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VESTIBULAR DISORDERS AND REHABILITATION
nystagmus, and mixed and central type patterns. e presence of interictal eye movement
abnormalities should alert the examiner to consider the possibility of either a dierent
disorder altogether (e.g. episodic ataxia type 2) or an underlying neurological disorder
causing a migraine phenotype. Pure-tone audiometry is usually normal in VM and can be
helpful in dierentiating VM from MD. In cases where the history is typical and examination ndings are normal, MRI scanning to exclude secondary causes may not be required.
Management
A clear explanation to the patient about the nature of the condition is essential since VM is
frequently chronic and patients need to become expert in self-management. e evidence
base for management of VM as a specic subtype is generally weak, and recommendations
are generally made on the basis of management of migraine in general.
Migraine headache should be managed along standard lines with analgesics or migraine-specic relief medicines such as the 5-hydroxytryptamine receptor 1-B/D (5-HT1B/D) agonists
(‘triptans’), taking care to avoid analgesic-overuse headache. Acute symptoms of vertigo can be
managed with vestibular sedatives such as prochlorperazine, cyclizine, or cinnarizine. When
symptoms of headache and vertigo together are suciently intrusive/frequent to justify the risk
of adverse eects, migraine prophylactic agents can be considered. Evidence-based guidelines
should be followed; beta blockers and tricyclics remain frequently recommended, but there are
many options. VR may be useful in patients with sensitivity to self- and visual motion.
Superior Semicircular Canal Dehiscence (SSCD)
Superior semicircular canal dehiscence syndrome (SSCD) is the dehiscence of otic capsule
bone overlying the superior semicircular canal. It encompasses a wide variety of vestibular
and auditory symptoms, and it creates a third cochlea window in addition to the oval and
round window.
Typical third window symptoms are a result of movement at the dehiscence from raised
intracranial pressure, or at the oval or round windows, from loud sounds or straining (e.g.
Valsalva manoeuvre). Alterations in inner ear uid dynamics due to the third window cause
increased ring of vestibular aerents and transient momentary vertigo.
Diagnosis
A 0.5–0.6% prevalence of SSCD has been observed in histological studies of cadaveric temporal bones. In comparison, reported prevalence from studies reviewing high-resolution
temporal bone computed tomography (CT) scans was 4–8%. Dehiscence alone is therefore
not sucient to cause the syndrome. SSCDS could be congenital, acquired, or a combination
where a genetic predisposition followed by a secondary event triggers SSCDS.
Symptoms can include hearing loss (typically a low-frequency conductive hearing loss, with
supranormal bone conduction), autophony, pulsatile tinnitus, and a description of hearing their eye movements or footfall. Transient vertigo, imbalance, and oscillopsia can all
occur with loud sounds (Tullio’s phenomenon) or intracranial/middle ear pressure changes.
Generalised imbalance can also occur.
High-resolution CT is the gold standard for identication of SSCD. Patients with SSCDS also
have ocular or cervical vestibular evoked myogenic responses present with lower thresholds
or higher amplitudes than normal for the aected ear.
Management
Patients with mild symptoms that are not intrusive or bothersome should be treated conservatively and given advice on avoidance of triggers. Surgery via either a transmastoid or middle fossa approach can be oered where symptoms are persistent/disabling, and techniques
include plugging, capping, and resurfacing of the SSC. Surgery typically does not improve
hearing, and it can be complicated by SNHL and chronic imbalance. ere is some evidence
to support patching of the round window to reduce third window symptoms.
38 e Ear
VESTIBULAR DISORDERS AND REHABILITATION
Neuropsychiatric Aspects of Vestibular Disorders
It has long been recognised that psychological factors can play a signicant role in the genesis
of dizziness.
e concepts of phobic positional vertigo, space motion discomfort, and chronic subjective
dizziness were brought together to produce the entity known as persistent perceptual postural dizziness (PPPD), referring to dizziness, unsteadiness, or non-spinning vertigo that
are present pervasively over 3 months or more and that are exacerbated by upright posture,
active or passive movement, and exposure to moving or complex visual stimuli and thought
to be a functional disorder. Models for explaining PPPD have been drawn from anatomical,
neurochemical, and cognitive behavioural theories, and it is considered to be a functional
neurological disorder.3 Anxiety and major depressive disorders are common in patients with
PPPD but do not occur in all cases.
