ENT - Ear Trauma & Infections

Question 1

External Ear Trauma

Pinna Haematoma
TM Perforation
Haemotympanum 
Lacerations 
Bites

Answer 1

1. ) Pinna Haematoma - see next slide
2. ) Temporal Bone Fracture - see next slides
3. ) TM Perforation - due to trauma or otitis media
   - causes pain and possible conductive hearing loss
   - watch and wait: advised to keep the ear dry, it should heal by itself within 6-8 weeks
   - myringoplasty if it hasn’t healed in 6 months
4. ) Lacerations - clean and close the skin with sutures
   - wound cleaning carried out under LA
   - consider tetanus boosters and antibiotic prophylaxis
   - skin coverage is essential, if significant skin loss, seek advice from a plastic reconstructive surgeon
5. ) Bites - ↑risk of infection from skin/oral commensals
   - leave wound open, wound irrigation and antibiotics

Question 2

Pinna Haematoma

Pathophysiology
Cauliflower Deformity
Management
Drainage

Answer 2

1. ) Pathophysiology - accumulation of blood/serum between cartilage and its overlying perichondrium
   - subperichondrial haematoma deprives cartilage of blood supply causing avascular necrosis of tissue
   - often due to blunt injury to the pinna (contact sports)
   - differential is an auricular pseudocyst
2. ) Cauliflower Deformity - complication if untreated
   - fibrosis –> new asymmetrical cartilage development
3. ) Management - urgent assessment by ENT
   - urgent drainage (<24hrs) and pressure dressing application to prevent re-accumulation of 2 layers
   - gauze padding over the ear and a tight headband applied, review in 24hrs, I+D if reaccumulates
   - simple needle aspiration is considered in small ones
4. ) Drainage - ideally performed in an operating theatre
   - LA (w/o adrenaline) instilled for a regional block
   - incision along the inside of the helical rim allows for the evacuation of the haematoma
   - dental roll can be placed on either side of the auricle to close the perichondrial space

Question 3

Temporal Bone Fracture

Classifications
Clinical Features
Management

Answer 3

1. ) Classifications - longitudinal (80%) or transverse
   - longitudinal: a lateral blow to the head and associated with conductive hearing loss
   - transverse: fronto-occipital head trauma associated with sensorineural hearing loss or facial nerve injury
2. ) Clinical Features
   - facial nerve palsy: most concerning, suggests direct nerve damage meaning low chance of recovery
   - Battle’s sign: post-auricular ecchymosis
   - haemotympanum: blood in the middle ear
   - CSF otorrhoea or rhinorrhoea
   - hearing loss: conductive or sensorineural, most cases resolve spontaneously
3. ) Management
   - full oto-neurological examination, CT if indicated
   - all should be admitted for neuro-observation
   - majority end up being managed conservatively

Question 4

Otitis Externa (‘Swimmer’s Ear’)

Pathophysiology
Clinical Features
Management
Malignant Otitis Externa

Answer 4

1. ) Pathophysiology - inflammation of external ear canal due to pathogen overgrowth due to disruption of the external ear canal’s protective mechanism. Causes:
   - interrupted wax formation (repeated water exposure), trauma (e.g. cotton buds) or blockage (e.g. debris)
   - bacterial: Pseudomonas most common (esp in swimmers, others include S aureus, S. epidermidis
   - in rarer cases, can be due to a fungal infection
2. ) Clinical Features
   - progressive ear pain with purulent discharge
   - itchiness, ear fullness, muffled hearing (discharge)
   - otoscopy: swollen, red, or eczematous ear canal/external ear
   - white/yellow discharge is bacterial, thick white grey w/ visible hyphae/spores suggests fungal
3. ) Management
   - topical antibiotics: gentamycin, Otomize ear spray (neomycin, dexamethasone, acetic acid) for 7-14 days
   - advised to keep the ear dry
   - codeine can be given for additional pain relief
   - PO flucloxacillin if the infection spreads to the external ear
   - referral to ENT: poor response to topical abx
   - swab discharge, micro-suction of pus/debris
   - severe: pope wick used to keep the canal open for treatment with topical antibiotics
   - antifungals for fungal infections
4. ) Malignant Otitis Externa - infection spreads from ear canal into the mastoid, temporal bones (osteomyelitis)
   - occurs in diabetics or immunocompromised patients
   - presents w/ chronic ear discharge despite treatment, severe ear pain, sometimes CN palsies (often CN VII)
   - treat w/ IV ciprofloxacin (covers Pseudomonas) AND topical Abx for an extended period (6wks)

