraosseous meningiomas, may cause OME. Similarly, disorders such as cle palate that impair ET function can cause OME.
OME may also arise due to acquired dysfunction of the Eustachian tube, most notably, radiotherapy to the head and neck has a strong dose-related relationship with OME. Equally, in
patients with prolonged sedation (and consequent lack of swallow), there is a very high incidence of OME. is is also seen in patients with ciliary dysfunction such as smokers and
patients with primary ciliary dyskinesia. Barotrauma and hyperbaric oxygen therapy may
also cause ETD and consequent OME, but this typically resolves spontaneously. OME has
also been associated with sning to suppress patulous eustachian tube symptoms.
Upper Respiratory Tract Inammation
While upper respiratory tract inammation can a priori cause ETD, it is worthwhile considering it as a dierent entity, because it may also aect the middle ear mucosa directly. e majority of adults report an URTI prior to episodes of OME, and about two-thirds of aspirates from
middle ear eusions are culture positive for pathogens such as S. pneumoniae, H. inuenza or
Candida spp. In contrast, pathogens cannot be cultured from irrigation of the middle ear in
people without OME. ere is also a high incidence of OME in patients with HIV.
e Ear 53
ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION IN ADULTS
ere is evid ence showing a higher i ncidence of OME in adults w ith allerg ic rhinitis. Fu rthermore,
there is an association with nasal polyposis, which is likely to be mediated by the underlying
mucosal inammation. e role of laryngopharyngeal reux in the aetiology of OME is controversial, given the high incidence of reux, and the uncertain signicance of the nding of pepsin
in middle ear aspirates, but it does seem likely there is a relationship. Other inammatory conditions associated with OME include granulomatosis with polyangiitis, and polyarteritis nodosa.
Eosinophilic otitis media (EOM) is distinct from OME and has a strong association with asthma
and allergy. It is characterised by eosinophilic inltrates in the middle ear mucosa and can be
associated with e usion, viscous discharge through a perforation, and/or middle ear granulation.
Diagnosis
History
In a case-control study, symptoms in OME suerers included the following:
Hearing loss: 97%
•
Aural fullness: 77%
•
Pulsatile or crackling tinnitus: 60%
•
e condition is usually bilateral, but it may be unilateral. Subjects frequently have predisposing factors including smoking, childhood ear infections, and nasal symptoms. A recent
URTI, AOM, and/or barotrauma is oen a feature.
Examination
Otoscopy reveals a dull tympanic membrane, with a loss of the light reex. e tympanic
membrane may be inamed, visibly thickened, or retracted. ere may be reduced movement of the tympanic membrane to pneumatic otoscopy. A uid level, or air bubbles, may
be seen. Fibreoptic nasoendoscopy is recommended in patients with unilateral symptoms to
rule out an obstructing nasopharyngeal lesion.
Differential Diagnosis
Cerebrospinal uid (CSF) in the middle ear secondary to a skull base defect may be mistaken
for OME. EOM and vasculitis-associated otitis media are distinct entities. ese require intensive anti-inammatory treatment in conjunction with respiratory/rheumatological physicians.
Investigations
Audiology and Tympanography
A pure–tone audiogram will show the level of impaired hearing function and typically reveal a
conductive hearing loss. Tympanography will commonly show a ‘type B’ pattern. Experienced
clinicians will usually make the diagnosis of OME from tympanic membrane appearance.
Myringotomy
e presence of uid at surgery conrms the condition of OME, but the absence of uid does
not necessarily refute it, as uid may still be present in the mastoid. Immediate pre-operative
tympanometry has shown that type B and type C2 tympanograms are 92% and 39% predictive of a middle ear eusion, respectively.
Imaging
Unilateral OME may be investigated with contrast magnetic resonance imaging (MRI) of
the nasopharynx and skull base, particularly in at-risk populations such as those of Chinese
descent. is is in recognition of the potential for skull base tumours or submucosal nasopharyngeal tumours to present in this way with normal endoscopic ndings. In addition,
certain MRI sequences are useful in dierentiating OME from CSF.
Management
ere are four management options in adults: (1) nonmedical treatment, (2) medical treatment, (3) hearing aids, and (4) surgical treatment.
