ENT Flashcards
Describe the anatomy of the external ear?
- Lined with skin
- Supplied by the greater auricular nerve, lesser occipital and facial nerve
- Includes the pinna, external auditory meatus, and tympanic membrane
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Auricle / pinna = visible ear: mostly made of elastic cartilage, thrown into folds, only the lobule is fatty
- Outer curvature = helix, inner curvature = antihelix
- Concha = hollow depression → external auditory meatus
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External acoustic/ auditory meatus: sigmoid shape, from deep part of concha to tympanic membrane
- External 1/3 is cartilage, inner 2/3 is temporal bone
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Tympanic membrane: connective tissue, skin on outside, mucous membrane on inside which is connected to temporal bone by fibrocartilaginous ring Divides external ear from middle ear
- The pars flaccida is the weakest and most flaccid area of TM
- Pars tensa forms the rest
- The tip of the handle of the malleus forms the umbo: deepest concavity
Is this image from the left or right side of the body?
Identify the indicated parts of the tympanic membrane
- Pars flaccida (attic region)
- Below this is pars tensa- the translucent region
- Lateral process of malleus
- Anterior malleolar fold
- Cone of light (light reflex)
- Umbo- fibrous attachment to tympanic membrane
- Handle of malleus
- Posterior malleolar fold
This image is from the right side of the body- the key difference is the cone-shaped light reflection of the otoscope light is seen at 4 to 5 o clock position in the right tympanic membrane, and 7 to 8 o clock position in the left
Identify the indicated parts of the external ear:
What is the pinna?
- Concha
- Tragus
- External acoustic meatus
- Lobule
- Antitragus
- Antihelix
- Helix
Pinna = auricle = the external ear that we see:
- Cartilage underlying skin
- Lobule is just fat
Identify the indicated parts of the external, middle and internal ear
- Auricle
- External acoustic meatus
- Cartilage
- Tympanic membrane
- Pharyngotympanic tube
- Pharynx
- Internal acoustic meatus
Describe the anatomy of the middle ear- what’s its function & how does it perform said function?
- Air-containing space connected to the nasopharynx via the eustachian tube
- Lined with respiratory epithelium (mucous membrane)
- Function is to amplify and transmit sound energy efficiently from air to a fluid medium in the cochlea
- Ossicles connected via synovial joints
- Sound waves cause movement in TM, creates movement or oscillation in auditory ossicles
- This movement helps transmit sound waves from the TM of external ear to oval window of inner ear (cochlea)
- Ossicle movement tampered by 2 muscles tensor tympani + stapedius - these contract if XS vibration due to loud noise: protective, acoustic reflex
- 3 ossicles
- Malleus
- Incus
- Stapes
Describe the anatomy of the inner ear
- 2 functions
- Convert mechanical signals from middle ear into electrical signals which can transfer info to auditory pathway of brain
- Maintain balance by detecting position + motion
- The inner ear is located within the petrous part of the temporal bone
- Lies between the middle ear and the internal acoustic meatus
- Fluid-filled
- Has a bony labyrinth and membranous labyrinth
- BONY LABYRINTH:
- Central vestible
- Spiral cochlea- fluid-filled tube with specialised hair cells that generate action potentials when moved = organ of hearing
- 3 semicircular ducts
- MEMBRANOUS LABYRINTH:
- 3 semi-circular canals: anterior, lateral, posterior = organs of balance
- Urtricle/ saccule
- Semicircular canals
- BONY LABYRINTH:
Identify the indicated structures related to the inner ear
- Central vestibule
- Semicircular canals
- Semicircular duct
- Facial nerve
- Vestibular nerve
- Vestibulocochlear nerve
- Internal acoustic meatus
- Cochlear nerve
- Cochlea
- Cochlear duct
What is the vestibular system?
- Somatosensory portion of the nervous system
- Detects motion, head position, and spatial orientation
- Central and peripheral portions
- Peripheral
- Vestibular labyrinth
- = proprioceptive components of inner ear
- Semicircular canals- contain cells that detect angular acceleration of head
- Utricle and saccule- contain cells that detect the linear acceleration of head & spatial orientation of head
- = proprioceptive components of inner ear
- Vestibular ganglion- receives inputs from the above receptors
- Vestibulocochlear nerve- transmits info to central portion
- Vestibular labyrinth
- Central
- Vestibular nuclei in brainstem
- Projections into cerebellum, spinal cord, thalamus, nuclei of occulomotor/ trochlear/ abducens nerve
- Peripheral
What is the sensory supply to the pinna?