Question 5

Acute Otitis Media (AOM)

Pathophysiology 
Clinical Features
Management
Antimicrobial Usage
Complications

Answer 5

1.) Pathophysiology - acute infection of the middle ear
- middle ear is a ‘continuation of the respiratory tract
so pathogen inc S. pneumonia, H.influenzae, Moraxella
- common in childhood (0-4) as their ET is short, wide, straight, which ↑likelihood of infection

2. ) Clinical Features
   - fever, malaise, coryzal sx, crying, poor feeding
   - ear pain: evident by ear pulling or cradling, irritability
   - ruptured TM: extreme pain that suddenly resolves followed by ear discharge (clear grey in AOM)
   - conductive hearing loss, cervical lymphadenopathy
   - TM is red +/- bulging or perforated w/ discharge
3. ) Management
   - often self-limiting (<3 days), analgesia, keep ear dry
   - TM perforation: keep ear dry, review in 6-8 weeks, avoid any ear/olive oil drops
   - consider admission if: <3mths w/ temp >38°C or 3-6 mths >39°C, AOM complication, cochlear implant
   - recurrent AOM: surgery (grommet insertion)
4. ) Antimicrobial Usage - PO amoxicillin, used only if:
   - systemically unwell, unwell >4 days w/o improvement
   - perforation or ear discharge (swabs before abx)
   - RF for complications: immunosuppressed, CHD
   - <2yrs with bilateral AOM
5. ) Complications - must assess for these
   - CN VII function, labyrinthitis, intracranial: mastoiditis, meningitis, intracranial abscess, sinus thrombosis
   - mastoiditis: boggy, red swelling behind the ear, IV abx for treatment, mastoidectomy if no improvement
   - petrositis: spreads to petrous temporal bone causing Gradenigo triad: otorrhoea, deep pain, CN VI palsy

Question 6

Otitis Media w/ Effusion (‘Glue Ear’)

Pathophysiology 
Risk Factors
Clinical Features
Investigations
Management

Answer 6

1. ) Pathophysiology - collection of fluid in the middle ear with an intact TM w/o signs of acute inflammation
   - due to ET dysfunction (more common in children)
   - in adults, considered a red flag as it is associated with post nasal space tumours
2. ) Risk Factors
   - bottle-fed, paternal smoking, atopy
   - genetic: CF, downs syndrome, ciliary dyskinesia
3. ) Clinical Features
   - conductive hearing loss (speech delay, sch problems)
   - pressure sensation w/ ‘popping/crackling’ noises
   - painless unless it becomes infected (AOM)
   - TM: dull, loss of light reflex, bubble behind TM
   - important differential is adenoidal enlargement
4. ) Investigations
   - tympanogram: normal canal volume w/ flat (type B) tracing suggesting reduced membrane compliance
   - PT audiogram: conductive hearing loss at low frequency
5. ) Management
   - active surveillance: most resolve after 2-3 months
   - grommets: if >3mths of bilateral OME and hearing level in best ear <25-30 dBHL, grommets ventilate and equalise pressure across the Eustachian tube
   - hearing aids whilst waiting for grommets, it’s also first line in patients with down syndrome as complications from grommets can be common
   - myringotomy: allows fluid to drain
   - adenoidectomy: to remove a source of infection, used in persistent disease or multiple grommets