Management
Uncontrolled trials indicate that selective serotonin reuptake inhibitors (SSRIs) and serotonin-noradrenaline (norepinephrine) reuptake inhibitors (SNRIs) may be of benet for
chronic dizziness with or without co-existing anxiety and depression. Psychotherapy (cognitive behavioural therapy [CBT]) also appears to be a helpful intervention. VR is eective in PPPD for hypersensitivity to motion, improving balance condence, and reduction
of avoidance behaviour. Outcomes appear to be variable. A multidisciplinary approach is
recommended.
Vestibular Rehabilitation (VR)
VR is oered for patients with head or visual motion intolerance, or imbalance, related to
vestibular disorders. VR is based on principles of vestibular compensation including habituation, adaptation, substitution, and/or sensory reweighting (table 6.2).
Table 6.2 Examples of commonly prescribed exercises in vestibular rehabilitation
Type of exercise Examples
Head exercises
(performed with eyes
open and eyes closed)
Eye movement exercises Head stationary follow movement of nger left and right/up and down
Visual xation exercises Perform head exercises while xating stationary target
Positioning exercises
(performed with eyes
open and closed)
Postural exercises
(performed with eyes
open; eyes closed
under supervision)
Bend head backwards and forwards
Turn head from side to side
Head movement to look back and forth between two vertical or
horizontal targets
Perform head exercises while xating moving target
While seated, bend down to touch the oor
While seated, turn to look over shoulder to left and then right
Bend down with head turned rst to one side and then the other
Lying down, roll from one side to the other
Sit up from lying supine and on each side
Practise static stance with feet as close together as possible
Practise standing on one leg, and heel to toe
Repeat head and xation exercises while standing and then walking
Practise walking in circles, pivot turns, up slopes, upstairs, and
around obstacles
Stand and walk in environments with altered surface and/or visual
conditions with and without head and xation exercises
Aerobic exercises, e.g. alternate touching the ngers to the toes,
trunk bends, and rotation
e Ear 39
VESTIBULAR DISORDERS AND REHABILITATION
Although components of the pioneering exercise programme by Cawthorne and Cooksey
may still be used today, good practice is now considered to be a customised programme based
on individual decits.
A VR assessment will include validated questionnaires around symptoms and disability,
objective and subjective tests to identify functional decit, and objective static and dynamic
balance tests and gait measures.
Treatment goals are devised to address each person’s individual subjective symptoms (i.e.
dizziness, giddiness, nausea) and objective symptoms (postural and gait instability, falls).
Various authors have discussed the potential benet of virtual reality as a therapeutic protocol to improve postural and gait stability, vestibulo-ocular reex (VOR) gain, and subjective
symptoms. Benets over standard approaches so far are not very striking, but the experience
may be more enjoyable with more sustained engagement as a result.
Outcome in VR can be inuenced by a number of factors which should be sought and
addressed especially if progress with therapy is limited (see Box 2, Chapter 5).
The Law and Vertigo
In the United Kingdom, the Driver and Vehicle Licensing Authority (DVLA) requires that
drivers declare any ongoing liability to sudden and unprovoked attacks of disabling vertigo,
because these could lead to loss of vehicle control while driving. It is the responsibility of the
driver to inform the DVLA, although clinicians have a responsibility to make patients aware
of this regulation.
e nature of the regulations means that some, but not all, individuals with vestibular paroxysmia, MD, PPPD, and VM may need to declare their condition. PC-BPPV would not
normally cause problems when driving, because when driving head movement is mainly in
the horizontal plane.
KEY POINTS
• MD causes episodes of incapacitating vertigo with unilateral auditory symptoms,
and treatment can be medical in the rst instance, or with intratympanic steroids or
gentamicin.
• BPPV is a common cause of episodic vertigo, which is diagnosed with positional
manoeuvres; management includes particle repositioning procedures that are highly
effective.
• VM is a common cause of episodic vertigo, and treatment of frequent or disabling
symptoms is usually with medical management.
• PPPD is a functional dizziness disorder.
• VR is offered for patients with head or visual motion intolerance, or imbalance, related
to vestibular disorders.
