ENT Flashcards
1
Q
Describe the anatomy of the external ear?
A
- Lined with skin
- Supplied by the greater auricular nerve, lesser occipital and facial nerve
- Includes the pinna, external auditory meatus, and tympanic membrane
-
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
-
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
-
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
2
Q
Is this image from the left or right side of the body?
Identify the indicated parts of the tympanic membrane
A
- 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
3
Q
Identify the indicated parts of the external ear:
What is the pinna?
A
- Concha
- Tragus
- External acoustic meatus
- Lobule
- Antitragus
- Antihelix
- Helix
Pinna = auricle = the external ear that we see:
- Cartilage underlying skin
- Lobule is just fat
4
Q
Identify the indicated parts of the external, middle and internal ear
A
- Auricle
- External acoustic meatus
- Cartilage
- Tympanic membrane
- Pharyngotympanic tube
- Pharynx
- Internal acoustic meatus
5
Q
Describe the anatomy of the middle ear- what’s its function & how does it perform said function?
A
- 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
6
Q
Describe the anatomy of the inner ear
A
- 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:
7
Q
Identify the indicated structures related to the inner ear
A
- Central vestibule
- Semicircular canals
- Semicircular duct
- Facial nerve
- Vestibular nerve
- Vestibulocochlear nerve
- Internal acoustic meatus
- Cochlear nerve
- Cochlea
- Cochlear duct
8
Q
What is the vestibular system?
A
- 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
9
Q
What is the sensory supply to the pinna?
A
- 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
10
Q
What are the branches of the trigeminal nerve & their functions?
A
- CN V1: Ophthalmic division
- CN V2: Maxillary division
- CN V3: Mandibular division
11
Q
How does a haematoma form in the auricle?
Why is it important to recognise pinna haematoma?
A
- 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
12
Q
How to recognise & treat a pinna haematoma?
A
- 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
13
Q
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?
A
- If ear clearly contaminated, haematoma older than 24 hrs, or signs of infection à give abx too eg oral amoxicillin or clarithromycin
14
Q
Causes of a tympanic membrane perforation? How do pts commonly present?
A
- 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
15
Q
How to assess & manage a tympanic membrane perforation?
A
- 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
16
Q
Red flags for temporal bone fracture?
A
- CSF otorrhoea/ rinorrhoea
- Facial nerve paralysis
- Post-auricular or periorbital ecchymosis
- Haemotympanum/ pinna haematoma/ lacerations
- Severe nystagmus
- Vertigo
17
Q
Why is it important to recognise a fracture of the temporal bone?
A
- Potential ENT short & long term complications include CSF leak, meningitis, hearing loss, facial nerve palsy
18
Q
Describe the management of temporal bone fracture?
A
- 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
19
Q
What is haemotympanum & what can it suggest?
A
- 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
20
Q
- 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?
A
- 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
21
Q
Suggest some examples of causative microorganisms of acute otitis externa?
A
- 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)
22
Q
What are some risk factors for developing otitis externa?
A
- 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
23
Q
What are some complications of otitis externa and who’s at risk of developing these complications?
A
- 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
24
Q
Most common causative organism of malignant otitis externa? What to do if you suspect it?
A
- 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
25
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
26
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
27
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
28
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
29
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)
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
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
* 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
40
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
41
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
42
What diseases can affect proprioceptive ability?
* Diabetes- neuropathy
* Joint replacements- loss of joint receptors
43
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
44
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
45
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
46
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
47
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
48
# 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
49
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
50
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
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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)
60
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
61
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
62
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
63
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
64
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)
65
What is tinnitus?
* Persistent addition sound that is heard but not present in surrounding environment
* Ringing in ears, buzzing, hissing or humming
66
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
67
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
68
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
69
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
70
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
71
Most common causes of hearing loss in the UK?
* Presbycusis and exposure to excessive noise
72
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
73
Why does presbycusis occur?
* Loss of hair cells in cochlea
* Loss of neurones in cochlea
* Atrophy of stria vascularis
* Reduced endolymphatic potential
74
Risk factors for developing presbycusis?
* Age
* Male
* FHx
* Loud noise exposure
* Diabetes
* HTN
* Ototoxic medications
* Smoking
75
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
76
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)
77
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
78
What is the diagnostic criteria for sudden sensorineural hearing loss?
* Audiological diagnostic criteria for SSNHL- rule of three:
1. Sensorineural loss worse than 30dB
2. In 3 consecutive frequencies
3. Within 3 days (72hrs)
79
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
80
What are the consequences of ear wax impaction?
* Conductive hearing loss
* Discomfort in ear
* Feeling of fullness
* Pain
* Tinnitus
81
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
82
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)
83
Briefly describe the types of hearing aids available?
* Behind the ear hearing aids- most common type
* In the ear hearing aids
* Completely in canal
84
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)
85
Indications for a cochlea implant?
* According to NICE:
* Unilateral cochlea implant for severe to profound deafness in adults who do not benefit from hearing aids, after a 3 month trial with the aids
* Simultaneous bilateral cochlear implant for:
* Children
* Adults who are blind or who have other disabilities that increase their reliance on auditory stimuli as a primary sensory mechanism for spatial awareness
86
Contraindications to consideration for cochlear implant?
* Lesions of cranial nerve VIII or the brainstem causing deafness
* Chronic infective otitis media, mastoid cavity or tympanic membrane perforation
* Cochlear aplasia
87
Difference between 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
88
Name some medications that cause sensorineural hearing loss?