- Upper lateral surface- CN V3- Auriculotemporal nerve
- Lower lateral surface & medial surface- C3- Greater auricular nerve
- Superior medial surface- C2/ C3- lesser occipital nerve
- External auditory meatus- auricular branch of vagus nerve
What are the branches of the trigeminal nerve & their functions?
- CN V1: Ophthalmic division
- CN V2: Maxillary division
- CN V3: Mandibular division
How does a haematoma form in the auricle?
Why is it important to recognise pinna haematoma?
- The pinna is a well vascularised area
- How does a haematoma form? Shearing forces can lead to separation of the anterior auricular perichondrium from the underlying tightly adherent cartilage- there can be tearing of the perichondrial blood vessels and subsequent haematoma formation
- If not drained early, the haematoma can compromise the viability of the auricular cartilage & lead to avascular necrosis, this can stimulate new & asymmetrical cartilage growth leading to cauliflower ear deformity- cosmetically unpleasant for pts
- Another complication if not drained is infection & abscess formation – due to the compromised blood supply to the cartilage
How to recognise & treat a pinna haematoma?
- Pinna will appear swollen, fluctuant & mildly erythematous
- Hx of trauma- determine mechanism of injury
- Exclude other head injuries & assess hearing function
- Drainage required within 24hrs of injury
- Can be done in A&E/ outpatient setting under aseptic conditions
- Local anaesthetic w/o adrenaline eg 1% lidocaine infiltration
- Smaller haematoma- aspiration with 10ml syringe attached to wide bore needle- though high recurrence rate
- Larger haematoma- incision & drainage w/ blade- incise along helical rim (most fluctuant part), squeeze out haematoma completely & wash cavity with saline, 2 dental rolls on either side of ear to close perichondrial space- prevent recollection of haematoma
- Tight bandage is placed with gauze used as padding in front of & behind ear- removed 2-3 days later in ENT clinic
Once a pinna haematoma has been drained, the patient can usually be discharged. Does the patient need to be sent home with antibiotics, if so which ones?
- If ear clearly contaminated, haematoma older than 24 hrs, or signs of infection à give abx too eg oral amoxicillin or clarithromycin
Causes of a tympanic membrane perforation? How do pts commonly present?
- Traumatic
- Blunt force trauma to external ear canal eg RTA, blow to side of head
- Penetrating trauma eg cotton buds, iatrogenic injury during microsuction
- Barotrauma eg explosions, scuba diving
- Otitis media
- Presentation: otalgia, hearing loss (conductive), aural fullness, tinnitus, serosanguinous discharge
How to assess & manage a tympanic membrane perforation?
- Assess facial nerve function & document
- Assess hearing- Rinne’s and Weber’s & document
- Battle’s sign- ecchymosis (bruising) behind ear- suggestive of skull base fracture- CT head
- Topical abx not routinely required for dry perforation; if evidence of contamination then they may be used. Advise pt to keep ear dry and clean to reduce risk of secondary infection
- When showering with shampoo or soap use water precautions such as soft ball of cotton wool rolled in petroleum jelly & placed gently against the canal
- A little blood is normal- if extensive, suspect a more serious injury
- Specialist follow-up not routinely required; they heal spontaneously with 8wks
- Advise if they get recurrent ear discharge or their hearing declines, then seek referral to ENT clinic
- For non-hearing perforations (after 6months) w/ persistent hearing loss/ recurrent infections- surgical repair: myringoplasty to repair the TM
Red flags for temporal bone fracture?
- CSF otorrhoea/ rinorrhoea
- Facial nerve paralysis
- Post-auricular or periorbital ecchymosis
- Haemotympanum/ pinna haematoma/ lacerations
- Severe nystagmus
- Vertigo
Why is it important to recognise a fracture of the temporal bone?
- Potential ENT short & long term complications include CSF leak, meningitis, hearing loss, facial nerve palsy
Describe the management of temporal bone fracture?
- CT head within 1 hour
- Assess for vascular injury- carotid canal involved on CT or suspected clinically
- Assess for complications
- Facial nerve palsy
- Eye protection, tape eye closed at night
- If delayed onset consider 5 days prednisolone (delayed onset is better prognosis)
- CSF leak
- β2-transferrin sample to confirm diagnosis
- Give pneumococcal vaccine
- Monitor for signs of meningitis- uncommon in traumatic CSF leak
- Elevate head & give stool softeners
- Most leaks will resolve with conservative mx- period of bed rest with measures to reduce fluctuations in ICP
- Consider lumbar drain if not settling
- Surgical repair if persisting >10 days
- Vertigo
- Manage conservatively where possible
- Use vestibular suppressants sparingly
- Perform otoscopy & anterior rhinoscopy
- Facial nerve palsy
- Follow up in ENT skull base clinic eg at 6wks- perform pure tone audiometry and tympanometry, refer for hearing aids if required
What is haemotympanum & what can it suggest?
