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188
CHAP TER6 Theear
cInjuries
Injuries localized to the external or middle ear include auricular haematoma, external auditor y canal abr asion or laceration, tympanic
membrane perforation, and ossicular chain dislocation. In addition,
barotrauma, such as a slap to the ear or a blast injury, can cause a tympanic membrane perforation or ossicular chain dislocation.
eTemporal bone fractures
These represent roughly 20% of all skull fractures. Blunt trauma to the
lateral surface of the skull (the squamous portion of the temporal bone)
often results in a longitudinally orientated fracture. These follow the axis
of the exter nal auditory canal to the middle ear space. In a longitudinal
fracture, the otic capsule is spared. In contrast, a blow to the occiput may
go through the foramen magnum and result in a transverse fracture of
the temporal bone. These cour se directly across the petrous bone, fracturing the otic capsule and geniculate ganglion (facial nerve). Longitudinal
fractures and transverse fractures represent 80% and 20% of temporal
bone fractures respectively.
Symptoms and signs include:
• Hearingloss
• Nausea and vomiting
• Vertigo
• Battle’s sign (post- auricular ecchymosis)
• External auditory canal laceration with bony debris within thecanal
• Haemotympanum
• CSF otorrhoea.
CT of the head is usually per for med due to the head trauma. Highresolution scanning of the temporal bone is valuable in delineating the
extent of the frac ture, but it is not required unless a complication is suspected (e.g. otic capsule fracture, facial nerve injur y, or CSF leak). Tuning
fork tests should always be per formed on patients with a temporal bone
fracture. The Weber tuning fork test r adiates to the fractured ear if conductive hearing loss is present and radiates to the contr alateral ear if
sensorineural hear ing loss is present . The presence or absence of facial
nerve paralysis should be documented in all patients with tempor al bone
fractures. Complications of these fractures include:
• Conductive hearingloss
• Sensorineural hearing loss and vertigo
• Facial nerveinjur y
• CSFleak
• Perilymphatic stula (uctuating vertigo and sensorineuralloss).
cCSFleak
There is usually clear otorrhoea or rhinorrhoea (CSF leak through
Eustachian tube into the nasophar ynx if ear dr um is intact), and a salt y
taste. Look for the ‘halo sign’. Fluid analysis (bet a- 2 transferrin) and CT
usually conrm the diagnosis. Management is initially bed rest, head
elevation, and diuretics (mannitol, acetazolamide, furosemide). If persistent, a lumbar drain or surgical exploration may be required. Refer
urgently to ENT/ neurosurgeons.
cDizziness following eartrauma
This is usually self- limiting with mild inner ear injury (post- concussion
syndrome). Injury to the vestibular labyrinth may cause a complete unilateral vestibular decit. Rarely it can be due to perilymphatic stulas.
High- resolution C T of temporal bones may be required.
cAuricular haematoma
These occur following direct trauma (Figure 6.1). Bleeding occurs in
the subperichondrial space supercial to the cartilage. This can result
in car tilage necrosis and predispose to infection, especially if there is
an overlying skin laceration. A haematoma presents as a painful, tender swelling with associated skin discolouration. Principles of treatment
are evacuation of the haematoma, reapposition of perichondrium to the
underlying car tilage, and removal of any ‘dead space’ to avoid infection
or a ‘cauliower ear’ deformity. Prompt wide- bore needle aspiration is
often eec tive. Incision and drainage may be required in cases of recurrence or in late presentation. Gentle pressure can be applied by means
of a pressure bandage, mattress suturing, or a silicone mould. Do not put
the bandage on too tight, this can result in car tilage necrosis. Early review is
required as haematoma can readily re accumulate.
cSeroma ofthepinna
This is serous uid that has collected between the perichondrial layer of
the pinna and the underlying cartilage. It can occur spontaneously or as
the result of trauma. Treatment involves aspiration and a pressure dressing; however, there is a high propensit y for recurrence.
INJURIES
189
Figure6.1 Auricular haematoma.
Repro duced from At las of Operat ive Maxi llofaci al Trauma Su rger y:Pri mary Re pair of F acial
Injuries, ‘Sof t Tissue Inj urie s’, 2014, Figu re14.1, eds M. Pe rry and S. H olme s, Copy righ t © 2014,
Spri nger- Verl ag Lond on. Wit h permiss ion of Sp ring er Nat ure.
190
CHAP TER6 Theear
cTraumatic perichondritis
Trauma, with haematoma formation and subsequent infection, is the
commonest cause. O ther causes of perichondritis include malignant
otitis externa , following ear piercing, or other sharp trauma which can
introduce infection directly. It can also occur following mastoid surgery.