* Loop diuretics eg furosemide
* Aminoglycoside abx eg gentamicin
* Chemotherapy drugs eg cisplatin
89
Causes of severe-to-profound hearing loss?
* Children
* Genetic- 50% cases
* Congenital- maternal CMV, rubella or varicella infection
* Idiopathic- 30% childhood deafness
* Infectious- eg post meningitis
* Adult
* Viral-induced sudden hearing loss
* Ototoxicity eg aminoglycoside abx or loop diuretics
* Otosclerosis
* Meniere’s disease
* Trauma
90
Signs/ symptoms of congenital deafness?
* Poor speech development
* Difficulty following verbal directions
* Difficulty with oral expression
* Poor response to auditory cues
91
How to recognise deafness in a child?
* Newborn hearing screening
* If babies fail, they repeat the test
* If they fail again they’re referred to ENT
* Audiometry to determine range of hearing
* It is important to recognise deafness within 12 months of life
92
What is an audiogram?
* Audiometry involves objectively assessing hearing by playing a variety of tones and volumes
* Headphones (air conduction) and an oscillator (bone conduction device) that delivers sound d irectly to the bones of the skull
* Audiometry results are recorded on an audiogram which help identify & differentiate conductive and sensorineural hearing loss
* X-axis: frequency in Hz (different tones)
* Y-axis: volume in dB (loud at bottom, quiet at the top- the higher up the y axis the more sensitive a pt’s hearing is)
* Normal hearing: all readings between 0 and 20 dB
* Sensorineural hearing loss: air and bone conduction are \>20dB
* Conductive hearing loss: BC normal, but air \>20dB
* Mixed hearing loss: both air and bone conduction \>20dB but there is a difference of \>15dB between the two
93
What is an acoustic neuroma?
* = Vestibular schwannoma
* Tumour surrounding vestibulocochlear nerve
* Schwann cells provide the myelin sheath and are found in the peripheral nervous system
* Occur @ cerebellopontine angle
* Usually unilateral
94
What are bilateral acoustic neuromas often associated with?
* Neurofibromatosis type II
* Autosomal dominant
* Chromosome 22
* Also causes multiple intracranial schwannomas, meningiomas and ependyomas
95
What symptoms does a patient with an acoustic neuroma experience? How to investigate?
* Unilateral sensorineural hearing loss- this is often the initial symptom
* Unilateral tinnitus
* Dizziness or imbalance
* Sensation of fullness in ear
* Ix- MRI of cerebellopontine angle, audiometry as only 5% pts will have a normal audiogram
96
How is an acoustic neuroma managed?
* Conservative- monitor if no symptoms or if it is inappropriate to treat
* Surgery- partial or total removal of tumour
* Radiotherapy- reduce the growth of the tumour
* Risks- vestibulocochlear nerve injury leading to permanent hearing loss, facial nerve injury, facial weakness
97
Describe the anatomical course of the facial nerve?
* Arises at the lower pons
* Begins as 2 roots- large motor and small sensory root
* Travel through the internal acoustic meatus to enter the petrous part of the temporal bone
* Still within temporal bone, the roots enter the facial canal- Z shaped.
* The 2 roots fuse together to form the facial nerve
* The nerve forms the geniculate ganglion
* The nerve gives rise to the following-
* Greater petrosal nerve
* Nerve to stapedius
* Chorda tympani
* Then the facial nerve exits the facial canal (and cranium) via stylomastoid foramen
* First extracranial branch is posterior auricular nerve
* Immediately distal to this, motor branches to posterior belly of digastric and stylohyoid muscles
* The motor root continues anteriorly & inferiorly into the parotid gland- 5 branches
* Temporal branch
* Zygomatic branch
* Buccal branch
* Marginal mandibular branch
* Cervical branch
98
What are the functions of the facial nerve?
* MOTOR FUNCTIONS
* Muscles of facial expression
* Stapedius in inner ear
* Posterior digastric, stylohyoid, platysma in neck
* SENSORY FUNCTIONS
* Taste from anterior 2/3 of tongue
* PARASYMPATHETIC FUNCTIONS
* Greater petrosal nerve- lacrimal gland, mucous glands of oral cavity, nose + pharynx
* Chorda tympani- submandibular + sublingual salivary glands
99
How to distinguish between an upper motor neurone and lower motor neurone facial nerve palsy?
* Pt with new onset umn facial nerve palsy- suspect stroke
* Lmn facial nerve palsy- less urgent
* Each side of the forehead has umn innervation by both sides of the brain
* However each side of the forehead only has lmn innervation from one side of the brain
* So in an umn lesion, the forehead is spared and the patient can move their forehead on the affected side
* In a lmn lesion, the forehead is NOT spared, the pt can’t move their forehead on the affected side
* How to differentiate- ask pt to raise their eyebrows, If they can raise both & wrinkle both sides of forehead = umn lesion
* If eyebrow on affected side can’t be raised and forehead remains smooth = lmn lesion
100
What causes upper motor neurone lesions of the facial nerve?
* Unilateral:
* Stroke
* Tumour
* Bilateral: rare
* Pseudobulbar palsies
* Motor neurone disease
101
Red flags to look out for when patient presents with facial nerve palsy?
* Facial nerve palsy associated w/ severe otalgia- ?mastoiditis, necrotising otitis externa
* Facial nerve palsy w/ parotid swelling in elderly pt- ?parotid malignancy
* Facial nerve palsy w/ trauma- urgent decompression may be required
* Other associated neuro symptoms- ?stroke
102
What is Bell’s palsy, what causes it & how is it managed?