- Blood in middle ear- seen behind tympanic membrane
- Associated w/ conductive hearing loss
- Can suggest a basilar skull fracture- other features:
- Battle’s sign (bruising over mastoid process)
- Raccoon eyes (bruising around eyes)
- CSF rinorrhoea/ CSF otorrhoea
- Urgent head CT
- What is otitis externa?
- How does it present?
- How would you expect the ear canal and tympanic membrane to appear?
- How is otitis externa managed?
- Inflammation of external ear canal
- Due to bacterial or fungal infection
- Always consider underlying otitis media as otitis externa may be secondary to otorrhoea from otitis media
- Hx- ear pain, discharge, aural fullness, conductive hearing loss, itchiness
- There may be trigger- eg swimming or cotton bud use
- Acute otitis externa: pre-auricular lymphadenopathy
- O/E- canal may be open or swollen close, tenderness in ear canal, pus or discharge in ear canal, lymphadenopathy, associated furuncle (infected canal wall hair follicle) may occlude canal
- Ix- ear swab for microscopy, culture & sensitivity
- Mx-
- Protect ear canal from water entry
- Topical abx first line eg ciprofloxacin, gentamicin drops- TDS, for 7-14days
- Topical acetic acid 2% spray for mild cases
- Failure to improve with abx may suggest fungal cause- topical fungal treatment eg clotrimazole drops
- +/- steroid drops to reduce canal inflammation and reduce swelling- allowing the abx to penetrate better and reduce pain
- Microsuction of pus/ debris which enables the drops to get to the source of infection
- Severe infection- wick may be used to hold canal open to allow topical treatment to diffuse through
- Analgesia
Suggest some examples of causative microorganisms of acute otitis externa?
- Bacterial-
- Pseudomonas aeruginosa- gneg, can colonise lungs in pts with CF, resistant to many abx, treat with aminoglycosides (gentamicin) or quinolones (ciprofloxacin)
- Staph aureus
- Fungal- candida albicans (whitish blobs of rice pudding)
What are some risk factors for developing otitis externa?
- Interfering with the protective mechanism of the external auditory canal
- Frequent water contact eg swimmers
- Humid environment
- Presence of ear polyps or foreign bodies
- Narrow ear canals
- Ear eczema or psoriasis
- Local trauma eg hearing aid or cotton buds
- Immunocompromised, diabetes
What are some complications of otitis externa and who’s at risk of developing these complications?
- Significant risk factors:
- Diabetes mellitus
- Age > 65
- Recurrent AOE
- Chemo or radiotherapy or immunocompromised in another way
- Complications:
- Necrotising otitis externa (previously known as malignant otitis externa)- infection spreads from external auditory canal to skull base
- Classic example is elderly diabetic man with severely painful chronically discharging ear
- Deep seated severe ear pain
- Cranial nerve palsy- commonly CN VII
- Most common causative organism: pseudomonas aeruginosa
- CT scan: thickening & enhancement of soft tissue, opacification of mastoid air cells & abscess formation
- Aggressive IV abx as well as topical treatment required to eradicate infection
- 6wks
- Localised abscess formation
- Cause: staph aureus
- Localised fluctuant swelling which may form in or around affected ear
- Rupture- purulent discharge
- Peri-auricular or pinna cellulitis
- Pain, erythema, swelling and warmth of pinna or around ear
- Systemic symptoms- fever, generalised illness, regional lymphadenopathy
- Chronic stenosis of ear canal
- Due to fibrosis within ear canal
- Formation of a false fundus covering the TM
- Distinct from irreversible acute stenosis (which is due to inflammation)
- Necrotising otitis externa (previously known as malignant otitis externa)- infection spreads from external auditory canal to skull base
Most common causative organism of malignant otitis externa? What to do if you suspect it?
- Pseudomonas aeruginosa
- Ix- microbiology/ swabs of discharge, IV access, FBC, U&Es, serum glucose, CRP, ESR
- Blood cultures if pyrexial
- Sepsis 6
- CT temporal bone (fine slice) if NOE suspected
Why is recognising & treating acute otitis externa important?
- AOE can progress to necrotising otitis externa (NOE) which is osteomyelitis of the temporal bone & skull base, sometimes CN (commonly VII) involvement
Describe the anatomy of the middle ear- describe the function?
- Lies within the temporal bone
- Extends from tympanic membrane to lateral wall
- Air containing space connected to nasopharynx via Eustachian tube
- Lined with respiratory epithelium (mucous membrane)
- Tympanic cavity- 3 ossicles
- Connected via synovial joints
- Malleus, incus, stapes
- Sound waves create movement in TM creating movement/ oscillation in the ossicles, which helps transmit sound waves to the cochlea (inner ear)
- Ossicle movement is tampered by 2 muscles- tensor tympani and stapedius- these contract if excess vibration due to loud noise for protection
What is acute otitis media? What causes it? What are risk factors for it?