Patients present with dull pain, er ythema, and inammation of the pinna.
If lef t untreated, abscess formation and cartilage necrosis can occur.
The most frequent microbe is Pseudomonas aeruginosa; others include
Staphylococcus aureus and Escherichia coli. Treatment in the majority of
cases is with IV antibiotics, with the addition of antimicrobial ear drops in
cases of suspected otitis externa. Incision and drainage may be required
where abscess formation is evident.
cLacerations/ tears and partial avulsions involving
theEAM
Injuries to the external meatus/ canal most commonly occur when a
patient is tr ying to remove his or her own earwax with a cotton- tipped
applicator or probe. The injur y is usually a simple abra sion or laceration.
Lacerations may also occur in association with fractures of the mandibular condyle. Treatment consists of using an antimicrobial drop to prevent
bacterial or fungal infection. Patient s with diabetes have a high risk of
developing external otitis from this type of injury. These patients need to
be followed up closely. Occasionally tears are associated with an underlying fracture. Meticulous repair is required to avoid trapping skin (causing implantation cholesteatoma) and canal stenosis.
cBarotrauma
A sudden pressure change in middle ear cleft can occur during diving or
ying. Symptoms var y depending on the pressure gradient:
• Otalgia (pressure dierential of 60mmHg)
• Eustachian tube dysfunction (pressure dierential of 90mmHg)
• Tympanic membrane per for ation (pressure dierential of
100 – 50 0mmHg).
Patients present with acute pain, haemotympanum, bloody otorrhoea,
acute hearing loss, dizziness, and tinnitus.
Types ofbarotrauma
• Middle ear squeeze:on a scent , the Eustachian tube may close, failing
to relieve pressure in the middle ear with decreasing pressure. This
can cause an ear drum perforation or haemot ympanum.
• Round window rupture may occur with an acute increase in CSF
pressure transmitted through the perilymph.
• Inner ear decompression sickness (Caisson disease):with increased
pressure (diving), nitrogen becomes more soluble and enters body
uids. If decompression occurs rapidly (rapid ascent), small gas
emboli may form and occlude micro- blood circulation leading to end-
organ damage causing blindness, deafness, paralysis, ordeath.
INFECTIONS OF THE EAM AND PINNA
cTympanic membrane perforation
This can occur following insertion of a cotton- tipped applicator, pin,
or pencil, or following barotrauma (slap to the ear or a blast injury).
Perforation is diagnosed by otoscopy. It is important to note how much
of the tympanic membrane has been perforated. A central perforation
does not involve the annulus of the eardrum, whereas a marginal perforation does. The Weber tuning fork test should be per formed and the
eyes checked for nystagmus. If the sound does not radiate to the aected
ear and the patient has nyst agmus, it is likely that an inner ear injury (perilymphatic stula or stapes dislocation) ha s also occurred and requires
urgent treatment. If no evidence of sensorineural hearing loss is found,
no specic treatment is required. Traumatic tympanic membrane perforations, especially central perforations, typically heal spontaneously.
Strict dr y ear precautions should be followed to prevent water from
getting into the ear. Instructions include no swimming and the placement of a cotton ball thoroughly coated with petrolatum (Vaseline®)
in the aected ear during bathing. If the per foration has not healed by
3months, a tympanoplasty may be needed.
cOssicular chain dislocation
Ossicular chain dislocation with an intact eardr um manifests as a maximal (60 dB) conductive hearing loss. Ossicular chain dislocation with a
perforated eardrum results in lesser degrees of hearing loss. Treatment
is middle ear exploration and ossicular chain reconstruction, with tympanoplasty if needed.
cInfections ofthe external auditory
meatus andpinna
cAcute otitis externa (‘swimmer’sear’)
This is often caused by a bacterial or fungal (lobomycosis, also known
as Singapore ear) infection involving the sk in of the external auditory
canal. Predisposing factors include aggressive ear cleaning, lack of cer umen, digital trauma (e.g. cotton buds, ngernails) and retention of water
(swimming). Pseudomonas aeruginosa is the most common pathogen, but
others include Gram- negative bacilli, staphylococci, and fungi. It is impor-
tant to rule out malignant external otitis (look for granulation tissue in the
canal, cranial nerve involvement , and diabetic patients).
Patients present with severe ear pain, tragal tenderness, and pr u-
ritus. The EAM is swollen and oedematous with purulent discharge.
There may be conductive hearing loss. In otomycosis, otoscopy reveals
greyish white, thick debris with its characteristic ‘wet blotting paper’
appearance.
