20 - Ears Flashcards
Label the different parts of the ear.
Label the different parts of the ear drum.
Anterosuperior quadrant is above the cone of light
What is the nerve supply to different parts of the pinna, and why is this important to know?
Can perform regional nerve blocks at the nerves if need to perform procedures on the pinna
Upper Lateral: Auricotemporal Nerve (CNV3)
Lower Lateral and Medial Surface: Greater Auricular Nerve (C3)
Superior Medial Surface: Lesser Occipital Nerve (C2/C3)
External Auditory Meatus: Auricular Branch of Vagus
With any trauma to the ear what important examination should you do?
Usually not urgent:
- Full Oto-Neurological exam
- If head injury may consider CT scan
How are lacerations and bites to the pinna treated?
Laceration: Primary closure with sutures after cleaning under local anaesthetic. Ensure any cartilage is covered with skin as gets its blood supply from here. If significant skin loss contact plastics
Bites: Need a strong history to find out what creature/person bit them to work out what organisms/commensals could cause an infection. Leave wound open, wound irrigation and antibiotics
What is the issue with a pinna haematoma?
When there is trauma to the ear (e.g rugby, boxer) the perichondrial blood vessels are torn and haematoma forms between auricular cartilage and the overlying perichondrium.
Cartilage can no longer get it’s blood supply from the perichondrium
If left untreated can lead to avascular necrosis and fibrocartilage overgrowth forming a structural deformity (cauliflower ear)
Also, haematoma at increased risk of infection so give abx cover
How is a pinna haematoma managed?
Drainage:
- Within 24 hours
- Aseptic field and give local anaesthetic for regional block (no adrenaline)
- Make incision along helical rim and allow haematoma to evacuate. Can then wash cavity with saline
- If only small haematoma can try needle aspiration but can reaccumulate
Pressure Dressing
- After evacuation need to apply gauze padding and tight headband or use two dental rolls with tight mattress sutures. Closes the perichondrial space and prevents re-accumulation
- If re-accumulates need to re-drain
How can temporal bone fractures be classified?
- Longitudinal (more common): lateral blow to the head and usually with conductive hearing loss
- Transverse: fronto-occipital head trauma and usually with sensorineural hearing loss or facial nerve injury
- Otic capsule sparing or otic capsule violating
What are some of the signs of a temporal bone fracture?
- Facial nerve palsy (if immediately after trauma means direct nerve damage so low chance of recovery)
- Post-auricular ecchymosis (Battle’s sign): basal skull fracture
- Haemotympanum or tympanic membrane perforation
- CSF otorrhoea or rhinnorhoea
- Hearing loss, either conductive or sensori-neural
How are temporal bone fractures managed?
- CT scan
- Admit for neuroobservation and consider surgery
- Most managed conservatively
What are some of the signs and symptoms of a tympanic membrane perforation?
Caused by blunt trauma, penetrating trauma, barotrauma and infection (e.g chronic otitis media)
- Pain (Otalgia)
- Sudden conductive hearing loss
- Ottorhoea
- Tinnitus
What investigations should you do when you suspect a TM perforation?
- View the size and location using otoscope. If any blood suction it out
- Facial nerve function tests
- Weber’s and Rinne’s test
How is a tympanic membrane perforation managed?
Uncomplicated perforation: Watch-and-wait as may heal spontaneously over 2-3 months. Strict water precauions to prevent infection e.g avoid swimming and getting water in ear when showering. Avoid blowing nose and flying
Persistent perforation: If not healed after 6/12 can refer for myringoplasty
What is haemotympanum and how should it be managed?
Blood in the middle ear due to trauma and often associated with temporal bone fracture. Can have conductive hearing loss
- Conservatively will settle over time
- Follow up in a few months to check no residual hearing loss or damage to ossicles
How does otitis externa present and what are some of the causative organisms?
Presentation: Erythematous, swollen, tenderness of the tragus and/or the pinna, and a warm ear. Can be discharging, itchy and hearing loss.
Due to any disruption in wax productive e.g repeated water exposure, trauma from cotton buds
Organisms: Pseudomonas Aeruginosa, S. Epidermidis, S. Aureus, Fungal Aspergillus
What are some risk factors of otitis externa and some differentials to consider?
Differentials:
- Otitis media with perforation
- Ramsey Hunt Syndrome
- Furuncle
How can you risk score otitits externa?