* Often idiopathic- commoner in the elderly \>age 70
* Other causes include central or peripheral nervous system lesions, trauma including iatrogenic causes eg surgery for acoustic neuroma, systemic infection & inflammations, Herpes zoster virus (Ramsay Hunt syndrome), mastoiditis, parotid tumours, previous SCC of the periocular or facial region
* Unilateral lmn facial nerve palsy
* Most pts recover over several weeks up to 1 year
* 1/3 left with residual weakness
* If they present within 72 hours of developing symptoms- treat w/ prednisolone
* 50mg for 10 days
* 60mg for 5 days followed by 5 day reducing regime of 10mg a day
* Lubricating eye drops to prevent eye on affected side drying out/ damaged
103
How does facial nerve palsy present?
* Facial weakness or droop
* Weakness can cause asymmetry at rest or only on movement of the face
* Hyperacusis (nerve to stapedius)
* Loss of taste sensation in anterior 2/3 of tongue (chorda tympani)
104
Differential diagnoses for facial nerve palsy?
* Idiopathic
* Bell’s palsy is the most common cause; diagnosis of exclusion
* Infection
* AOM +/- mastoiditis
* NOE
* Lyme disease
* Ramsey-Hunt syndrome (Herpes zoster)
* Trauma
* Temporal bone #
* Damage during surgery to middle ear or parotid
* Neoplastic
* Parotid carcinoma
* Acoustic neuroma
* Cholesteatoma (benign)
* Neurological
* Stroke
* GB syndrome
* Sarcoidosis
* MS
105
What is Ramsey Hunt syndrome caused by & how is it managed?
* Caused by Herpes zoster virus
* Presents as unilateral lmn facial nerve palsy
* Painful and tender vesicular rash in ear canal, pinna and around the ear on the affected side
* The rash can extend to the anterior 2/3 of the tongue and hard palate
* Mx- within 72 hrs initiate prednisolone & acyclovir
* Lubricating eye drops
* PPI cover- gastroprotection
* (RH syndrome is a common MCQ)
106
Describe the skeletal structure of the external nose?
* Bony component- superiorly, contributions from nasal bones, maxillae and frontal bone
* Cartilaginous component- inferiorly, inflect into tip of nose
107
Causes of saddle-shape nose deformity?
* Granulomatosis with polyangiitis (Wegener’s granulomatosis)
* Direct trauma to septal bone or cartilage
* Untreated nasal septal haematoma- leads to avascular necrosis of cartilaginous septum
108
Describe the nerve innervation to the nose and nerve cavity?
* Sensory- trigeminal nerve
* Motor- facial nerve
109
Describe the blood supply to the nasal mucosa?
What are the implications of this in an infection?
* Arterial supply comes from branches of ophthalmic artery and maxillary artery
* Anterior and posterior ethmoidal branches from ophthalmic artery (from internal carotid)
* Sphenopalatine branch of maxillary artery (from external carotid)
* Arterial anastomoses in anterior septum- Kisselbach’s plexus/ Little’s area
* Venous drainage from nasal cavity into pterygoid venous plexus, cavernous sinus, and facial vein
* This is known as the danger triangle of the face
* Infection from the nasal area can spread to the brain because the cavernous sinus is in the bran
* Retrograde spread of infection can cause cavernous sinus thrombosis, meningitis, brain abscess
110
Where does bleeding from the nose usually originate?
* Majority is anterior
* Little’s area on the anterior septum
* Posterior- small minority
111
How to advise patients on how to manage a nosebleed?
* Sit up & tilt head forwards
* Squeeze the soft part of the nostrils together for 10-15 mins
* Spit out any blood in the mouth (don’t swallow)
112
How to treat nosebleeds?
* Conservative measures for 15 mins- squeeze soft parts of nostrils together
* Nasal cautery using silver nitrate sticks- first line
* Nasal packing using nasal tampons or inflatable packs- try the above before nasal packing- drawbacks of packing:
* Mucosal trauma
* Pain and discomfort for pt
* Obstruction of nasal airway in COPD etc à may need to sleep semi-upright or require supplementary O2
* Need for admission/ increased length of stay. Tend to stay in for 24-48hrs max. prolonged packing à abx
* After bleed- Naseptin nasal cream (chlorhexidine and neomycin) QDS for 10 days can reduce crusting, inflammation, infection
* Contraindicated in peanut/ soya allergy
113
Advice for patients following a nosebleed?
* Don’t blow or pick nose
* Avoid piping hot food and drink for a day
* Avoid strenuous activity/ exercise for a couple of days
* Apply antiseptic cream twice a day for 2 weeks
* First-aid measures in case of re-bleed
* Attend A&E If nosebleed \>20mins
114
Complications of nasal fracture?
* Septal haematoma
* Very important- can lead to septal abscess & ascending cavernous sinus infection, necrosis of septal cartilage, saddle deformity, septal perforation
* CSF leak
* Anosmia
* Septal deviation leading to nasal obstruction
115
How to manage nasal fracture?
* Isolated nasal injuries can be managed as outpatient as the nose is too swollen immediately after trauma
* Discharge from A&E and book into emergency ENT clinic 7-10 days later for manipulation under anaesthesia
116
What is septal haematoma?