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CHAP TER6 Theear
Management
• Thorough aural toileting with ne suction.
• Topical ear drops (acetic acid, antibiotic, or antibiotic/ corticosteroid
combination drops for 7– 10days).
• Consider placing a wick if the exter nal auditory canal is too
oedematous.
• Oral antibiotics are not required unless there are signs of
periauricular cellulitis, or systemic illness.
• Avoid prescribing antibiotic and steroid drops in fungal otitis externa.
• Advise the patient to keep the ear dr y and avoid self- cleaning of
theears.
cChronic otitis externa
Thickening of the EAM skin can occur as a result of longstanding infection
or inammation. Often the patient’s ear feels itchy and they scratch the
canal prolonging irritation and symptoms.
cEczematous otitis externa
This is a dermatological condition that aects the EAM (e.g. atopic dermatitis, contact dermatitis, psoriasis).
cPerichondritis
This is an infection of the perichondrium of the ear cartilage. It may arise
from extension of inadequately treated otitis externa, periauricular cellulitis, or following exposure of the cartilage from trauma . It is also a
known complication of surgery involving incisions within the cartilage
(e.g. correction of bat ears). Clinically the pinna is tender, erythematous, and warm. Pseudomonas aeruginosa, Staphylococcus aureus, and
Streptococcus are the common organisms involved. Treatment is with
high- dose systemic antibiotics. There is a risk of cauliower ear deformity if not treated quickly or ag gressively enough.
cInfections ofthe middleear
cOtitismedia
Inammation of the middle ear (otitis media) is a common condition, usually occurring bilater ally. It may be acute or chronic. Acute otitis media
is commonly seen in children often following an upper respiratory tract
infection. It may be viral or bacterial in origin. Streptococcuc pneumoniae
and Haemophilus inuenzae are common bac terial pathogens.
cAcute otitismedia
Acute otitis media begins with mucosal inammation and oedema, resulting in exudates in the middle ear. Oedema prevents drainage through the
Eustachian tube and as pus accumulates, pressure builds up. This causes
the ear drum to bulge. Untreated, the t ympanic membrane eventually
perforates. As the middle ear can now drain, the infection will slowly
resolve.
INFECTIONS OF THE MIDDLEEAR
Presentation
Patients complain of a throbbing ear ache (otalgia) which progresses in
intensity until perforation of the drum relieves some of the pressure.
Aconductive deafness is usually present , possibly with tinnitus. Patients
are often systemically unwell. The tympanic membrane r anges in appearance from the loss of the light reex, to red and bulging, culminating in
perforation with discharge. Deafness in children is a treatable cause of
developmental delay— early detection and appropr iate investigation and
treatment are therefore imperative.
Management
• Antibiotics:penicillins are often the rst line of treatment , but culture
and sensitivities of known pathogens may alterthis.
• Analgesics/ antipyretics:paracetamol,NSAIDs
• If a bulging tympanic membrane persists, despite adequate antibiotic
therapy, myringotomy under general anaesthetic enables the ear
todrain.
• Patient s who present with a discharging ear (perforation) should be
started on broad- spectrum antibiotics after microbiology swabs have
been sent for culture and sensitivities.
• If signs and symptoms do not resolve, consider altering the choice
of antibiotic and consider under lying infection elsewhere (mastoid,
nasopharynx, sinuses).
cOtitis media witheusion:‘glueear’
This condition is said to aect 30 – 40% of children at some stage in their
development and presents with deafness and a mild otalgia, occasionally
associated with tinnitus. Otitis media with eusion is due to a build- up
of uid in the middle ear and although many cases will spontaneously
resolve, a short course of antibiotics may prove useful if there is suspicion of underlying infection. If pain or hearing loss persists for >10 weeks,
surgery should be considered. Myringotomy and grommet insertion is performed under general anaesthesia. A small incision is made in the tympanic membrane; a plastic grommet (drainage tube) is inser ted. These
often self- extrude after an aver age period of 6months— repeated insertions may be necessary if the eusion persists. Adenoidectomy may be
benecial in the long- term treatment of ‘glueear’.
cChronic suppurative otitismedia
Chronic suppurative otitis media (CSOM) is a chronic inammatory process aecting the middle ear and mastoid cavity. Patients can present
with painless per sistent or recurrent otorrhoea, with an associated tympanic membrane perforation. There is often some degree of conductive hearing loss. On auroscopic examination, the position of tympanic
membrane perforation is important. Atticoantral perforations are more
likely to be associated with cholesteatoma (described as ‘unsafe’ CSOM).