Further Reading
1. Lopez-Escamez JA, Carey J, Chung WH, et al. Diagnostic criteria for Meniere’s disease
according to the Classication Committee of the Barany Society. HNO 2017; 65(11):
887–93. doi: 10.1007/s00106-017-0387-z.
2. IHS. Headache Classication Committee of the International Headache Society (IHS)
e International Classication of Headache Disorders, 3rd edition. Cephalalgia 2018;
38(1):1–211. doi: 10.1177/0333102417738202.
3. Popkirov S, Staab JP, Stone J. Persistent postural-perceptual dizziness (PPPD): a common, characteristic and treatable cause of chronic dizziness. Practical Neurology 2018;
18(1):5–13. doi: 10.1136/practneu rol-2017-001809.
40 e Ear
CONDITIONS OF THE EXTERNAL EAR
7. CONDITIONS OF THE EXTERNAL EAR
Wax
Wax is a combination of desquamated skin and cerumen, formed by glands in the base of the
hair follicles of hair-bearing skin, in the lateral third of the external auditory canal (EAC).
Most external canals are self-cleaning, but a common nding on otoscopy is partial occlusion of the canal that is usually asymptomatic. Wax is amenable to removal by non-specialists
by water syringing most commonly using a pressure-controlled irrigator. Specialists prefer
to remove wax under direct vision with the aid of a headlight, microscope, or endoscope,
via a speculum with ear wax hooks or similar instruments, or suction. Various wax-soening agents including olive oil and sodium bicarbonate are frequently used to ease removal.
However, there is no evidence to support the use of one agent over another.
1
Otitis Externa
Otitis externa (OE) is characterised by erythema and oedema of the EAC, associated with
itch, pain, discharge, and debris in the meatus. Predisposing factors include a narrow/
obstructed EAC, dermatological conditions of the ear canal (e.g. eczema or psoriasis), maceration of the skin, excessive moisture (swimming or bathing), and active chronic otitis media.
OE aects approximately 10% of the population during their lifetime. Water and moisture
are thought to change the ora in the ear from predominantly gram-positive organisms to
gram-negative organisms. Most patients will culture multiple organisms, with Pseudomonas
aeruginosa being the most prevalent.
e main treatment of OE is a combination of regular topical medications, with or without
an oto-wick/aural toileting, and prevention of aetiological factors. A topical combination of
antibiotic/steroid drops or spray, for a minimum of 7 days, is regarded as the best rst-line
treatment; however, randomised trials comparing treatments are few and with small patient
numbers.2 Systemic antibiotics are indicated for patients with pinna cellulitis or evidence
of necrotising OE (see later). Most otolaryngologists reserve microbiological investigations
for refractory cases. Water precautions using cotton wool with petroleum jelly or custom
moulds can be helpful in patients with recurrent infections. In patients with refractory OE,
sensitivity to topical agents including steroid drops may contribute to ongoing symptoms.
Patients with recurrent OE that is exacerbated by air-conduction hearing aids may benet
from bone conduction devices or middle ear implants, depending on the inner ear function.
Otomycosis
Otomycosis or fungal OE accounts for approximately 10% of OE cases. It is more common
in hot, humid climates or following prolonged treatment with topical antibiotics. e diagnosis must be considered in patients with OE who fail to respond to appropriate treatment.
Aspergillus accounts for 80–90% of cases, with Candida accounting for the remaining cases.
e most common nding is discharge with debris and occasionally visible fungal hyphae or
spores. Treatment is similar to OE but with topical antifungal drops, and longer courses of
treatment are typically required.
Furunculosis
Furunculosis is an infection of a single hair follicle. e lateral aspect of the EAC, which has
hair follicles, is the site of furunculosis. Bacterial infection of the hair follicle can progress
from a deep skin infection to form a local abscess with associated cellulitis and oedema.
Symptoms can be similar to severe OE; however, characteristically oedema and inammation are restricted to the lateral canal. Staphylococcus aureus is the most common organism.
Recurrent furunculosis may result from colonisation of the external nares by S. aureus and
decolonisation therapy should be considered in these cases.
e Ear 41
CONDITIONS OF THE EXTERNAL EAR
Treatment choices include the following:
Aspiration or incision and drainage for an abscess
•
Oral or intravenous anti-staphylococcal antibiotics
•
Topical antibiotics/antiseptics
•
Perichondritis
Perichondritis is an infection or inammation involving the perichondrium of the externa l ear.