* Blood collecting under the lining of the septal cartilage- between the nasal septal cartilage and overlying perichondrium + mucosa
* Causing a red-purple fluctuant swelling on both sides of the nasal septum
* Early diagnosis and treatment is important to prevent abscess formation, septal perforation, saddle nose deformity
* Most common symptoms in children- nasal obstruction, pain, rhinorrhoea, fever
* Mx- urgent surgical drainage to reduce risk of cartilage necrosis
117
How to determine CSF rhinorrhoea?
* Send a sample of the watery nasal discharge to the lab for β-2-transferrrin/ tau protein to determine if it is CSF or not
* You can give a small plastic sterile container to the pt to catch the discharge at home if necessary
118
Identify the important causes of rhinitis? How to diagnose, investigate and manage it?
* Acute or chronic
* Allergic or non-allergic
* Allergic: IgE mediated inflammatory disorder of the nose where the nasal mucosa becomes exposed + sensitised to allergens, to produce typical symptoms of sneezing, nasal itching, discharge (rinorrhoea), and congestion
* Mx- nasal irrigation w/ saline, avoid allergens, intranasal corticosteroid during periods of allergen exposure, add-on treatments include intranasal decongestant, intranasal anticholinergic
* Non-allergic can be caused by a cold or the flu, spicy foods
119
Key features of acute rhinosinusitis?
* Nasal blockage
* Rinorrhoea (nasal discharge)
* Hyposmia (reduced smell
* Facial or dental pressure/ pain
* Tenderness over the sinuses
* Usually no swelling- any swellings below zygoma (cheek or jaw) consider dental abscess or salivary gland infection
* The above 4 are the most predictive symptoms; not all 4 have to be present
* Also may have systemic malaise, fever, cough, sore throat
120
What is acute rhinosinusitis?
* Acute inflammatory condition following a viral URTI
* Increase in symptoms following initial viral illness- double sickening
121
How to manage acute rhinosinusitis?
* Symptomatic care- simple analgesia (paracetamol, ibuprofen), 5 day course nasal decongestant
* Should not prescribe abx unless persistent infective symptoms \>10 days or suspecting sepsis, or immunosuppressed
* Penicillin V 500mg qds 5 days
* Pts who are systemically unwell/ more serious illness/ high risk of complications/ not responding after 2-3 days- co-amoxiclav 500/125m tds 5 days
122
What is sinusitis?
* Inflammation of the paranasal sinuses in the face
* This can be accompanied by inflammation of the nasal cavity – rhinosinusitis
123
Describe the anatomy and function of the paranasal sinuses?
* 4 paranasal sinuses
1. Frontal sinuses (2, above eyebrows)
2. Maxillary sinuses (either side of nose below the eyes)
3. Ethmoid sinuses (in ethmoid bone in middle of nasal cavity)
4. Sphenoid sinuses (in sphenoid bone at back of nasal cavity)
* Function- various roles are suggested
* Lightening the weight of the head
* Supporting immune defence of nasal cavity
* Humidifying inspired air
* Increasing resonance of voice
124
Why can sinusitis present with toothache?
* Maxillary nerve supplies both the maxillary sinus and maxillary teeth so inflammation of the maxillary sinus can present with toothache
125
Causes of sinusitis?
* Infection- viral URTI
* Allergies- hayfever
* Obstruction of draining eg foreign body, trauma, polyp
* Smoking
* Asthma is associated with higher incidence of sinusitis
126
How do patients with sinusitis present?
* Nasal congestion
* Facial pain or headache
* Nasal discharge
* Facial pressure
* Facial swelling
* Loss of smell
* Tenderness to palpation over affected areas
* Fever
* Chronic sinusitis= \>12wks
127
Management of acute and chronic sinusitis?
* Acute-
* Analgesia for pain/ fever
* Abx? – if worsening or not improving within a week
* High dose intranasal corticosteroids in adults with severe or prolonged symptoms
* Chronic-
* Manage any associated disorder eg allergic rhinitis, asthma
* Avoid triggers
* Nasal irrigation with saline solution
* Intranasal corticosteroids
* Long term abx? Consult specialist
* Surgery-
* Functional endoscopic sinus surgery- inserting small endoscope through nostrils and sinuses to remove any obstructions to the sinuses – eg swollen mucosa, bone, polyps, deviated septum (septoplasty)
* CT required beforehand to confirm diagnosis
128
How to explain the use of a steroid nasal spray to patients?
* Tilt head slightly forward
* Use the left hand to spray into the right nostril and vice versa
* NOT sniffing hard during the spray
* Very gently inhaling through the nose after the spray
129
What are nasal polyps?
* Growths of nasal mucosa that occur in the nasal cavity or sinuses
* Often associated with inflammation – chronic rhinitis
* Grow slowly & obstruct nasal passage gradually
* Usually bilateral
* Unilateral = red flag for tumour
130
What conditions can nasal polyps be associated with?
What are some symptoms patients may experience?
* Chronic rhinitis/ sinusitis
* Asthma
* Samter’s triad- nasal polyps, asthma, aspirin sensitivity
* Cystic fibrosis
* Eosinophilic granulomatosis with polyangiitis (Churg Strauss syndrome)
* Symptoms- difficulty breathing, snoring, nasal discharge, anosmia
131
How to manage nasal polyps?
* Unilateral- urgent 2WW referral, suspect malignancy
* Medical- intranasal topical steroid drops or spray
* Surgery- if medical mx fails- intranasal polypectomy (for more visible polyps) or endoscopic nasal polypectomy (where they’re deeper inside)
132
What is the oropharynx?