‘Safe’ CSOM is seen in those cases without evidence of cholesteatoma.
There may also be evidence of granulation tissue in the external auditory
canal. ENT referr al is of ten required to carr y out aural cleaning to allow
eective administration of topical antibiotics.
193
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CHAP TER6 Theear
Symptoms of otalgia, vertigo, systemic upset, or evidence of postauricular
inammation should prompt urgent referral to exclude intratemporal or intracranial involvement.
cHerpeszoster
A rare complication of varicella zoster virus (V ZV ) reactivation is herpes
zoster oticus (Ramsay Hunt syndrome) which classically presents as a
triad of lower motor neuron facial paralysis, otalgia, and vesicles in the
auditory canal and auricle. Some patient s may also present with tinnitus
or hyperacusis and vertigo. Commonly patients are aged over 60years
but it can aect all ages. VZ V reactivation in the geniculate ganglion can
also spread to involve the eight cranial nerve. Cases have been reported
in association with herpes simplex t ype 2. Diagnosis is based on clinical ndings. Eye care and early treatment with steroids and antivirals
is recommended, but there is little evidence of ecacy and complete
recovery, especially of facial par alysis which is less likely compared to
Bell’spalsy.
Be careful prescribing steroids in VZV (and other viral) infections. If there
is viraemia, the patient is at risk of developing viral encephalitis. Discuss the
need for steroids with ENT (or follow local guidelines).
cInfections ofthe adjacentbones
cOsteomyelitis ofthe skull base (necrotizing
or malignant external otitis)
This is an extension of infection from the EAM into the temporal bone,
resulting in progressive osteomyelitis. It is usually caused by Pseudomonas
aeruginosa and seen in immunocompromised patients (diabetics, HIV,
radiation exposure). Patients present with relentless severe otalgia (out of
proportion to patient’s signs), granulation tissue in the EAM, and cranial
nerve involvement. Diagnosis often requires CT of temporal bones, or
technetium or gallium bone scans. It may also require biopsy and culture
of the granulations. Untreated or late diagnosis can lead to cranial neuropathy, sinus thrombosis, septicaemia, and intracranial infections (meningitis), and carries mortality.
Management
This includes prolonged parenteral anti- Pseudomonas antibiotics (up to
6months), antibiotic/ corticosteroid ear drops (gentamicin with hydrocortisone), meticulous cleaning, and debridement. Hyperbaric oxygen
has been used in recalcitrant cases. Screen for diabetes.
cMastoiditis
Mastoiditis is another potentially serious complication of acute otitis
media. Infection passes into the mastoid air cells causing furth er suppuration and bone necrosis. Remember that infection can travel elsewhere—
always consider other potential complications. These include:
• Intracranial (meningitis, brain abscess, extra and subdural abscess,
Lateral sinus thrombosis)
• Extracranial (labyrinthitis, facial nerve paralysis, mastoiditis).
OTALGIA (‘E AR ACHE’) AND OTORR HOEA
Presentation
Patients complain of a persistent and throbbing pain with increasing deafness. Discharge is present which is usually creamy and may be profuse.
They are pyrexic and t achycardic. There is usually tenderness over the
mastoid prominence, of ten with a postauricular swelling that pushes the
pinna forwards. Otoscopy may show bulging of the roof or posterior wall
of the exter nal auditory canal. The tympanic membrane is usually red,
perforated, and discharging.
Investigation
Mastoid X- rays may show opacit y of the air cells. CT scans will give far
more information but are not always indicated.
Management
• Patient s often need admission for IV antibiotics and pain relief. If the
causative or ganism is unknown then broad- spectrum antibiotics are
given, e.g. amoxicillin and metronidazole.
• In the absence of a rapid or complete response to antibiotics or if a
subperiosteal abscess is present, surgery may be indicated. Acor tical
mastoidectomy is per formed. Here the mastoid air cells are opened
to remove any necrotic debris whilst leaving the middle ear intact.
cOtalgia (‘earache’) and otorrhoea
Otalgia is a common symptom and is usually due to local disease. But
pain may also be referred. If the ear looks normal, check distant sites (TMJ,
oropharynx, nasopharynx, larynx, teeth,etc.).
Localcauses
• Acute otitis externa— a short course of antibiotic/ steroid drops or
dressing may be required
• Furuncles (infected hair follicles)— drain and prescribe antibiotics
• Acute and ‘malignant’ otitis externa
• Perichondritis— the pinna is swollen and tender due to infection of
the cartilage
• Barotrauma
• Herpeszoster
• Tumours.