- Infection of the middle ear
- Causes- often preceded by viral URTI, bacteria- strep pneumoniae, H influenzae, M catarrhalis, Staph aureus
- Risk factors- male, young age- mainly affects children, viral URTI, FHx
Features of acute otitis media, including on examination?
- Ear pain- caused by increased pressure in tympanic cavity
- Discharge- TM rupture- pus from middle ear- pain stops at this point
- Reduced hearing in affected ear
- Fever, feeling generally unwell
- Symptoms of URTI- cough, coryzal symptoms, sore throat
- O/E- bulging, red, inflamed tympanic membrane
- TM perforation- discharge in ear canal, hole in TM
How is acute otitis media managed?
- Conservative- analgesia for pain & fever
- Advise that the usual course of AOM is 3 days, can be 1 wk, advise paracetamol/ ibuprofen for analgesia
- Admit children <6months
- Abx- considered if systemically unwell, high risk of complications, co-morbidities, those <2 years w/ bilateral infection, those with otorrhoea
- Amoxicillin 5-7 days first-line
- Clarithromycin- penicillin allergy
- Erythromycin- in pregnant women allergic to penicillin
- Surgical- recurrent AOM- grommet insertion (ventilation tube)
Describe some complications of acute otitis media?
- Extracranial complications
- Labyrinthitis- dizziness or vertigo
- Perforated TM- pain, reduced hearing, discharge
- Otitis media with effusion
- Facial palsy- w/o forehead sparing, usually recovers once infection resolves
- Mastoiditis- infection spreads from middle ear to form an abscess in the mastoid air spaces of the temporal bone
- Petrositis- infection spread to the apex of the petrous temporal bone, signs of sepsis and symptoms of mastoiditis
- Intracranial complications
- Meningitis- sepsis, headache, vomiting, neck rigidity, photophobia, positive Kernig’s sign (pain on meningeal stretch eg chin to chest or straight leg raise)
- Sigmoid sinus thrombosis
- Brain abscess- sepsis w/ neuro signs
Key diagnostic criteria for mastoiditis?
- Septic- pyrexia, anorexia, lethargy, irritable child, not feeding
- Features of ear infection- red bulging TM, purulent ear discharge
- The sharp angle between the ear and the mastoid is lost (the auriculomastoid sulcus)- compare to normal ear
- The pinna is classically pushed downwards and forwards w/ boggy oedema of the mastoid
Clinical features of meningitis?
- Sepsis, headache, N&V, photophobia, drowsiness, seizures
- Signs- neck rigidity, purpuric rash, positive Kernig’s sign- pain on meningeal stretch- chin to chest or straight leg raise
What is otitis media with effusion? What causes it & what are the complications?
- Glue ear
- Characterised by a collection of fluid within the middle ear space w/o signs of acute inflammation
- Exact cause is uncertain but 50% cases are thought to follow AOM episode esp. in ch. <3 years old
- Causes-
- Impaired ET function causing poor aeration of middle ear
- Low grade viral or bacterial infection
- Persistent local inflammatory reaction
- Adenoidal infection or hypertrophy
- Complications-
- Conductive hearing loss
- Speech/ language development difficulties
- Chronic TM damage
What is otosclerosis?
What is the mode of inheritance and who does it affect?
How is it managed & what imaging may be done?
- A condition where there is remodelling of the small bones in the middle ear- normal bone is replaced by vascular spongy bone
- Causes a progressive conductive hearing loss due to fixation of the stapes at the oval window
- May also cause tinnitus
- Mode of inheritance: autosomal dominant
- Who it affects: young adults, age 20-40
- Imaging: high resolution CT scan can detect bony changes but not always required
- Mx:
- Conservative- hearing aid
- Surgical- stapedectomy: removing stapes bone & replacing w/ prosthesis; stapedotomy: removing part of stapes & leaving the base of the stapes attached to the oval window, with a small hole made for prosthesis that can transmit sound from the incus to the cochlea
What is a cholesteatoma?
- Abnormal collection of squamous epithelial cells in the middle ear
- Benign
- Can invade local tissues, nerves, and erode middle ear bonds
- Can pre-dispose to significant infections
What is the pathophysiology behind a cholesteatoma formation?
- Not fully understood
- Squamous epithelial cells originate from the outer surface of the TM
- The main theory is this: ET dysfunction causes negative pressure in the middle ear, causes a pocket of the TM to retract into the middle ear, the squamous epithelial cells of this pocket continue to grow into the surrounding space, bones and tissues
- It can damage the ossicles resulting in permanent hearing loss
How do patients with cholesteatoma present?