Brighton Grading Scheme
How is otitis externa managed?
- Prevention: remove any debris with microsuction, avoid swimming
- Aural Toileting: e.g irrigation or microsuction
- Topical antibiotics e.g acetic acid
- Topical steroid drops if inflammation e.g gentamicin with hydrocort
- Analgesia
- Swab any discharge in resistant cases
- If severe can use wick with topical treatment
Why is it important to check for perforations before giving treatment for otitis externa?
Gentamicin is ototoxic so don’t want it to get into middle ear
What are some complications of otitits externa?
- Malignant otitis externa
- Mastoiditis
- Osteomyelitis
- Intracranial spread
What is malignant otitis externa, how does it present and how is it managed?
- Spread of infection from soft tissue of ear to the bone usually in diabetics and immunocompromised. Usually due to P.Aeruginosa.** **Osteomyelitis of temporal bone
- Presentation: chronic ear discharge despite topical treatment, deep seated ear pain, CN palsies (usually CN VII)
- Management: refer urgent to ENT, diagnose with HRCT, urgent debridement and IV antibiotics
What is a key sign on clinical examination that points to malignant otitis externa?
Granulation tissue at the junction in between the bone and cartilage of the ear canal.
What are some causes of referred otalgia?
- TMJ dysfunction
- Larynx (e.g cancer)
- Tonsils (e.g warn after tonsillectomy may have otalgia)
- Posterior 1/3rd tongue
- Cervical spondylosis
What are the different types of otitis media?
What is the pathophysiology of acute otitis media?
- Usually in childhood due to ET dysfunction
- ET is shorter, straighter and wider in children so easier for organisms to migrate from nasopharynx
- Pathogens are usually respiratory as respiratory epithelium (S.Pneumoniae, Haemophilus Influenzae, Moraxella species, RSV, Rhinovirus )
What are some risk factors for acute otitis media?
- Age (peak age 6-15 months)
- Boys
- Passive smoking
- Bottle feeding
- Craniofacial abnormalities
- Winter
What are some clinical features of acute otitis media?
Symptoms: Pain due to increase pressure in tympanic cavity, malaise, fever, coryzal symptoms, tugging at ear, discharge if rupture
Signs: On otoscopy will have red bulging TM, may have tear and discharge, conductive hearing loss, cervical lymphadenopathy
If you do an ear exam and find a patient to have acute otitis media, what other exams should you do?
- Lymph nodes
- Facial nerve function tests as close to ear
- Oral and throat
- If any discharge send for MC&S
How is acute otitis media managed?
Conservative: Most resolve conservatively in 24-72 hrs, give analgesia and watch-and-wait. Can give delayed prescription
Medical: Avoid antibiotics unless risk factors for complications, continuing over 4 days, discharge from ear (swab first), systemically unwell but not requiring admission. <2 and bilateral otitis media.
Usually amoxicillin first line. If penicillin allergy, give erythromycin or clarithromycin.
Surgery: If recurrent AOM may benefit to have grommet insertion
What are some complications of acute otitis media?
- Mastoiditis
- Meningitis
- Facial Nerve Palsies
- Intracranial Abscess
- Sigmoid sinus thrombosis
- Chronic Otitis media
- TM perforation
How does mastoiditis present and how is it managed?
Infection spreads to mastoid air cells and causes necrosis and subperiosteal abscess. This can lead to intracranial spread and meningitis
Erythematous swelling behind the ear that can push the pinna forward. TM will show AOM (bulging red TM)
Management: IV antibiotics. If no improvement after 24h do CT head and consider mastoidectomy
What is the definition of recurrent AOM and why is it important to refer these to ENT?
3 or more distinct episodes of AOM in the past 6 months
OR
4 or more in the past twelve months, 1 of which was in the last 6 months
Could be a nasopharyngeal cancer that is blocking the ET. If have conductive hearing loss, persistent cervical lymphadenopathy or nasal obstruction with recurrent AOM also refer
Which patients with AOM should you admit?
What are the different types of chronic otitis media?
- Active (discharging) or Inactive
- Squamous (Retraction pocket) or Mucosal (Ruptured TM)
What is the aetiology of chronic mucosal otitis media?
- Recurrent acute otitis media (most common)
- Grommets
- Craniofacial abnormalities
- Previous traumatic TM perforation
What are the clinical features of chronic mucosal otitis media?