54 e Ear
ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION IN ADULTS
Non-Medical Treatment
Autoination techniques have a role to play in adults as well as children. Although the
benet is modest, the risks are negligible. Autoination is commonly encouraged through
the Politzer technique, although mechanical devices such as the OtoventTM balloon and
EarPopperTM can be employed to achieve the same eect.
Medical Management
ere is limited evidence for topical nasal steroids or decongestants, such as xylometazoline, in the treatment of OME. However, they are likely to be benecial in patients who
have rhinitis. Antibiotics and antihistamines are ineective, despite being oen prescribed.
Short courses of oral steroids have been shown to be ineective in a paediatric population.
Hearing Aids
Hearing aids are highly eective for conductive hearing loss provided there is adequate inner
ear function, and they can be oered to adults with long-term OME.
Surgical Treatment
Ventilation Tubes
Ventilation tubes are commonly used for OME in adults for hearing restoration. Several
studies have shown evidence for their short-term ecacy. Aer grommet extrusion, around
25–35% of patients will have recurrent OME depending on the underlying aetiology of the
OME. Grommets are not without complications; about 20% of patients will have grommetrelated otorrhoea, and persistent perforation rates of 2% with short-term tubes rise to 17%
when long-term tubes are used.
Chronic otorrhoea has meant that conservative management is oen recommended in
patients who have had radiotherapy for nasopharyngeal carcinoma. Actual rates of otorrhoea are relatively low in these patients, so surgery can be oered. Extra-annular tubes may
stay in situ for longer periods, and do not cause tympanic membrane perforation, but require
a more invasive initial operation.
Laser Myringotomy
e use of a laser to produce fenestration of the tympanic membrane produces a short-term
solution. A mean of around 3 weeks for a functioning myringotomy has been reported.
Eustachian Tuboplasty
A meta-analysis including 1155 patients concluded that the balloon Eustachian tuboplasty
(BET) oers short-term benet in the majority of cases and medium to longer term benet in
a smaller number of patients. For that reason it has been proposed as a treatment for patients
with recurrent OME aer grommet insertion. Laser tuboplasty has also been reported.
KEY POINTS
• AOM, which is symptomatic after tympanic membrane perforation, is more likely to be
associated with pathogenic bacteria such as group A streptococcus.
• Vascularity of the normal tympanic membrane should not be confused with the
bulging red tympanic membrane seen in AOM.
• Persistent clear uid during unilateral ventilation tube insertion indicates a CSF leak.
• Complications associated with ventilation tube insertion include otorrhoea (20%) and
persistent perforation (2–17% depending on type of tube).
• AOM in adults is usually managed with antipyretics for 72 hours to allow spontaneous
resolution.
Unilateral OME requires investigation with nasoendoscopy and/or MRI to exclude a
nasopharyngeal lesion.
e Ear 55
CHRONIC OTITIS MEDIA
Further Reading
1. NICE Clinical Knowledge Summary: Acute Otitis Media. https://cks.nice.org.uk/
otitis-media-acute#!topicSummary
2. Perera R, Glasziou PP, Heneghan CJ, McLellan J, Williamson I. Autoination for
hearing loss associated with otitis media with eusion. Cochrane Database Syst Rev.
2013;31 (5): CD006285.
3. Fish BM, Banerjee AR, Jennings CR, et al. Eect of anaesthetic agents on tympanometry and middle-ear eusions. J Laryngol Otol 200 0;114 (5): 336–338 .
10. CHRONIC OTITIS MEDIA
Introduction
Chronic otitis media may manifest in a variety of clinical phenotypes, including middle ear
eusion (glue ear), cholesteatoma, tympanic membrane retraction, or tympanic membrane
perforation (which may be associated with infection). Tympanosclerosis and myringitis are
also discussed here, although their relation to chronic otitis media is less clear.
Aetiology
e cause of chronic inammation of the middle ear is poorly understood. e traditional
theory assigning it to a functional abnormality of the Eustachian tube has little evidence to
support it (although this mechanism may be important in syndromic cases related to craniofacial malformation).
It seems probable that recurrent bacterial ingress into the middle ear in early childhood triggers inammation, which in some (genetically) predisposed individuals leads to non-resolving mucosal inammation (Figure 10.1), with resulting tissue dysfunction and damage.