Facial palsy, disproportionately severe pain, and progressive deafness are
worrying features and warrant careful consideration.
Distant causes (referredpain)
Due to its var ied inner vation, pain can also arise secondarily from the
followingsites:
• Tonsillitis and upper respiratory tract disease
• Eustachian tube dysfunction
• Dental pathology
• Disorders of theTMJ
• Parotid disease
• The oropharynx and nasopharynx
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CHAP TER6 Theear
• The lar ynx and pharyn x
• Cervical spondylosis
• Malignancy of any of the above- listed, but particularly the
tonguebase.
Never forget tumours of the upper aerodigestive tract as possible causes of
earache in adult s.
cOtorrhoea
Discharge from the ear may arise from several causes. The commonest
is due to middle ear infections. The nature of the discharge may give a
clue to itscause:
• Watery:CSF oreczema
• Mucoid:chronic suppurative otitismedia
• Purulent:furunculosis or local abscess
• Bloody:trauma/ acute otitis media/ malignancy
• Foul smelling:cholesteatoma.
cDeafness
Hearing loss is extremely common and has a wide spectrum ranging
from a nearly undetectable degree of disability, to a profound loss. It
can present at any age. Nearly 10% of the adult population has some
hearing loss and around one- third of individuals over the age of 65 have
loss sucient to require a hearing aid. Hearing loss can result from
disorders of the auricle, external auditory canal, middle ear, inner
ear, or central auditory pathways. In general, lesions in the auricle,
external auditory canal, or middle ear cause conductive hearing loss.
Sensorineural hearing loss results from lesions in the inner ear or
eighth cranial nerve (Table 6.1). Sensorineural hearing loss may result
from damage to the hair cells caused by intense noise, viral infections,
fractures of the temporal bone, meningitis, cochlear otosclerosis,
Ménière’s disease, and ageing. Many drugs can produce sensorineural
hearing loss (e.g. salicylates, quinine, aminoglycosides, loop diuretics,
and some chemotherapeutic agents).
Classication ofhearingloss
Sensorineural
Nerve impulses are prevented from reaching the brain by a defect
of either the auditory nerve (CN VIII) itself or the functioning of the
cochlea.
Conductive
Sound is prevented from reaching the cochlea apparatus by some form of
mechanical obstruction in the outer or middleear.
Mixed deafness
A combination of sensorineural and conductive deafness in the sameear.
Table6.1 Aetiology ofsensorine ural hear ingloss
Aetiology Diagnosis
Developmental and hereditary
Syndromic Alport syndrome, Usher syndrome
Non- syndromic Large vestibular aqueduct syndrome
Infectious Otitis media, viral, syphilis
Pharmacological toxicity Aminoglycosides, loop diuretics
Tra uma Head injury, noise- induced, barotrauma
Neurological disorders MS
Bone disorders Paget disease
Neoplasms Acoustic neuroma, meningioma
Unknown aetiology Presbycusis, Ménière’s disease
Assessment
A simple clinical assessment may be made by an examiner repeating certain words at dierent intensities and at dierent distances to each ear
in turn. By convention this is recorded as (for example) WV @ 200cm
(whispered voice at 200cm).
Tuning forktests
• Rinne’s test:a 512hz tuning fork is str uck and held close to the ear; it
is then placed rmly on the ipsilateral mastoid process. The patient is
asked to say whether the tuning fork is heard better by BCorAC.
• AC >BC Rinne +ve (middle/ outer ear functioning normally).
• BC >AC Rinne – ve (defective middle/ outerear).
• Weber’s test :a struck tuning fork is held on the vertex of the
patient’s head. They are then asked to say whether the sound is
heard centr ally or more to one ear than theother.
• Conductive deafness:sound heard in deaferear.
• Sensor ineural deafness:sound heard in better hearingear.
• Audiometry specialist tests are carried out in soundproofedrooms.
Causes ofhearing loss inchildren
Deafness in children is a treatable cause of developmental delay – early detection and appropriate investigation and treatment are therefore imperative.
Otitis media witheusion (‘glueear’)
This is the commonest cause of deafness in children with around 60% of
cases going undetected in the rst year. Commonly presenting with hear ing loss and otalgia there is a higher incidence in children with Down’s
syndrome or cleft palate. Treatment in the shor t ter m involves antibiotics and decongestants, progressing to surger y if symptoms persist (myringotomy and grommets). Otitis media with eusion is rare in adults and
so further investigation must be undertaken to exclude a neoplastic growth.
Progressive unilateral sensorineural deafness must raise the suspicion of an
acoustic neuroma.
DEAFNESS
197