- Chronically discharging ear (<6 weeks)
- Absence of fever or otalgia
- Possible conductive hearing loss
- TM perforation on otoscopy
What investigations should you do with chronic mucosal otitis media?
- Test facial nerve function
- Audiograms and Tympanometry
- Microbiological swabs
- If any suspicion of cholesteatoma do CT scan of the petrous temporal bone
How is chronic mucosal otitis media managed?
Medical
- Aural toileting, topical steroids, topical abx
- Keep ear clean and dry
- Should resolve spontaneously
- Refer to ENT if symptoms >6 weeks
Surgical (close perforation to restore hearing)
- Myringoplasty: closure of perforation in pars tensa by patching on graft from tragal cartilage
- Tympanoplasty: myringoplasty with reconstruction of ossicular chain
What is the aetiology of chronic squamous otitis media?
- Acquired (most common): chronic negative middle ear pressure from Eustachian tube dysfunction causes retraction pocket
- Congenital: choleasteatoma with no previous trauma or ear surgery
Retraction pocket can trap keratinised squamous cell debris, leading to formation of cyst-like structure which may evolve into a cholesteatoma
Which type of retraction pockets are at high risk of developing into a cholesteatoma and why are cholesteatomas so dangerous?
High risk: attico-antral (postero-superior)
Low risk: tubotympanic (antero-inferior)
Choleasteatoma can induce inflammation in the adjacent temporal bone. This can lead to destruction of the following and the following symptoms:
- Ossicles (conductive hearing loss)
- Semicircular canals (vertigo)
- Cochlea (sensorineural hearing loss)
- Facial canal (CNVII palsy)
- Erosion into intracranial cavity (meningitis, intracranial abscess, sinus thrombosis)
What are some risk factors for chronic squamous otitits media (cholesteatoma)?
- Recurrent acute otitis media
- ET dysfunction
- Prior otological surgery
- Children (more aggressive course)
What are the clinical features of chronic squamous otitis media?
Inactive stage: asymptomatic
Active stage:
- Purulent discharge resistant to treatment
- Unilateral conductive hearing loss
- Tinnitus, Vertigo, Facial nerve palsy
- NOT otalgia
How is cholesteatoma diagnosed and investigated?
Diagnosis: Otoscopy shows pearly, keratinized, or waxy mass in the attic region. Has purulent discharge
Investigations:
- Pure tone audiogram (extent and type of hearing loss)
- CT scan of the petrous temporal bone
How is chronic squamous otitis media (cholesteatoma) managed?
Sometimes cannot tell if cholesteatoma present or not so if persistent discharge go to surgery and treat based on findings (squamous or mucosal)
- Surgery to remove whole cholesteatoma as otherwise will recur
- Create mastoid cavity, remove all of the cholesteatoma then wash out mastoid air cells (mastoidectomy)
- Reconstruction of ossicles if any damage (tympanoplasty)
What is the aim of a mastoidectomy in chronic squamous otitis media and what are some risks associated with this?
- Restore hearing but keep safe dry ear
- Risks: facial nerve palsy, altered taste due to chorda tympani damage, CSF leak, tinnitus, vertigo, complete hearing loss
What is the difference in the surgical treatment for chronic mucosal and chronic squamous otitis media?
What is otitis media with effusion and what is the aetiology of this?
Viscous inflammatory fluid present in the middle ear but with intact tympanic membrane. Leads to conductive hearing loss
Children: dysfunction of ET as shorter, straighter and wider so infection more likely
Adults: blockage of ET by infection or tumour. RED FLAG URGENT REFERRAL TO LOOK AT POST NASAL SPACE IF ADULT HAS UNILATERAL OME
What are some risk factors for developing otitis media with effusion?
- Bottle-fed
- Parental smoking
- Atopy
- Genetic disorders e.g mucociliary disorders like CF, craniofacial abnormalities like Downs
What are the clincal features of otitis media with effusion and what will you see on otoscopy?
- Conductive hearing loss (speech delay and issues at school - OLLIE)
- Sensation of pressure, popping, cracking in ear
- Otoscopy: TM appears dull, lost light reflex, bubble behind TM, retracted
What investigations should you do when you find a patient has glue ear (OME) on examination, and what will these investigations show?