It occurs usually secondary to trauma and is mostly caused by P. aer ugi nosa but can be polymicrobial. It should be dierentiated from cellulitis of the ear, classically by being lobule sparing.
e presentation is usually with dull pain increasing in severity, and there is inammation
of the cartilaginous pinna. Relapsing polychondritis is an autoimmune condition, and it may
present similarly but is dierentiated on the basis of the systemic nature of the condition,
which may also aect joints, the eye, and cartilage of the nose and airway. Perichondritis
is treated with prompt broad-spectrum antibiotics with anti-pseudomonal cover, ideally
intravenously. If there is a subperichondrial abscess it should be drained. If perichondritis is
untreated, it could result in avascular necrosis of the cartilage and deformity of the pinna.
Myringitis
Myringitis is inammation of the tympanic membrane (TM). Acute bullous myringitis
(BM) and chronic granular myringitis (GM) are dierent clinical entities.
BM is characterised by bullae or vesicles on the TM, which are believed to develop between
the middle brous and outer squamous layers. e aetiological pathogens are similar to acute
otitis media (AOM) such as Streptococcus pneumoniae, Haemophilus inuenzae, and respiratory viruses. It is more common in winter and in children between the ages of 2 and 8 years.
is diers from AOM, which is more common in children under 2 years.
Patients typically present with unilateral sudden-onset severe otalgia lasting for 1–2 days.
ere is a high incidence of associated middle ear eusion resulting in a conductive loss.
However inner ear involvement with sensorineural hearing loss (SNHL) and vertigo is not
uncommon and usually resolves spontaneously. As BM is usually self-limiting the treatment
is usually symptomatic.
GM is a chronic inammation characterised by the de-epithelialisation of the outer (squamous)
layer of the TM being replaced by granulation tissue, with the absence of middle ear disease. e
aetiology is unknown, but there is a high incidence following myringoplasty. It usually presents
with otorrhoea and granulation on the TM. Treatment of GM includes microsuction/debridement with topical antimicrobial, steroid, or astringent preparations for prolonged periods. Laser
resurfacing and surgical excision + graing are usually reserved for recalcitrant cases.
Acquired Canal Atresia
Acquired canal atresia is progressive stenosis leading to closure of the EAC resulting in a blind
sac. is is usually following chronic ina mmation and occurs in the medial aspect of the EAC.
Solid atresia consists of a continuous block of brosis from the TM. Membranous atresia is
typied by a brous tissue that has a covering of canal skin on both sides, separating the ear
canal into two segments. e medial segment inevitably collects keratin, which may become
erosive. Stenosis may also cause this. Atresia may be caused by the following processes:
Inammation
•
Chronic OE
•
Chronic otitis media
•
Trauma
•
Burns
•
Surgery especially involving a meatal approach
•
It is useful to use computed tomography (CT) imaging to help identify the extent of atresia
and ascertaining the presence of middle ear pathology.
42 e Ear
CONDITIONS OF THE EXTERNAL EAR
Patients with atresia will have a conductive hearing loss. is may be managed in some cases
with a conventional behind-the-ear hearing aid (especially when the atresia is medial), a
bone-conducting device, a middle ear implant, or surgical treatment. Surgery involves
removing the brosed segment, down to the lamina propria of the TM. e exposed bone
and TM is sometimes graed with a split-thickness skin gra. ese patients require intensive post-operative aural toilet and restenosis is not uncommon.
Exostosis
Exostoses are benign growths of the periosteal bone in the medial aspect of the external ear
canal. Exostoses are usually multiple and bilateral. ey are usually found incidentally and
are associated with a history of prolonged cold-water exposure.
e diagnosis of exostosis is made clinically and can be dierentiated from osteomas, which
are generally unilateral, solitary, arise from the lateral EAC, and can oen be pedunculated
as opposed to the sessile base of exostoses. Most exostoses are incidentally found and are
asymptomatic; however, more severe cases may result in keratin accumulation, recurrent
OE, and rarely cholesteatoma. Treatment may include regular aural toilet or surgical excision. Avoidance of cold water may help prevent progression.