Question 7

Chronic Suppurative (Mucosal) Otitis Media (CSOM)

Pathophysiology
Clinical Features
Investigations
Management

Answer 7

1. ) Pathophysiology - chronic inflammation of the middle ear causing persistent/recurrent ear discharge
   - due to TM perforation leading to inflammation
   - cause of TM perforation: infection (AOM), iatrogenic (grommets), trauma, down syndrome (risk factor)
   - active: chronic discharge through TM
   - inactive: no active infection or discharge
2. ) Clinical Features
   - otorrhea (>6w) w/o ear pain or fever
   - sometimes will have conductive hearing loss
   - otoscopy: painless ear exam w/ perforated TM
   - h/o recurrent AOM, OME, ear trauma, or grommets
3. ) Investigations
   - audiograms and tympanometry
   - swabs for MC+S useful when treatment options fail
   - CT petrous temporal bone if suspect cholesteatoma
   - assess CN VII function
4. ) Management - should be seen by an ENT specialist
   - aural toileting, topical antibiotic or steroid treatments
   - surgery for large perforations that persist:
   - myringoplasty: closure of perforation in pars tensa
   - tympanoplasty: myringoplasty + reconstruction of the ossicular chain
   - complications are the same as AOM

Question 8

Chronic Squamous Otitis Media (Cholesteatoma)

Pathophysiology
Clinical Features
Investigations
Mastoidectomy

Answer 8

1. ) Pathophysiology - chronic inflammation of the middle ear causing persistent/recurrent ear discharge
   - due to retraction of the TM caused by chronic negative middle ear pressure from ET dysfunction
   - retraction pocket traps keratinised squamous cell debris leading to the formation of a cholesteatoma
   - usually acquired but can also be congenital
2. ) Clinical Features
   - painless, purulent/smelly ear discharge
   - asymptomatic in inactive phase (pockets are made)
   - when active –> inflammatory process in the adjacent temporal bone which damage structures:
   - hearing loss: cond..(ossicles) or sens.. (cochlea)
   - vertigo/tinnitus: destruction of semi-circular canals
   - facial nerve palsy: the destruction of the facial canal
   - intracranial complications if it spreads
   - otoscope: pearly, keratinized/waxy mass in attic area
3. ) Investigations
   - PT audiogram: determine extent/type of hearing loss
   - CT petrous temporal bone
4. ) Mastoidectomy - definitive management
   - create a mastoid cavity where the cholesteatoma is removed and the mastoid is ‘cleaned out’
   - ossicles can be reconstructed depending on damage
   - can treat w/ antibiotics if also infected
   - complications: CN VII palsy, altered taste (chorda tympani), CSF leak, tinnitus, vertigo, complete deafness

Question 9

Otosclerosis

Pathophysiology
Clinical Features
Investigations
Management

Answer 9

1. ) Pathophysiology - abnormal bone remodelling of the ossicles, mainly the footplate (base of the stapes)
   - causes thickening and fusion w/ cochlea which –> ↓sound transmission –> conductive hearing loss
   - can be inherited (autosomal dominant)
   - often presents under the age of <40, F>M, may be precipitated by pregnancy in genetically predisposed
2. ) Clinical Features - can be unilateral or bilateral
   - hearing loss: affects lower-pitched sounds more
   - quiet speech: hear their own voice as loud compared to the environment due to intact sensory hearing
   - tinnitus
3. ) Investigations
   - otoscopy: may see Schwartz sign (pink hue to TM)
   - audiometry: conductive hearing loss pattern, bone > air conduction, deafness greater at lower frequencies
   - tympanometry: ↓ admittance (absorption) of sound as the TM is stiff and reflects most sound back.
   - HR-CT: detect boney changes (not always required)
4. ) Management - conservative or surgical
   - conservative: use of hearing aids
   - stapedectomy: replace stapes w/ a prosthesis
   - stapedotomy: remove stapes leaving the footplate, prosthesis is put inside the footplate to transmit sound