Pure tone audiogram: conductive hearing loss
Tympanogram: Type B tracing, reduced membrane compliance but normal canal volume. Helps to distinguish from otosclerosis
Adults: need to do flexible nasendoscopy and full ENT exam
How is OME managed?
What procedure can be done if it is recurrent?
1st line
Active surveillance. Most resolve spontaneously within 3 months
2nd line
- Myringotomy and Grommet insertion if > 3 months of bilateral OME and hearing level in better ear < 25-30dBHL
- Can also give hearing aid if don’t want surgery e.g Down’s
- If persistent and need multiple grommet insertions do adenoidectomy
What advice do you need to give parents after grommet insertion?
- Can swim but don’t go diving as forces water in
- Will fall out after about 3-12 months then need to recheck hearing
- When fall out may leave a small hole which may need surgery
What is otosclerosis and what causes it?
- Remodelling of the ossicles leading to conductive hearing loss once stapes footplate becomes fixed to the oval window
- Autosomal dominant transmission and more common in women
How does otosclerosis present?
- Progressive bilateral conductive hearing loss (especially low-pitch sounds)
- Tinnitus
- Improved hearing in noisy surroundings during early stages
- Family history
- Talking quietly
When you peform an exam on a patient with otosclerosis what will you find?
- Otoscopy: normal or slight pink hue (Schwartze’s sign)
- Weber: normal if bilateral, if unilateral will be louder in affected ear
- Rinne’s: BC>AC
What investigations should you peform for otosclerosis and what will it show?
- Tympanogram: Type A normal trace
- Pure tone audiogram: Conductive hearing loss, Carhart Notch at 2kHz
How is otosclerosis managed?
Conservative: hearing aid
Surgical: stapedectomy and replace with prosthesis
Where is the inner ear found and how can it be split up anatomically?
- Found in the petrous part of the temporal bone
- Vestibule (utricle and saccule) and Semicircular canals: position
- Cochlea: hearing
What fluid is contained in the inner ear?
Membranous labyrinth is filled with endolymph and suspended in perilymph within the bony labyrinth
Perilymph resembles CSF as it communicates with the subarachnoid space via the cochlear aqueduct
How does sound get from the stapes to the brain?
Stapes –> Oval Window –> Moves perilymph and round window stabilises –> Vibrations travel through to endolymph to –> Tectorial membrane –> Movement of hair cells –> Depolarisation of Cochlear Nerve fibres
High frequency sounds at base of cochlea, Low frequency at apex
What types of movement do the semicircular canals, utricle and saccule detect?
Semicircular canals: rotary movements
Utricle and Saccule: linear movements
What three things are needed for balance?
- Proprioception
- Vestibular system
- Visual inputs
What is vertigo and what are the causes of this?
Hallucination of movement
Central Caues (Brainstem and Cerebellum): MS, Posterior stroke, Migraine, Intracranial SOL, Drugs
Otological (peripheral): BPPV, Meniere’s, Vestibular Neuronitis, Labrynthitis, Vestibular Neuroma
How can you tell the difference between central and otogenic causes of vertigo?
Vestibular (peripheral):
- Severe and may be accompanied by loss of balance
- Nausea, vomiting
- Hearing loss and tinnitus
- Nystagmus (usually horizontal)
- Diaphoresis
Central:
- Less severe
- No hearing loss or tinnitus
- Nystagmus can be horizontal and vertical
When somebody presents with vertigo, what examination should you do?
- Assess CNs and ears
- Test cerebellar function (DANISH) & reflexes: nystagmus, gait
- Romberg’s test (+ve if balance is worse when eyes are shut, implying defective joint position sense or vestibular input).
- Do provocation tests (Head thrust test and hallpike test)
- MRI to look for vestibular schwanomma
What is the pathophysiology and aetiology of BPPV?
Pathophysiology
- Presence of canaliths (calcium carbonate) in the semi-circular canal instead of the utricle
- When the patient moves their head the crystals move and move the endolymph in the semicircular canals producing vertigo
Aetiology
- Previous head trauma
- Older patients
- Previous history of labrynthitis
How does BPPV present?
- Vertigo attack that last seconds to a minute with certain head movements
- Nausea and vomiting
How is BPPV diagnosed and managed?