Keratosis Obturans and External Auditory Canal Cholesteatoma
Keratosis obturans (KO) results from failure of epithelial migration, which causes accumulation of keratin in the medial bony EAC with expansion and remodelling.
EAC cholesteatoma is characterised by invasion of squamous epithelium into bone (Table 7.1
and Figur e 7.1).
Table 7.1 Differential diagnosis of non-neoplastic conditions eroding the bony EAC
External auditory canal
Keratosis obturans
Aetiology Abnormal epithelial
migration
Symptoms
and
ndings
Pathology Keratin plug
Treatment Remove plug
Differential
diagnosis
Source: Modied from Shire JR, Donegan JO. Cholesteatoma of the external auditory canal and
keratosis obturans. Am J Otol 1986; 7: 361–364.
Severe otalgia
Conductive hearing loss
Lung or sinus disease
Younger
Occasionally bilateral
Tympanic membrane
thickened
Widened deep canal
Hyperaemia of skin
canal with granulations
Treat granulations
Occasionally biopsy
Canaloplasty
Wax impaction with
infection
Otitis externa
Neoplasm
cholesteatoma
Abnormal bone leading to
epithelial migration into
bone
Otalgia mild
No hearing loss Itchiness
Older
Usually unilateral
Keratin in random pattern
Tympanic membrane normal
Localised osteitis/erosion of
ear canal usually
posteroinferior
Sequestration of bone
Surgically remove
cholesteatoma graft with
cartilage and fascia
Biopsy
Necrotising otitis externa
Neoplasm
Necrotising otitis
externa
Immunocompromise
Patient with necrotic
bone in ear canal
Severe penetrating pain
Cranial nerve palsy
Diabetic/renal failure or
otherwise
immunosuppressed
Raised inammatory
markers
Chronic inammation
Pseudomonas
aeruginosa
Treat cause of
immunosuppression
High-dose long-term
antibiotics
Surgical debridement
Malignant neoplasm
e Ear 43
CONDITIONS OF THE EXTERNAL EAR
Figure 7.1 (a) Canal cholesteatoma – a sac of canal skin invades bone. (b) Keratosis obturans –
the bony canal is widened.
Necrotising Otitis Externa
Necrotising otitis externa (NOE) is a skull base osteomyelitis of the temporal bone occurring
as a complication of OE. It was previously termed malignant OE due to its associated mortality.
Whilst oen described as a rare condition there is evidence of increasing incidence, the cause of
which is unclear. ere is no universally agreed diagnostic criteria; however, most would agree
that the condition presents with otalgia, oen severe and nocturnal; otorrhoea; and evidence
of ear canal inammation, frequently with granulation tissue inferiorly. It is almost invariably
seen in immunocompromised individuals either due to age, diabetes, or other causes.
Progression of disease can result in cranial neuropathies, including facial and bulbar nerves.
Diagnosis is clinical combined with radiological assessment which may utilise CT (showing bone
erosion) and contrast magnetic resonance imaging (MRI) and bone scans. Biopsy of granulation
tissue should be considered to exclude malignancy. Treatment should be guided by microbial
sampling. P. aer uginosa is the most common pathogen and therefore agents should target this.
Anti-microbia l treatment is usua lly prolonged, typically la sting 6–12 weeks, and may benet from
a multidisciplinary guidance by microbiology colleagues. Rarely NOE can be fungal. Treatment
response is assessed clinically (most importantly resolution of pain), with inammatory markers
and in some units with imaging (nuclear medicine scans or MRI). e role of surgery is limited
to obtaining microbiological samples, removing bony sequestra, and draining abscesses. ere is
evidence from cases series for the therapeutic benet of hyperbaric oxygen in NOE.
Osteoradionecrosis of the Temporal Bone
Osteoradionecrosis of the temporal bone is dened as necrosis of a previously irradiated
petrous temporal bone which fails to heal. e temporal bone is dense, which results in
greater absorption of radiation than so tissue. e tympanic ring is particularly susceptible, likely due to its poor vascular supply.3 Oen there is loss of skin and so tissue exposing bone, bony sequestration, and secondary infections. In an established case, ruling out an
underlying recurrence of malignancy is vital.
Localised disease can be managed with regular aural toileting of the sequestra and topical
antibiotic treatments. For more extensive cases or those complicated by chronic infection,
prolonged antibiotic treatment and surgical debridement with possible reconstruction using
vascularised tissue may be required.