Clinical
phenotypes
Bacteria virulence
and load
Host response
genetics
Chronic mucosal
inammation
Acute otitis
media
Inammatory
eusion
Submucosal
brosis
Eustachian tube
inammation
Lysis of tympanic
membrane
Disrupted gaseous
exchange
Epithelial –
mesenchymal
interaction
Secondary
bacterial infection
Glue ear
Tympanic
membrane
retraction
Cholesteatoma
Chronic
suppurative
otitis media
Tympanic
membrane
perforation
Grommets
Trauma
Figure 10.1 Clinical phenotypes of chronic otitis media and presumed aetiology.
56 e Ear
CHRONIC OTITIS MEDIA
Goblet cells in the middle ear mucosa hypertrophy and secrete mucus, leading to middle ear
eusion or ‘glue ear’.
Mucosal dysfunction can disrupt gaseous exchange and lower middle ear pressure (the relative role of this versus the Eustachian tube in maintaining normal middle ear pressure is
debated), and if combined with lysis and weakening of the brous layer of the tympanic
membrane from chronic inammation, can lead to tympanic membrane retraction.
Many cases of tympanic membrane perforation are also thought to be caused by lysis from
chronic inammation, although this may also occur secondary to acute otitis media, trauma,
or non-healing aer grommet extrusion. Some perforations are asymptomatic, whereas others are prone to recurrent infections, and if this occurs, the disease is termed chronic suppurative otitis media (CSOM).
Cholesteatoma can be dened as ‘the presence of squamous epithelium in the middle ear
cle’. Aetiology is uncertain, but acquired cholesteatoma has been demonstrated to arise
from the squamous epithelium of the tympanic membrane, as a result of active proliferation and medial growth. is seems to occur in response to chronic mucosal inammation,
but the underlying molecular signalling is uncertain. Cholesteatoma is more likely to occur
within a retraction pocket. In a few cases cholesteatoma may be iatrogenic, arising from
implanted squamous epithelium from previous surgery. Some consider cholesteatoma to be
a subtype of CSOM.
Symptoms and Signs
Chronic otitis media typically presents with hearing loss, otorrhoea, and/or otalgia.
Hearing loss will be conductive in nature, and it may result from middle ear eusion, tympanic membrane perforation, or erosion of the ossicles (most oen the long process of the
incus). Recurrent otorrhoea may be seen with tympanic perforation, retraction, or cholesteatoma. Mild otalgia is sometimes a feature in cholesteatoma. Typically, disease has to be
present for at least 3 months to be called chronic, but for CSOM some authors use 6 weeks.
Symptoms alone cannot determine diagnosis, and otoscopy is critical to visualise middle ear
pathology (using a microscope or endoscope where available), and an audiogram to evaluate
hearing loss. A tympanogram can conrm the presence of eusion or perforation.
In some cases, granulation tissue may preclude a full view of the tympanic membrane.
Granulation tissue should be treated with topical steroids, but if it fails to settle, surgical exploration is indicated for denitive diagnosis and treatment (including excluding
cholesteatoma).
Chronic Otitis Media with Effusion (Come; Glue Ear)
is is covered in more detail in Chapter 9. COME is common in childhood, aecting
5–6% of children at the age of 2, but it becomes rare aer the age of 7. Amongst adults
who suer chronic otitis media in some form, the majority will give a history of COME in
earlier life.
Tympanic Retraction
is typically aects either the pars accida or the posterosuperior pars tensa. e retraction
pocket may become adherent to and then erode the ossicles. In more advanced cases there
can be bony erosion (typically the scutum) or retraction of the entire membrane, with adhesion to the promontory. Retraction may be graded, and the Sade and Tos systems are most
commonly used (Table 10.1). Inter-observer reliability of these systems is poor.
Epidemiological studies suggest that up to 15% of adults have tympanic membrane retraction. Asymptomatic cases may need monitoring for risk of progression, including development of cholesteatoma, although the frequency and duration of monitoring is unclear. ose
with recurrent infection or hearing loss (air-bone gap greater than 20 dB) may benet from
cartilage tympanoplasty ± ossiculoplasty. Others advocate grommet insertion or excision
of retraction pockets, but there is little evidence on long-term results from such treatment.
e Ear 57
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