Diagnosis:
- Ensure vertigo is not persistent, no nystagmus, no CN palsies
- Dix-Hallpike test (look for torsional nystagmus that lasts <1min)
Treatment:
- Self limiting
- Epley manouvre if persisitent
- Brandt-Darroff exercises
What are some contraindications for the Dix-Hallpike test?
(LEARN IMAGE)
- Neck trauma
- Spinal fractures
- Cervical disc prolapse
- Vertebrobasilar insufficiency
- Carotid sinus syncope
- Recent stroke
- Recent CABG
What is some advice you should give to a patient following an Epley manouvre?
- For 48 hours do not drive, bend down, look up and sleep upright
- Resolution is not always complete so may need another manouvre
What is the pathophysiology of Meniere’s disease?
- Idiopathic
- Could be due to increased pressure in endolymph
- Dysfunctioning Na channels, an osmotic gradient is set up that draws fluid into endolymph, increasing endolymphatic pressure
What is the presentation of Meniere’s disease?
TRIAD OF:
- Severe paroxysmal vertigo that lasts minutes to hours with N+V
- Tinnitus
- Fluctuating sensorineural hearing loss (can become permanent over time in later stages)
Lasts minutes to hours but less than 24 hours. Sometimes aural fullness
How is Meniere’s disease investigated and managed?
Ix
- Otoscopy normal
- Tympanometry Type A
- Audiometry sensorineural hearing loss
Mx
- Diet: reduce salt, avoid chocolate and caffeine
- Acute attack: Prochlorperazine buccal or IM (Vestibular Sedative)
- Prevention: Regular betahistine and Thiazide diuretics
- Surgical: Steroid injection, Getamicin injection, Endolymphatic Sac destruction, Labyrinthectomy
What are some risk factors for developing Meniere’s disease?
What is the difference between vestibular neuronitis and labrynthitis?
- Vestibular neuritis is inflammation of the vestibular nerve, NO HEARING LOSS
- Labyrinthitis is inflammation of the labyrinth, HEARING LOSS
- Both are usually triggered by viral infection so preceding URTI. Treat the same way
How does vestibular neuronitis present?
- Sudden onset and severely incapacitating vertigo
- Preceded by URTI
- Nausea and Vomiting
- Horizontal nystagmus
- No hearing loss
- Neurological exam is normal
Lasts for several days to a week. Can have a long term vestibular deficit afterwards so may be unsteady for a number of weeks whilst the brain compensates for this
How is vestibular neuronitis managed?
- Vestibular sedatives e.g Prochlorperazine or Cyclizine
- Vestibular rehabiliation exercises if prolonged poor balance (Cawthorne-Cooksey exercises)
- Once acute attack is over need to stop taking vestibular sedatives as this will delay recovery
What are some causes of non-genetic hearing loss in children?
- Intrauterine infection eg CMV, rubella, toxoplasmosis, HSV, syphilis
- Perinatal causes: Prematurity, hypoxia, IVH, kernicterus
- Infections: meningitis, encephalitis, measles, mumps
- Other causes: Ototoxic drugs, acoustic or cranial trauma
What are some hearing tests that can be done in children?
- Universal Newborn Hearing Screening: OAE
- Distraction testing
- Visually reinforced audiometry
- Speech discrimination
What is the difference between a bone anchored hearing aid (BAHA) and a cochlear implant?
Cochlear implant: implanted surgically with electrodes so directly stimulates the auditory nerve with electrodes
BAHA: Sound is transmitted to the cochlear via bone conduction
What are some causes of conductive and sensorineural hearing loss?
Conductive:
- External canal obstruction (wax, foreign body)
- Drum perforation (trauma, barotrauma)
- Problems with the ossicular chain (otosclerosis, infection, trauma)
- Inadequate Eustachian tube ventilation of the middle ear (eg with effusion secondary to nasopharyngeal carcinoma)
Sensorineural:
- Acoustic Neuroma
- Ototoxic drugs e.g Gentamicin, Hydroxychloroquine
- Post infective e.g meningitis, mumps
- Presbyacusis
What serious pathologies do you need to consider with unilateral sensorineural hearing loss?
- Acoustic Neuroma: do MRI
- Choleasteatoma
- Effusion secondary to nasopharyngeal cancer
If a patient presents with sudden onset hearing loss what investigations should you do?
- Pure tone audiogram and Tuning Fork tests as need to find out if sensorineural or conductive
- MRI: exclude acoustic neuroma
What is the definition of sudden onset sensorineural hearing loss and how is this managed?