* Posterior 1/3 of tongue
* Tonsils on both sides
* Uvula
* Soft palate
* (Hard palate is oral cavity)
133
Describe the sensory supply to the tongue?
* Anterior 2/3
* Sensation- trigeminal- lingual branch of V3 (mandibular)
* Taste- facial- chorda tympani branch
* Posterior 1/3
* Sensation & taste- glossopharyngeal (IX)
134
How do salivary gland stones present, where are they commonly located & how to treat?
* = sialolithiasis
* Formation of calculi (sialoliths) inside the ducts or parenchyma of salivary glands
* Most common in submandibular gland
* Symptoms- stimulated by eating- pain in gland, swelling, infection
* Diagnosis- X-ray, sialogram
* Mx- conservative, hydrate, moist head, NSAIDs, sucking something sour to increase saliva production
135
* Most common- viral infection
* Bacteria- commonest is group A strep (strep pyogenes)
* Strep pneumoniae
* Haemophilius influenzae
* Moraxella catarrhalis
136
How do patients with tonsillitis present?
* Sore throat
* Fever
* Pain on swallowing (however if they can still swallow good amount of fluid, they don’t need to be admitted)
* Cervical lymph nodes
* Bad breath
* O/E- red, inflamed, enlarged tonsils, +/- exudates (small white patches of pus on tonsils), anterior cervical lymphadenopathy
137
Red flags in patients with suspected tonsillitis?
* Severe sore throat, hoarse croaky voice, dysphagia and fever – epiglottitis until proven otherwise
* Pts may develop stridor as late sign and can decompensate very quickly
* Severe sore throat where you cant see evidence of tonsillitis- epiglottitis until proven otherwise
* Hot potato voice, stertor, trismus (reduced mouth opening)- peritonsillar abscess or quinsy
138
What is the Centor criteria and what is the function?
* Used to estimate the probability that tonsillitis is due to a bacterial infection and will benefit from abx
* A score of 3 or more gives 40-60% chance of bacterial so will offer abx
* A point for each of the following:
* Fever \>38
* Tonsillar exudates
* Absence of cough
* Tender anterior cervical lymph nodes
(CENT: cant cough, exudate, nodes, temperature)
139
What is the FeverPAIN score used for?
* Used as an alternative to the Centor criteria
* A score of 2-3 gives a 34-40% chance, and 4-5 gives 62-65% chance of bacterial cause of tonsillitis (strep pyogenes)
* A point for each of the following:
* Fever during previous 24 hrs
* Pus on tonsils
* Attended within 3 days of onset of symptoms
* Inflamed tonsils
* No cough or coryza
140
How to manage tonsillitis?
* Calculate Centor criteria or FeverPAIN score
* Safety net
* Simple analgesia for pain and fever
* Advise pts to return if pain hasn’t settled within 3 days or fever \> 38.3
* Antibiotics if:
* Centor \>3
* FeverPAIN \>4
* Young infants
* Immunocompromised
* Co-morbidities
* Rheumatic fever hx
* Consider a delayed prescription, where you advise the pts or parents about the likely viral nature of sore throat & if symptoms worsen within 3 days to collect the abx prescription
* Which abx?
* Penicillin V 10-day course
* Clarithromycin if penicillin allergy
141
Patients with tonsillitis- who to admit? How to manage?
* Admit if-
* Immunocompromised
* Systemically unwell
* Dehydrated
* Stridor/ stertor
* Respiratory distress
* Peritonsillar abscess or cellulitis
* IV access
* FBC, U&Es, LFTs, glandular fever screen
* Regular basic IV/ PO analgesia- paracetamol + ibuprofen, stronger PRNs
* Topical analgesic spray eg benzydamine spray
* Fluids- 1 L normal saline over 1-2 hrs often needed as majority pts are often young and dehydrated
* Single stat dose steroid eg 6.6mg dexamethasone sodium phosphate IV, or 40mg prednisolone PO, esp. for those with stertor
* Abscesses may need aspiration
142
Suggest some complications of tonsillitis?
* Quinsy (peritonsillar abscess)
* Otitis media
* Scarlet fever
* Rheumatic fever
* Post-strep GN
* Post-strep Reactive arthritis
143
What is a peri-tonsillar abscess?
* A complication of acute tonsillitis
* Where a collection of pus forms in the peritonsillar space
* This pushes the affected tonsil inferomedially into the oropharyngeal space
144
When to suspect peri-tonsillar abscess?
* Similar symptoms as tonsillitis-
* Sore throat
* Painful swallowing
* Fever
* Neck pain
* Referred ear pain
* Swollen tender lymph nodes
* Additional symptoms that can indicate peritonsillar abscess-
* Trismus- unable to open mouth
* Change in voice- due to pharyngeal swelling = hot potato voice
* Swelling and erythema in the area behind the tonsils
145
Cause of quinsy?
* Usually due to a bacterial infection
* Most commonly strep pyogenes (group A strep)
* Other causes- staph aureus, H influenzae
146
How to manage patients with quinsy?
* Admit into hospital (ENT)
* Admit anyone unable to swallow enough fluid to stay hydrated
* Incision and drainage of abscess under general anaesthetic
* Abx before & after surgery
* Broad spectrum: co-amoxiclav (IV)
* Some ENT surgeons give dexamethasone to settle inflammation & aid recovery
147
What are they key signs that differentiate quinsy from tonsillitis?