Otalgia
Otalgia can be primary, arising from the ear, or secondary/referred, as a result of pathology elsewhere. In children otalgia is usually otogenic; however, in adults referred otalgia is
more common. e sensory supply to the ear is complex and therefore the potential origin of
the referred otalgia is widely distributed, which can cause diagnostic diculty (Fig u re 7.2).
44 e Ear
CONDITIONS OF THE EXTERNAL EAR
Auriculotemporal N. (CN V)
Po
Sensory aer
•
•
Etiogles in Referred O
•
• Herpes zoster
• Geniculate neuralgi
sterior Auricular N. (CN VII)
Posterior wall of EAC
Posterior auricular skin
Cerebeliopontine angle tumors
Posterior Auricular N.
Lesser Occipital N. (C2, V3)
Sensory aerents
• Posterior auricle
• Pre-auricular skin overlying parotid
• Skin overlying mastoid
Etiogles in Referred Otalgia
• Cervical spine degenerative diseases
• Whiplash/trauma
• Cervical menigiomas
ents
talgia
a
Sensory aerents
• Anterior auricle
• Tragus
Etiogles in Referred Otalgia
• TMJ disease
• Dental pathology
• Parotid tumour/infection
Jacobsons N. (CN IX)
Sensory aerents
• Medial surface of TM
• Eustachian tube
• Promontory
Etiogles in Referred Otalgia
• Tonsilitis/pharnygitis
• Eagle’s syndrome
• Sinusitis
• Pharyngeal tumour
Arnold’s N. (CN X)
Sensory aerents
• Floor of EAC
• Concavity of concha
• Lateral surface of TM
Etiogles in Referred Otalgia
• GERD
• Laryngeal tumor
C1
• Thyroid tumor/inflammation
C2
C3
Figure 7.2 The origin of referred pain can be grouped into the following: Malignancy: Malignant
tumours of the upper aerodigestive tract can present with otalgia as part of a symptom complex or
can be the sole symptom. Therefore, a full examination of the oral cavity and exible nasoendoscopy
is essential for patients with unexplained otalgia. Dental: Dental causes are the most common
cause of referred otalgia and can be referred from the teeth, periodontal tissues, or the temporomandibular joint (TMJ). The pain in acute apical abscess tends to be severe and can be localised;
however, if the inammation is mild and chronic, localisation may be poor. In TMJ dysfunction
there is diffuse pain in or around the TMJ joint, including tenderness of the masticatory muscles.
Intraoral palpation of the lateral and medial pterygoids frequently reveals tenderness in patients with
referred otalgia. Treatment of TMJ pain includes a soft diet and analgesics including non-steroidal
anti-inammatories. Other treatment options include tricyclic antidepressants, occlusal splints, and
TMJ surgery. Cervical: Cervical spine degenerative disease is an increasingly common cause of
referred otalgia. The pain is usually retroauricular or infra-auricular and related to neck movement.
Neuralgia: Numerous neuralgias have been implicated as causes of referred otalgia, but all are
rare. Trigeminal and post-herpetic neuralgias are the most common. In glossopharyngeal neuralgia,
there can be severe transient pain in the ear usually triggered by swallowing. Jacobsen’s nerve has
been implicated as well. If there is an elongated styloid process or mineralisation of the stylohyoid
ligament it can result in neuralgia known as Eagle’s syndrome. Depending on the cause of neuralgia,
treatment options include neuropathic pain killers, styloidectomy, section of the tympanic branch of
the glossopharyngeal nerve, or microvascular decompression. Neurology and pain team consultations may be helpful in management. For patients with a unilateral otalgia and unclear cause, further
imaging with contrast enhanced magnetic resonance imaging scan should be considered.
e Ear 45
EUSTACHIAN TUBE DYSFUNCTION
Otalgia in the absence of discharge, hearing loss or otoscopic abnormality should raise suspicion of referred otalgia.
KEY POINTS
• The incidence of NOE appears to be increasing, and the complex management of
these patients may benet from an multidisciplinary team approach.
• Underlying malignancy should be excluded in patients presenting with granulation or
bone erosion in the EAC.