- Hearing loss over 72 hours with no conductive cause. Loss of at least 30 decibels in 3 consecutive decibels
- Needs urgent referral to ENT as otological emergency within 24 hours
- Management: High dose steroids PO or intratympanic, ?Antivirals, Hyperbaric oxygen
What is presbyacusis and what is the cause/risk factors of this?
- Age-related sensorineural hearing loss
- Usually gradual, bilateral and affects high-pitched sounds first
- Loss of hair cells in cochlea, loss of neurones in cochlea, atrophy of stria vascularis and reduced endolymphatic potential
- Loud noise exposure is biggest risk factor
How does presbyacusis present?
- Not being able to hear in loud environments
- Not paying attention in conversations or missing details
- Can hear males better than females
- Tinnitus
How is presbyacusis diagnosed and managed?
Diagnosis
- Pure-tone audiometry: worse at high frequencies
Management (CANNOT BE REVERSED)
- Optimising environment e.g reduce ambient noise during conversations
- Hearing aids
- Cochlear implants (in patients where hearing aids are not sufficient)
What is tinnitus and what is the pathophysiology of this?
Perception of sound in the absence of auditory stimuli. Could be ringing, buzzing, hissing, humming, pulsatile
Background sensory signal produced by the cochlea that is not effectively filtered out by the central auditory system
What are some of the causes and classificications of tinnitus?
Primary – no underlying cause identified, often associated with sensorineural hearing loss
Secondary – underlying cause identified, further sub-classified into subjective (only heard by the patient) or objective (also audible to the examiner)
What are some examples of objective tinnitus?
Patient can hear an actual sound within their head and the examiner can auscultate it with a stethoscope e.g
- Carotid artery stenosis (pulsatile carotid bruit)
- Aortic stenosis (radiating pulsatile murmur sounds)
- AV malformations (pulsatile)
- Eustachian tube dysfunction (popping or clicking noises)
What are some important questions in a history and exam for a patient presenting with tinnitus?
History:
- Unilateral/Bilateral? Pulsatile/Non-Pulsatile?
- Hearing loss?
- Vertigo?
- Stress?
Examination
- Otoscopy to look for ear wax
- Weber’s and Rinne’s test
- IF UNILATERAL DO MRI FOR ACOUSTIC NEUROMA
When is tinnitus an otological emergency? (e.g red flags associated with tinnitus)
What investigations should you do for a patient with tinnitus?
- Blood tests: FBC (anaemia), TFTs, lipid levels (hyperlipidaemia), blood glucose (diabetes)
- Blood Pressure
- Pure tone audiometry and Tympanometry
- If persistent unilateral then MRI for acoustic neuroma
How is tinnitus managed?
- Treat any underlying cause
- Reassure often gets better with time on it’s own
- CBT
- Psychological help
- If associated hearing loss give hearing aid
- Sound therapy to mask the sound
What is an acoustic neuroma?
- Benign tumour of Schwann cells that surround the vestibulocochlear nerve
- Form at the cerebellopontine angle of the vestibular nerve and when they grow they are space-occupying lesions in the brain
- Most are unilateral, if bilateral suggests neurofibromatosis type II
What is the presentation of an acoustic neuroma?
Gradual Onset Triad:
- Unilateral sensorineural hearing loss
- Unilateral tinnitus
- Dizziness
If grows large enough can cause facial nerve compression and palsy, headache, seizures, increased ICP
How are acoustic neuromas diagnosed?
MRI with contrast
(also send for audiometry)
How are acoustic neuromas managed and what are the risks with the treatment?
Conservative: slow growing so do interval MRI scanning
Surgery: if large can resect whole tumour, partial tumour if risk of facial nerve damge
Stereotactic Radiotherapy: reduce growth
Complications with surgery: Vestibulocochlear damage so dizziness and hearing loss, Facial nerve palsy
What is the halo sign?
If a patient has a petrous fracture may have CSF leak into ear, drop discharge onto filter paper and will show a halo if CSF
Where should you hold your head when administering steroid nasal spray for shrinkage of nasal polyps?
Hold upside down, do not tilt head backwards
How should you manage a vestibular schawnnomma?
- If <40mm do interval MRI scanning every 6/12
- If >40mm need surgery as becoming life threatening as will start to encroach on brainstem and cerebellum