* Trismus
* On the affected side, the anterior arch is pushed medially
* On the affected side, the palate will bulge toward you, ie the normally concave palate becomes convex
* The uvula may be pushed away from affected side
* On the affected side, the mucosa of the arch and palate look angrily erythematous
148
What is a tonsillectomy and what are the indications for it?
* Surgical removal of tonsils
* Prevents further episodes of tonsillitis
* Patients can still get a sore throat from other causes such as pharyngitis
* Generally a day case procedure under GA
* Indications-
* 7+ episodes of acute sore throat in 1 year
* 5 per year for 2 years
* 3 per year for 3 years
* Recurrent tonsillar abscess (2 episodes)
* Enlarged tonsils causing difficulty breathing, swallowing or snoring
149
Complications of tonsillectomy?
* Sore throat where the tonsillar tissue has been removed (can last 2wks)
* Damage to teeth
* Infection
* Post-tonsillectomy bleeding
* Risks with GA
150
How to manage post tonsillectomy bleeding?
* This is the main significant complication after a tonsillectomy
* Occurs in ~5% pts who have had a tonsillectomy
* Happens up to 2 wks after
* Get IV access, send bloods- FBC, clotting screen, G&S, cross match
* Call ENT reg
* Keep pts calm and give adequate analgesia
* Sit pts up and advise to spit out blood rather than swallowing
* Suction should be available if needed
* Make pts NBM in case of surgery
* IV fluids for maintenance & resuscitation as required
* Ice pack on back of neck
* IV tranexamic acid
* If very severe bleeding, compromise to airway- call anaesthetist- may intubate
* For less severe bleeds
* Hydrogen peroxide gargle
* Adrenaline soaked swab applied topically
151
Describe the borders of the anterior triangle?
* Superior border: mandible
* Medial border: midline of neck
* Lateral border: scm
152
Describe the borders of the posterior triangle?
* Inferior border: clavicle
* Posterior border: trapezius
* Lateral border: scm
153
Causes of a neck lump?
* Congenital- branchial cyst, cystic hygroma, TGDC
* Acquired
* Trauma, infection, neoplasia, connective tissue, endocrine
* Benign- thyroglossal duct cyst
* Malignant- metastatic cancers, thyroid cancer, lymphoma
* Inflammatory- reactive nodes, tonsillitis, glandular fever
* Granulomatous diseases- toxoplasmosis, tuberculosis, sarcoidosis
* Infective- abscess, CMV, EBV
* Endocrine- thyroid, parathyroid
154
Differentials for a neck lump in adults?
* Normal structures- bones etc
* Skin abscess
* TB
* Lymphadenopathy
* Tumour
* Lipoma
* Goitre or thyroid nodules
* Salivary gland stones or infection
* Carotid body tumour
* Haematoma
* Thyroglossal cysts
* Brachial cysts
155
Differentials for a neck lump in children?
* Cystic hygromas
* Dermoid cysts
* Haemangioma’s
* Venous malformation
156
Who gets referred for a 2WW for suspected H&N cancer?
* Unexplained neck lump in someone \>45 years
* Persistent unexplained neck lump any age
* For a lump growing in size-
* Urgent 2 week USS if age \>25
* Within 48hrs if age \<25
* And then refer 2WW if the USS suggests soft tissue sarcoma
157
How to investigate neck lumps?
* Bloods
* FBC and blood film for leukaemia and infection
* HIV test
* IM test- EMV antibodies
* TFTs- goitre, thyroid nodules
* ANA- SLE
* LDH- Hodgkin lymphoma
* Imaging
* USS often first line
* CT or MRI
* Nuclear medicine scan- for toxic thyroid nodules or PET scans for metastatic cancer
* Biopsy
* FNA cytology
* Core biopsy
* Incision biopsy
* Removal of lump
158
Causes of lymphadenopathy?
* Reactive- viral URIT, dental infection, tonsillitis
* Infected- TB, HIV, IM
* Inflammatory- SLE, sarcoidosis
* Malignancy- lymphoma, leukaemia, mets
159
Enlargement of which lymph nodes are most concerning for malignancy of cervical lymph nodes?
* Supraclavicular nodes
160
Infectious mononucleosis: what causes it, how is it spread, and how does it present?
How do we investigate & treat?
* Caused by EBV
* Spread via saliva
* Presentation- classic triad of sore throat, pyrexia, lymphadenopathy
* Fatigue
* Very itchy maculopapular rash in response to amoxicillin or cephalosporins
* Splenomegaly ~50% pts
* Hepatitis, transient rise in ALT
* Ix-
* First-line- Monospot test = heterophil antibody test
* NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever
* IgM (acute infection)
* IgG (immunity)
* Mx-
* Supportive- rest, drink plenty fluids, simple analgesia for aches or pains
* Avoid alcohol- risk of alcohol impairment
* Avoid sports for at least 8 weeks after having glandular fever- splenic rupture
161
Where is the thyroid located?
What is the function of the thyroid?
* Mid-line of neck
* Anterior to trachea
* Inferior to larynx
* 2 lateral lobes
* Central isthmus
* Surrounded by fibrous capsule
* Located at level of vertebrae C5-T1
* Function- produce T3 and T4- following stimulation by TSH
162
Blood supply to thyroid?
* External carotid artery
* Superior thyroid arteries (1st branch ECA)
* Hyoid artery
* Scm branches
* Superior laryngeal artery
* Cricothyroid branch
* Thyrocervical trunk
* Inferior thyroid arteries
* Inferior laryngeal
* Oesophageal
* Tracheal
* Ascending cervical
* Pharyngeal
163
What is the recurrent laryngeal nerve?
