ENT Flashcards
Describe the sensory supply to the external ear
Upper lateral= CN V3 (auriculotemporal)
Lower lateral and medial= C3 (greater auricular nerve)
Superior medial= C2/3 (lesser occipital)
External auditory meatus= auricular branch of vagus nerve
These nerves can be blocked with local for various procedures
What is important to asses in lacerations of the external ear?
that all the cartilage is covered with skin. if significant skin loss where primary closure will not be possible, plastic surgery reconstruction may be needed
How should bites to the external ear be managed?
- significant risk of infection from skin and oral commensals
- wound left open
- irrigate wound
- prophylactic/ abx for infection
How should pinna haematomas be managed?
Drainage and pressure dressing application (prevents reaccumulation)
How should traumatic (direct or indirect) tympanic membrane perforations be managed?
Most will heal by themselves- watch and wait.
If hasnt healed after 6 months, myringoplasty to repair tymp membrane if its causing problems.
How should haemotymapnum be managed?
- may be associated with temporal bone fracture (head CT) and conductive hearing loss
- treat conservatively as will settle with time but follow up to ensure no residual hearing loss from damage to ossicles
How does otitis externa present?
- painful discharging ear
- swelling to external ear canal
- often history of swimming
How is otitis externa managed?
- topical ear drops (neomycin)
- can get mixed antibacterial + antifungal drops
- swab if resistant
- microscution of pus/ debris may be needed to help get drops to source of infection
- a wick can be helpful to hold ear canal open to allow topical treatment to diffuse through if infection is severe
- advise: avoid swimming for 7-10 days while being treated, ear plugs for showers/ baths, dry ears after swimming with hair dryer on low heat, OTC aceitic acid drops after swimming/ bathing,
What is malignant otitis externa? how is it managed?
- aggressive infection usually seen in diabetic or immunocompromised pts
- spreads from soft tissue into the bone
- presents with chronic ear discharge despoite dopical treatment, deep seated severe ear pain and sometimes CNVII palsies
- treat w/ IV abc + extended topical treatment
What organisms commonly cause acute otitis media and how does it present?
- strep pneumonia and H. influenza
- eat pain (child pulling ear) which improved but then ear starts discharging (as tymp membrane ruptures) and fever
- Otoscopic exam: A distinctly red, yellow, or cloudy tympanic membrane. Moderate to severe bulging of the tympanic membrane, with loss of normal landmarks and an air-fluid level behind the tympanic membrane (indicates a middle ear effusion). Perforation of the tympanic membrane and/or discharge in the external auditory canal.
How is acute otitis media managed?
- most conservativley with analgesia, severe or persistent cases need abx (amoxicillin)
- surgery for grommet if recurrent
How can chronic otitis media (conductive hearing loss + discharge for >6/52) be classified? (2 ways)
Active (discharging) vs inactive (not)
Squamous (cholestaetoma if active, retraction pocket if inactive) vs Mucosal (chronic discharge into middle ear- active if discharging through perforation, often develops from AOM where membrane fails to heal)
How does active squamous chronic otitis media develop?
kertinised squamous cells introduced into middle ear from retraction pocket or perforation
What feature is reassuring if seen in squamous COM?
if anterioinferior part of tymp membrane as carries low risk of cholesteatoma
What needs to be arranged if suspect cholesteatoma and why?
CT scan of petrous temoral bone to assess invasion before removal (wont metastasise but local invasion can cause significant damage)
How can most chronic otitis media be managed?
- aural toileting
- topical abx and steroid treatments until symptoms resolve
- if >6 weeks go to specialist - myringoplasty or tympanoplasty can be done to close large or troublesome perforations
How does otitis media with effusion present?
- usually in children and due to eustachian tube dysfunction (if adult be away of post nasal space tumours)
- conductive hearing loss (may be speech/ lang delay or school problems) and middle ear effusion on otoscopy
- not painful in itself but can lead to AOM which is
How should otitis media with effusion be investigated and what findings would you expect?
- do tympanogram (flat (type B) tracing with normal canal volume)
- pure tone audiogram showing conductive hearing loss
How is otitis media with effusion managed?
- conservative 1st line- most will resolve in 3 months
- hearing aids
- grommets +/- adenoidectomy
how does otosclerosis present?
- in elderly, F>M
- progressive conductive hearing loss
- which is improved in noisy surroundings during early stages of the disease
- often tinnitus and fhx
How should otosclerosis be investigated and what results would you expect?
- tympanogram shows normal type A tracing
- pure tone audiogram shows conductive hearingloss with characteristic carhart notch at 2kHz
How can otosclerosis be managed?
- hearing aids
- surgically with stapedectomy
What is the difference between the cochlear and the vestibular system?
cochlear is for hearing- stapes taps on window and moves hair cells.
Vestible is for balance- 3 of semicircular canals at 90degrees to eachother so movement in different planes causes movement of perilymph within them. The utricle has hair cells sticking up to detect horizonal movement. The saccule has hair cells sticking out so detects verticle movements
What contributes to good balance?
- vestibular system
- proprioception
- vision
integrated centrally by - vestibular nerve
- peripheral nerves and dorsal column
- cranial nerves
- brain/ brainstem/ cerebellum
Describe the differences in signs and symptoms of central and peripheral vertigo
Central: - gradual onset - constant and milder - unaffected by head position and movement - N+V less predictable - motor function, gait instability and ataxia common Peripheral: - sudden onset - intermittent but severe symptoms - affected by head position and movement - N+V severe and more frequent - motor function, gait and coordination usually intact
Give 3 central causes of vertigo?
- stroke
- migraine
- neoplasms
- demyelination eg MS
- drugs (gent, loop diuretics, chemo, amlodipine, SSRIs, anti epileptics, diazepams)
Give 3 peripheral causes of vertigo
- BPPV
- Menieres
- Vestibular neuritis
- labyrinthitis
What causes BPPV?
otoliths (crystals) in semicircular canals (most commonly posterior) causing abnormal stimulation of hair cells causing hallucination of movement when disturbed
How is BPPV diagnosed and treated?
diagnosis is with dix hallpike test and treatment is with epley manoruvre or brandt daroff exercises
What is thought to cause menieres disease?
- endolyphatic hydrops (increased fluid in endolymphatic compartment)
- not sure why exactly though
How does menieres present?
- tinnitus in affected ear
- episodic vertigo lasting mins-hrs with N+V
- fluctuating sensorineural hearing loss which becomes more apparent overtime
- aural fullness feeling
- initially well between attacks but feel unsteady and get sensorinueral hearing loss in between attacks as it progresses
- disease burns out overtime so dont have acute vertigo but have reduced hearing and generally poor balance (good ear can compensate to improve balance but takes time esp in elderly)
How can menieres be managed?
- reduce salt, chocolate, alcohol, caffeine, chinese food
- thiazides, betahistines and vestibular sedatives eg prochlorperazine (for acute attacks only) can help
- surgical options inc grommet, dexamethasone injections into middle ear, endolymphatic sac decompression, vestibular destruction w/ gent injection and surgical labyrinthectomy (rare)