- Foul-smelling, non-resolving discharge
- Hearing los
- Local invasion- vertigo, facial nerve palsy, altered taste, cerebellopontine angle syndrome
- Otoscopy: attic crust seen in upper part of ear drum; retraction pocket in attic
How to manage a suspected cholesteatoma?
- CT scan to assess local invasion
- Surgical removal
- Canal wall up mastoidectomy, allowing removal of cholesteatoma w/ canal wall intact
- 9-12 months later a second-look procedure is required to examine for residual or recurrent disease
What does the vestibular system comprise & what does it do?
- Somatosensory portion of nervous system
- Function? Detects motion, head position and spatial orientation
- Central and peripheral portions:
Peripheral:
- Vestibular labyrinth (vestibular apparatus)- inner ear
- 3 semi-circular canals, - lateral, posterior, superior- at right angles to each other, detect angular acceleration of head / rotational movements- nodding up/down, shaking side to side, tilting R to L
- Canals are filled with endolymph fluid- when head is rotated, endolymph moves corresponding to the movement
- The endolymph flows into ampulla, an expansion of the canal, here there are hair cells (sensory receptors) stereocilia at end of hair cells leads to release of neurotransmitters
- Otolith organs- lie in the vestibule- Utricle (horizontal movements) and saccule (vertical movements)- detect the forward/ backward movements- stops you falling over
- 3 semi-circular canals, - lateral, posterior, superior- at right angles to each other, detect angular acceleration of head / rotational movements- nodding up/down, shaking side to side, tilting R to L
- Vestibular ganglion- receives inputs from above, transmits to vestibulocochlear nerve which transmits info to central portion
Central:
- Vestibular nuclei in brainstem
- 2 branches of vestibular nerve- superior and inferior
- Projects into cerebellum, spinal cord, thalamus, nuclei of oculomotor, trochlear, abducens nerves
Briefly describe how the vestibular system works?
- Movements of head à endolymph fluid in semi-circular canals moves
- This fluid shift is detected by tiny hairs- stereocilia- in ampulla
- Transmits input to vestibular nerve
- Vestibular nerve carries signals from the vestibular apparatus to the vestibular nucleus in the brainstem & cerebellum
- The vestibular nucleus then sends signals to oculomotor, trochlear and abducens nuclei that control eye movements and the thalamus, spinal cord and cerebellum
- Cerebellum- co-ordinates movement throughout the body
What systems of the body affect balance?
- Vestibular system (ears)
- Eyes- giving information on the relationship between position & environment
- Proprioception- joint receptors, ability to establish a sense of position in space, somatosensory input
- Sensation- cerebellar inputs tell you how to link surroundings, cerebral inputs- psychological
What diseases can affect proprioceptive ability?
- Diabetes- neuropathy
- Joint replacements- loss of joint receptors
What is the function of the vestibulo-ocular reflex?
- The VOR is a reflex acting to stabilise gaze during head movement, and hence preserve visual acuity during head movements
- It does so by generating slow-phase movements in exactly the opposite direction and of almost equal velocity to the head movement
- 3 -neuron arc (don’t need to know these details, just appreciate and have an understanding)
- Vestibular nerve- primary sensory afferent
- Vestibular nucleus neuron in ponto-medullary region
- Oculomotor neuron in the III, IV, VI nuclei in the brainstem
An ENT consultant advised it is always important to get the patient from the waiting room yourself during clinics, what is the wisdom behind this?
- You can observe the patient before even speaking to them
- If the patient doesn’t want to move their head/neck – this tells you there may be a problem with the VOR
- Patient gets up and pauses before walking - this tells you they may have postural hypotension
How are vestibular disorders classified? Give some examples of drugs that can affect the vestibular system.
- Disease affecting ventral vestibular system
- Cerebrovascular disease
- Migraine
- Multiple sclerosis
- Cerebellar tumours
- Disease affecting peripheral vestibular system
- Benign paroxysmal positional vertigo
- Meniere’s disease
- Vestibular neuronitis
- Ototoxicity
- Drugs
- Gentamicin
- Loop diuretics
- Metronidazole
- Co-trimoxazole
How do you test for VOR impairment?
- Assess for nystagmus by asking the patient to turn their head to one side and then quickly move it back into the centre
Define dizziness?
- Generic term that may refer to light-headedness, faintness, giddiness, swimming or floating sensation, unsteadiness, imbalance, mental confusion, minor seizures or even true vertigo
Define vertigo?
What causes vertigo?