• Patients with unilateral otalgia should have a full head and neck examination; if cause
is not identied imaging with contrast-enhanced MRI should be considered.
Further Reading
1. Roland PS, Smith TL, Schwartz SR, et al. Clinical practice guideline: cerumen impaction. Otolaryngol Head Neck Surg 2008; 139(3 Suppl 2), S1–S21.
2. Rosenfeld RM, Schwartz SR, Cannon CR, et al. Clinical practice guideline: acute otitis
externa. Otolaryngol Head Neck Surg 2014; 150(1 Suppl), S1–S24.
3. Ramsden RT, Bulman CH, Lorigan BP. Osteoradionecrosis of the temporal bone. J
Laryngol Otol 1975; 89, 941–55.
8. EUSTACHIAN TUBE DYSFUNCTION
Introduction
e Eustachian tube (ET) is a narrow passage approximately 40 mm in length that connects
the nasopharynx and the middle ear (ME). e medial two-thirds is formed from cartilage
and other so tissue, whilst the lateral third is within the temporal bone. e lumen of the
ET is lined with respiratory-type cuboidal epithelium and has an hourglass shape, with the
anatomical isthmus located within the cartilaginous portion, approximately 20 mm from
the nasopharyngeal ostium. In the healthy state the cartilaginous ET lumen is collapsed for a
5- to 10-mm long segment, usually located a few millimetres from the isthmus.
e ET opening may be active or passive. Active opening typically lasts 300–600 ms and is
due to contraction of paratubal muscles, predominantly the tensor veli palatini. Most active
opening is involuntary and due to swallowing. Passive ET opening occurs if the nasopharyngeal or ME pressure exceeds the periluminal pressure that holds the lumen closed, for
example, during a Valsalva (forcible exhalation with the nose and mouth occluded).
e ET is shorter and more horizontal and compliant in children, which may contribute to
an increased incidence of ME disease in children.
ETD in Clinical Practice
e ET has three primary functions: (1) gas transfer and pressure equalisation between the
ME and nasopharynx; (2) clearance of ME secretions via both muscular action and mucociliary transport; and (3) prevention of sound, uid, and pathogen reux into the ME from
the nasopharynx.
ET dysfunction (ETD) is usually caused by failure of the tube to adequately open or close. It
is important to recognise ET function as a continuous spectrum, with a permanently open
46 e Ear
EUSTACHIAN TUBE DYSFUNCTION
Figure 8.1 Cross section along the length of the Eustachian tube.
(patulous) tube at one end, and a permanently closed (obstructed) tube at the other. e
healthy state falls in the middle of this spectrum.
Obstructive ETD, due to inadequate ET opening, is estimated to aect 0.9% of British adults.
Reported symptoms are typically aural fullness or pressure, popping or crackling sounds,
tinnitus, mued hearing, and otalgia. Some patients with obstructive ETD only experience
symptoms in situations of rapid ambient pressure change, such as when ascending or descending in a plane, or undertaking scuba diving. is may represent a milder form of the disorder,
although objective testing does not fully support this. Most ME disorders have a multifactorial
etiology; however, an association has been demonstrated between obstructive ETD and otitis
media with eusion, chronic otitis media, tympanic membrane retraction, and cholesteatoma.
Patulous ETD, due to inadequate ET closure, is estimated to aect 0.3% of the population,
although with screening, prevalence has been found to be as high as 6.6% in adults. Symptoms
are similar to those for obstructive ETD, although oen with a heightened awareness of the
patient’s own voice (autophony) and breath sounds (aerophony). Patulous ETD is usually
intermittent, with symptoms oen worse with exercise and better when supine. Sequelae of
patulous ETD include atelectasis, retraction pockets, perforations, and cholesteatoma as ME
pressure can vary from negative to positive with sning and Valsalva, respectively.
It is useful to classify ETD as acute or chronic if present for more than 3 months. ere
have been further attempts to develop a classication for ETD, notably making a distinction
between baro-challenge induced and other forms of obstructive ETD.
e pathogenesis of ETD is poorly understood. Chronic obstructive ETD is oen attributed
to mucosal inammation, and it has been associated with gastroesophageal reux, allergy,
rhinosinusitis, and smoking, though to date evidence of a causal relationship is lacking.
Failure of active ET opening appears to account for the association between cle palate and
e Ear 47
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