* Branch of vagus nerve
* The right side branches at level of subclavian artery
* The left side branches from arch of aorta
164
Functions of the recurrent laryngeal nerve?
* Motor
* Intrinsic muscles of larynx (except cricothyroid muscle)
* Sensory
* Glottis
* Subglottis
* Trachea
165
What are the salivary glands?
* Parotid glands
* Submandibular glands
* Sublingual glands
166
Causes of enlarged salivary glands?
* Stones- blocking the drainage- sialolithesis
* Infection
* Tumours
167
Features of carotid body tumour?
* Slow growing lump in upper anterior triangle of the neck
* Painless
* Pulsatile
* Associated with a bruit on auscultation
* Mobile side-to-side but not up & down
* May compress glossopharyngeal, vagus, accessory, hypoglossal nerves
* Pressure on vagus nerve- Horner syndrome
* Ptosis
* Miosis
* Anhidrosis
* Imaging- splaying of internal & external carotid arteries- Lyre sign
168
Features of a lipoma?
Soft, painless, mobile, no skin changes
169
Features of a thyroglossal cyst?
How is it treated?
* Patent thyroglossal duct causing a fluid filled cyst
* Midline of neck
* Mobile, non-tender, soft, fluctuant
* Move up & down w/ tongue movements
* Due to the connection between the thyroglossal duct and the base of tongue
* US or CT scan to confirm diagnosis
* Mx- surgical removal & histology
* Main complication- infection of cyst
170
What is a branchial cyst?
* Congenital abnormality
* Second branchial cleft fails to form properly during fetal development
* Round, soft, cystic swelling between the angle of the jaw and the scm in the anterior triangle of the neck
* Transilluminates w/ light
171
Suggest some locations of head and neck cancers
* Nasal cavity
* Paranasal sinuses
* Mouth
* Salivary glands
* Pharynx (throat)
* Larynx (epiglottis, supraglottis, vocal cords, glottis, subglottis)
172
What are the common/ less common locations for head and neck cancers?
* Increasing incidence- detection (thyroid), HPV (oropharynx)
* Decreasing incidence- hypopharynx/ larynx (smoking reduction)
173
Risk factors for developing H&N cancer?
* Smoking
* Chewing tobacco
* Chewing betel quid
* Alcohol consumption
* Virally mediated- HPV (16), EBV
* Sexually transmitted- HPV
174
Red flags for H&N cancers?
* Lump in mouth of on lip
* Unexplained ulceration in mouth lasting \> 3 weeks
* Erythroplakia (red patches) or erythroleukoplakia (white patches)
* Persistent neck lump
* Unexplained voice hoarseness
* Unexplained thyroid lump
175
What is cetuximab?
* Monoclonal antibody
* Used in treating SCC’s of H&N, bowel cancer
* Targets epidermal growth factor receptor, blocking activation of this receptor and inhibiting growth and metastasis of the tumour
176
How might patients with nasopharyngeal cancer present? How is it treated?
* Blocked nose
* Blocked ear
* Epistaxis
* Weight loss
* Often EBV induced
* Treatment- chemoradiation, rarely surgery
177
Types of thyroid cancer?
* Thyroid follicular epithelial derived cancer:
* Papillary (70%)
* Follicular (20%)
* Anaplastic (1%)
* Medullary thyroid cancer
* Primary thyroid lymphoma
178
How is papillary and follicular cancer managed?
* Total thyroidectomy
* Followed by radioiodine (I-131) to kill residual cells
* Yearly thyroglobulin levels to detect early recurrent disease
179
Risk factors for (papillary/ follicular) thyroid cancer?
* Radiation exposure esp. in childhood
* Fhx
* Female
* Others- obesity, endemic goitre, FAP, Cowden’s syndrome
180
Clinical features of thyroid cancer?
* Thyroid nodule/ mass
* Hoarseness/ change in voice
* Cervical lymphadenopathy
* Stridor
181
Causes of glossitis?
* Iron deficiency anaemia
* B12 deficiency
* Folate deficiency
* Coeliac disease
* Injury or irritant exposure
182
Causes of angioedema?
* Allergic reaction
* ACEi
* C1 esterase inhibitor deficiency (hereditary angioedema)
183
Risk factors for oral candidiasis?
* Inhaled corticosteroids
* Abx
* Diabetes
* Immunodeficiency- HIV?
* Smoking
184
How to treat oral thrush?
* Miconazole gel
* Nystatin suspension
* Fluconazole tablets
185
What is a strawberry tongue and what is it caused by?
* Swollen, red tongue
* Papillae enlarged, white, prominent
* 2 key causes
* Scarlet fever
* Kawasaki disease
186
What is leukoplakia?
* White patches in mouth, often tongue or insides of cheeks (buccal mucosa)
* Pre-cancerous condition- increases risk of SCC of mouth
* Asymptomatic, irregular, slightly raised patches
* Fixed in place- can’t be scraped off
* Mx- stop smoking, reducing alcohol, close monitoring, potentially laser removal or surgical excision
187
What is gingivitis?
Risk factors?
* Inflammation of gums à swollen gums, bleeding after brushing, painful gums, halitosis
* Can lead to periodontitis if not adequately managed
* Risk factors-
* Plaque build up on teeth
* Smoking
* Diabetes
* Malnutrition
* Stress
188
Treatment of gingivitis?