- Sensation that there is movement between the patient and their environment
- May feel that they are moving or the room is moving
- Often this is a horizontal spinning sensation
- Often associated w/ N&V, sweating, feeling generally unwell
- Vertigo is either caused by-
- Peripheral problem- vestibular system
- BPPV
- Meniere’s disease
- Vestibular neuronitis
- Labyrinthitis
- Central problem- brainstem, cerebellum
- Posterior circulation stroke
- Tumour
- Multiple sclerosis (MS)
- Vestibular migraine
- Peripheral problem- vestibular system
What is the most common cause of vertigo?
Describe the characteristic symptoms, how it is diagnosed & managed?
- BPPV
- Displacement of otoconia (= otoliths ie calcium carbonate particles displaced from cells in endolymph in semi-circular canals)
- Brief intense bouts of rotatory vertigo lasting <1minute, provoked by head turning
- N&V
- Classically, pts wake & on rolling out of bed experience severe rotatory vertigo
- No hearing loss or tinnitus
- Diagnosis- Dix-Hallpike manoeuvre
- Mx- watchful waiting, canalith repositioning manoeuvres eg Epley’s, Brandt-Darrof exercises
Describe the cause and underlying mechanism of BPPV?
- Small fragments of debris (calcium carbonate crystals) are deposited in inner ear
- When head is still, fragments sit at bottom of canal
- Certain head movements cause the fragments to be swept in fluid-filled canal
- This sends confusing messages to the brain causing vertigo
Describe the Dix-Hallpike manoeuvre?
- Ask pt to sit upright on a couch and to focus on a point straight ahead, then bring head and torso down to level of bed, ensure eyes remain open
- Move head directly downward below level of bed and turn left or right
- Watch for nystagmus for 30-60 seconds
- Sit the pt up and repeat, turning head to other side
What is the Epley manoeuvre?
Suggest some contraindications?
- Purpose is to reposition displaced otoconia from the semi-circular canals into the utricle
- To treat BPPV
- Contraindications- neck trauma, spinal fractures, cervical disc prolapse, vertebrobasilar insufficiency, carotid sinus syncope, recent stroke or CABG, back/ spinal pain
- Successful in ~80% pts
What are some common causes of dizziness in the elderly?
- Polypharmacy
- Multifactorial disequilibrium with age- naturally as we age, we lose balance function through loss of sensory elements, the ability to integrate information & issue motor commands, and because we lose musculoskeletal function
- Cerebral/ cerebellar degeneration- causes include cerebral vascular disease, stroke, hereditary
Describe the pathophysiology & clinical features of Meniere’s including disease progression?
- Pathophysiology- increased fluid in endolymphatic compartment (membranous labyrinth) of inner ear -increased pressure of endolymph = endolymphatic hydrops
- Typical pt is 40-50 years old
- Clinical features-
- Episodic vertigo- lasting hrs
- Fluctuating sensorineural hearing loss
- Unilateral tinnitus
- Aural fullness in affected ear
- Other features include nystagmus + positive Romberg test (swaying or falling when asked to stand with feet together & eyes closed)
- Disease progression
- Permanent sensorineural hearing loss
- Vertigo episodes settle
- Vestibulopathy (vestibular hypofunction)
- Generalised imbalance
- Helped by vestibular rehabilitation exercises
- May develop bilateral disease
Suggest some risk factors for Meniere’s disease?
- A lot of the time Meniere’s disease is idiopathic
- Average age diagnosis 30-60
- Affects more women than men
- Autoimmunity, genetics, metabolic disturbances involving levels of sodium and potassium in inner ear, vascular factors, viral infection, head trauma, syphilis, migraines
How is a diagnosis of Meniere’s made?
- According to nice, all of the following criteria need to be met-
- Vertigo- at least 2 spontaneous episodes lasting 20 mins- 12hrs
- Fluctuating hearing loss, tinnitus, +/- aural fullness in affected ear
- Sensorineural hearing loss confirmed by audiometry
- No alternative vestibular diagnosis
- MRI scan may be organised to exclude alternative diagnoses such as vestibular schwannoma
How is Meniere’s disease managed?
- Psychological- supportive
- Diet- reduce salt, caffeine, chocolate, alcohol
- Other lifestyle measures- avoid triggers such as stress, excessive fatigue, allergies
- Medical-
- Betahistine- labyrinthine vasodilator (helps reduce frequency/ severity of attacks)
- Acute attacks- oral or IM prochlorperazine (helps alleviate N&V and vertigo)- short course 1-2wks
- Thiazide diuretics (poor evidence but may help reduce number of vertigo attacks)
- Surgical- rare, last resort
- Grommet insertion- if functional hearing exists in the affected ear
- Intratympanic dexamethasone or gentamicin (injected, small risk of hearing loss)
- Endolymphatic sac decompression- controversial procedure but pts have found it helpful
- Surgical labyrinthectomy – for unilateral cases of intractable vertigo, involves the opening of the semi-circular canals & vestibules with excision of the neurosensory epithelia, results in deafness in affected ear but prevents vestibular input with the hope of eliminating vertigo
Can patients with Meniere’s disease drive?
- They must inform DVLA
- Current advice is to cease driving until there is satisfactory control of symptoms achieved
Vestibular neuronitis- define? Causes? Clinical features?
- Define: self-limited episode of vertigo, presumably due to inflammation of the vestibular division of CN VIII
- This distorts the signals travelling from the vestibular system to the brain, confusing the signal required to sense movement of the head
- Cause: unclear aetiology; probable viral cause
- Symptoms & signs:
- Single attack of severe vertigo, N&V, persistent nystagmus toward affected side
- Nystagmus is unidirectional, horizontal, spontaneous, with fast-beat oscillations in the direction of the unaffected ear
- Sudden onset, lasts 3-7 days & gradually resolves
- NO loss of hearing- cochlea and cochlear nerve not affected- if tinnitus/ hearing loss consider labyrinthitis or Meniere’s
- Treatment:
- Supportive
- Vestibular sedatives- prochlorperazine
- If symptoms don’t resolve after 6 wks- vestibular rehabilitation therapy (VRT)
What is the head impulse test?
- Used to diagnose peripheral causes of vertigo- problems with the vestibular system eg vestibular neuronitis, labyrinthitis
- Pt sits upright and focuses on examiner’s nose, hold patients head and rapidly jerk it 10-20 degrees in one direction whilst pt continues to focus on your nose, head is slowly moved back to centre before repeating in opposite direction
- Ask about neck pain beforehand
- Observe for eyes rapidly moving back and forth
What is the Unterberger’s stepping test?
- Identifying peripheral causes of vertigo
- Ask pt to remain stationary and step for 60 seconds with eyes closed and arms outwards
- Positive test- rotational movement of pt toward side of lesion
Describe the difference in the length of the vertigo experienced in BPPV, Meniere’s disease and vestibular neuronitis?
- BPPV: seconds
- Meniere’s: minutes- hrs
- Vestibular neuronitis: days
What is acute labyrinthitis?
- Labyrinthitis is inflammation of the labyrinth in the vestibular system of inner ear
- Acute onset
- Often preceded by viral URTI
- Features- acute onset vertigo, exacerbated by movement, N&V, sensorineural hearing loss, disequilibrium tinnitus, preceding URTI symptoms
- Positive head impulse test
- Mx- vestibular suppressant/ anti-emetic- promethazine, cyclizine
What should you see on otoscopy of a normal tympanic membrane?
- Healthy tympanic membrane is concave, not flat
- Lateral process of malleus
- Cone of light- 5 o’clock on R, 7 o’clock on L TM
- If the pressure of middle ear increases- TM bulges. If pressure decreases- TM retracts
- Pars tensa (greater part of TM)
- Pars flaccida (flaccid part of TM)
What is tinnitus?
- Persistent addition sound that is heard but not present in surrounding environment
- Ringing in ears, buzzing, hissing or humming
Causes of tinnitus?
- Primary- often occurs w/ sensorineural hearing loss, no identifiable cause
- Secondary-
- Impacted ear wax
- Ear infection
- Meniere’s
- Noise exposure
- Medications eg loop diuretics, gentamicin, chemotherapy- cisplatin
- Acoustic neuroma
- MS
- Trauma
- Depression
- Systemic conditions may be associated w/ tinnitus-
- Anaemia
- Diabetes
- Hypo/ hyperthyroidism
- Hyperlipidaemia
Differentiate between conductive & sensorineural hearing loss
- Conductive
- Sound not reaching inner ear
- Obstruction or trauma in external or middle ear, interfering with ability for sound to reach inner ear
- Sensorineural
- Problem in inner ear or cranial nerve 8
- Permanent- because human inner ear + hair cells have limited ability to repair themselves
How to differentiate between conductive and sensorineural hearing loss?
- Rinne’s test
- Normally: Rinne’s positive: AC > BC
- Conductive hearing loss: BC > AC
- Weber’s test
- Central is NORMAL
- Lateralised is ABNORMAL
- Towards- conductive hearing loss
- Away- sensorineural hearing loss
What are the types of hearing loss?
Which imaging would you choose for each one?