* Good oral hygiene
* Stop smoking
* Dental hygienist to remove plaque and tartar
* Chlorhexidine mouth wash
* Abx for acute necrotising ulcerative gingivitis eg metronidazole
* Dental surgery may be required
189
Possible causes of gingival hyperplasia?
* Gingivitis
* Pregnancy
* Vit C deficiency- scurvy
* Acute myeloid leukaemia
* Medications- CCBs, phenytoin, ciclosporin
190
Causes of aphthous ulcers?
* IBD
* Coeliac disease
* Behcet disease
* Vit deficiencies- iron, B12, folate, vit D
* HIV
191
How to treat aphthous ulcers?
* Topical treatments
* Choline salicylate
* Benzydamine
* Lidocaine
* Topical corticosteroids
* Hydrocortisone buccal tablets applied to lesion
* 2WW referral- unexplained ulceration lasting \>3 wks
192
What common organisms are implicated in mastoiditis?
* Staph aureus
* Strep pneumoniae
* H influenzae
193
How is mastoiditis managed?
* Early IV abx- third gen cephalopsorins such as ceftriaxone have good bone penetration and are also able to cross the BBB
* Penicillin/ beta lactam allergy à vancomycin, gentamicin are good alternatives with good bone penetration
* Surgical options-
* Mastoidectomy to drill out the mastoid bone and allow infection to drain
* Myringotomy and grommet insertion in addition to abx to help infection drain via the middle ear
194
What important relations of the middle ear/ mastoid are at risk when performing a cortical mastoidectomy?
* Facial nerve
* Inner ear
* Sigmoid sinus
* Brain
195
Suggest why patients with cholesteatoma present with a deterioration in hearing?
* Conductive hearing loss caused by debris
* Erosion of ossicles by cholesteatoma
196
Following a cholesteatoma surgical removal, a patient presents 2 years later with foul-smelling non-resolving discharge and hearing loss, and new onset vertigo. Why might this be?
* Disease recurrence with breach of the otic capsule bone causing dizziness on pressure change transmitted from the middle ear to the vestibular system
197
What would you expect to see during the Dix-Hallpike manoeuvre in patients with BPPV?
* When the affected ear is undermost-
* Latency
* Torsional geotropic nystagmus
* Fatigue
* Habituation on repeating the test
198
Describe how a saddle shape nose can be the result of trauma
* Untreated nasal septal haematoma leads to avascular necrosis of cartilaginous septum
199
How do you identify a nasal septal haematoma?
* Anterior rhinoscopy and palpation of the bulging septum
200
What recreational drug is commonly implicated in nasal septal defects, and what is the method of damage?
* Cocaine
* Causes loss of blood supply to cartilage of septum
201
Describe the management of chronic rhinosinusitis?
* Nasal steroid sprays
* Possible nasal steroids if polyps present
* Long course of abx- 6-8 weeks
202
What are the potential complications of sinus surgery?
* Bleeding
* Infection
* CSF leak
* Visual loss or disturbance
203
Describe the relations of the submandibular gland
* 2 parts- superficial and seep to the posterior border of the mylohyoid muscle in a U fashion
* The larger superficial part is in the digastric triangle and partly deep to the mandible, covered superficially by the platysma and skin
* The deep part is between mylohyoid and hyoglossus
* The duct runs from the deep part and is crossed by the lingual nerve
* The hypoglossal nerve lies deep to the gland
* The cervical branch of the facial nerve runs superficial to the gland and can be damaged in a high skin/ platysma incision
204
Describe the complications of surgery to remove submandibular gland that was cancerous?
* Bleeding
* Infection
* Damage to lingual nerve/ hypoglossal nerve/ cervical branch of facial nerve
205
Suggest some features that may suggest a malignant parotid gland?
* Facial nerve paresis
* Lymph nodes involvement
206
What is Frey’s syndrome and why does it occur?
* Rare, neurological disorder causing pt to sweat excessively whilst eating
* Most often occurs as a complication of surgery involving the parotid gland
* Injury to auriculotemporal nerve- when the nerve heals it reattaches to sweat glands instead of the original salivary gland which has been removed during surgery
207
When performing a neck dissection, what important structure in the posterior triangle is at risk of damage? If damaged, how might this affect the patient?
* Accessory nerve
* Shoulder drop
208
Clinically how do you differentiate a thyroglossal cyst from a thyroglossal mass?
* On clinical examination a thyroglossal cyst will move upwards on tongue protrusion
* A tongue nodule would move upwards on swallowing
209
What are the risks of carrying out thyroid surgery on someone who is hyperthyroid?
* Thyrotoxic storm
* Higher risk of bleeding
210
What are the complications of carrying out thyroid surgery on a euthyroid patient?
* Bleeding
* Infection
* Injury to recurrent laryngeal nerve
* Hypothyroidism
* Hypoparathyroidism
211
Describe the course of the recurrent laryngeal nerve on the left and on the right
* The nerves branch off the vagus nerves in the neck
* The left side loops under the aortic arch
* The right side loops under the right subclavian artery
* Both then pass upwards to supply the laryngeal muscles passing deep to the thyroid and entering the larynx posterior to the cricothyroid joint
212
What is the most important blood test to check after a routine total thyroidectomy and what symptoms suggest that this blood test was going to be low?
* Calcium
* Symptoms- tingling around mouth and fingertips
* If severely decreased- muscle spasm