- Conductive- abnormality of outer or middle ear which impairs conduction of sound waves from external ear (pinna, ear canal or TM) through the ossicles in middle ear to cochlea in inner ear
- CT scan
- Sensorineural- abnormality of cochlea, auditory nerve or other structures in neural pathway leading from the inner ear to auditory cortex
- MRI scan
- Mixed- both conductive & sensorineural hearing loss is present
Causes of hearing loss?
- Conductive-
- Impacted earwax
- Foreign body eg cotton bud tip
- TM perforation
- Infection eg otitis externa or otitis media
- Cholesteatoma
- Middle ear effusion
- Otosclerosis
- Neoplasm eg scc of external ear
- Exostoses- hard bony growths in ear canal associated with cold water swimming
- Sensorineural-
- Presbycusis- most common cause
- Noise exposure- temporary or permanent
- Sudden sensorineural hearing loss- within 72hrs, idiopathic, temporary or permanent
- Meniere’s disease
- Ototoxic substances- gentamicin, loop diuretics, NSAIDs, aspirin
- Labyrinthitis
- Vestibular schwannoma
- Neurological condition- MS, stroke
- Malignancy- nasopharyngeal cancer, intracranial tumour
- Trauma to head or ear
- Systemic infection eg meningitis, CMV
- Hereditary eg Alport’s syndrome
- Autoimmune eg RA, SLE, sarcoidosis
Most common causes of hearing loss in the UK?
- Presbycusis and exposure to excessive noise
How does presbycusis present & how is it diagnosed?
- Gradual and insidious hearing loss- pts may not initially notice change in hearing
- Loss of high-pitched sounds
- May be associated tinnitus
- Diagnosed via audiometry- sensorineural hearing loss pattern, with normal or near-normal hearing at lower frequencies and worsening hearing loss at higher frequencies
Why does presbycusis occur?
- Loss of hair cells in cochlea
- Loss of neurones in cochlea
- Atrophy of stria vascularis
- Reduced endolymphatic potential
Risk factors for developing presbycusis?
- Age
- Male
- FHx
- Loud noise exposure
- Diabetes
- HTN
- Ototoxic medications
- Smoking
How can presbycusis be managed?
- Irreversible hearing loss
- Optimise environment eg reduce ambient noise during convo’s
- Hearing aids
- If aids are insufficient, cochlear implant may be considered
What are the causes of sudden sensorineural hearing loss (SSNHL)?
- 90% cases are idiopathic ☹
- Infection eg meningitis, HIV, mumps
- Meniere’s
- Ototoxic medications
- MS
- Migraine
- Stroke (ix- MRI)
- Acoustic neuroma (ix- MRI)
- Cogan’s syndrome (a rare autoimmune condition causing inflammation of the eyes and inner ear)
How do patients with sudden sensorineural hearing loss present?
- Sudden hearing loss
- Almost always unilateral
- Many go to bed fine and awaken with deafness
- May be associated tinnitus or vertigo
- No significant otalgia, discharge, or other neuro signs eg nystagmus
What is the diagnostic criteria for sudden sensorineural hearing loss?
- Audiological diagnostic criteria for SSNHL- rule of three:
- Sensorineural loss worse than 30dB
- In 3 consecutive frequencies
- Within 3 days (72hrs)
How is sudden sensorineural hearing loss managed?
- Oral steroid eg 60mg prednisolone reducing over 10 days
- Gastric protection
- MRI IAM (internal auditory meati) as a routine outpatient
- Assess in next ENT clinic with Audiology support
- Hearing recovers spontaneously 66% of the time
- Presence of vertigo = poor prognostic sign
- Intra-tympanic steroid injections if no hearing improvement within 1-3 weeks
- Persistent hearing loss- consider hearing aids
What are the consequences of ear wax impaction?
- Conductive hearing loss
- Discomfort in ear
- Feeling of fullness
- Pain
- Tinnitus
How to manage build-up of earwax?
- Ear drops- olive oil or sodium bicarbonate 5%
- Ear irrigation- squirting water in ears to clean away wax- performed by GP, contraindications: perforated TM, infection
- Microsuction- to suck out the wax, performed by ENT specialist
What are the 4 levels of hearing loss?
How are they determined?
- The thresholds are based on the quietest sound that can be heard in decibels on pure tone audiometry
- Mild (25-39dB)
- Moderate (40-69dB)
- Severe (70-94dB)
- Profound (>95 dB)
Briefly describe the types of hearing aids available?
- Behind the ear hearing aids- most common type
- In the ear hearing aids
- Completely in canal
Common types of hearing implants & who gets them?
- Bone conduction hearing aids
- Conductive hearing loss
- Mixed hearing loss
- Bone conduction > 65
- Middle ear implant
- Cochlear implants
- Auditory brainstem implant
- Bilateral acoustic neuroma (neurofibromatosis II)