ENT Flashcards
Where are the inputs for balance from?
Visual- eyes
Vestibular
Proprioception
Also; auditory, cerebral/cerebellar
What is the role of the vestibular system?
Detects motion, head position and spatial orientation
What is the composition of the CNVIII?
Vestibular nerve- both superior and inferior.
Cochlear nerve
Where does the balance proportion occur?
Semilunar canals which are filled with endolymph that move around with movement:
-Anterior, posterior and horizontal. The horizontal pairs with the horizontal on the other side i.e. L with R. Anterior of L will pair with posterior of R and vice versa.
Otolith organs:
Utricle- Flat plane where hair sits, detecting movement in the horizontal plane. (Hair points up)
Saccule- Detecting movement in the vertical plane, anti-gravity. (Hair points to the side)
The collected information is then transmitted to the central portion via the CNVIII.
How does the vestibular system work?
Head movement moves the endolymph in SCC.
Fluid shift is detected by the stereocilia in the ampulla.
Input is transmitted to the vestibular nerve.
CNVIII carries the info to the vestibular nuclei in the brainstem and cerebellum.
Vestibular nuclei then sends info to the nuclei of CNIII, CNIV, CNVI and cerebellum, SC and thalamus which helps co ordinate movement.
What is the importance of visual input in balance?
-Vision is important for depth perception.
Some people begin to have visual preference- where they rely heavily on their visual system to determine their balance- disregarding their vestibular system.
This is usually a big problem in supermarkets, crowds f people, in the dark/eyes closed. Px will feel symptoms of disorientation, symptoms of panic, and severe discomfort, since they can’t determine a focus point to help them balance.
What is the importance of proprioception in balance?
Receive input from pressure receptors, i.e. in the feet, ankles, knees and hip.
Interfered with by joint replacement or peripheral neuropathy i.e. in diabetes.
What is the importance of sensory input in balance?
-Sensation (where cerebellum uses this and links to the surroundings)
What is the pathophysiology of visual preference?
Usually a unilateral vestibular insult- viral, toxic, BPPV.
Px is given medication to suppress the irritability, half Px will recover being asymptomatic, other half will have the brain compensate using the visual system. The brain will not return back to normal compensation and so the Px will become heavily reliable on the visual system.
What is the importance of postural hypotension in balance?
Px will take a pause when standing up.
Diagnose with supine and erect BP- drop by 20mmHg.
Ask about medications (anti-hypertensives), getting out of a bed or out of the chair in the morning.
Encourage cycling in the bed before standing, placing legs out and plantar and dorsiflexing in the chair before standing.
Dizziness due to pooling of blood at the legs.
What is the vestibular ocular reflex (VOR)?
Stabilises gaze during head movement, allowing the preservation of visual acuity during this movement.
What happens when the VOR stops working?
If the VOR stops working on one side, the body thinks the head has moved to the working side (since increased innervation on that side compared to the non-working side). I.e. if the right side is not working, since there is more stimulation of the left, it is believed the head is moving to the left. The eyes then move to the right as part of the VOR.
The visual cortex quickly recognises this is incorrect, now the eyes move back- causes nystagmus.
To compensate for this Px keep their head still whilst moving.
How do you test for VOR impairment?
Ask the Px to turn their head to one side then quickly move it back into the centre, looking for nystagmus.
How are vestibular disorders classified?
Affecting the central vestibular system:
- Cerebrovascular disease
- Cerebellum tumours
- MS
- Migraine
Affecting the peripheral vestibular system:
- Otoxicity
- BPPV
- Meniere’s
- Vestibular neuronitis.
Which drugs can affect the vestibular system?
Gentamicin
Loop diuretics
Metronidazole
Co-trimoxazole
What is dizziness?
Generic term used to describe; Light headedness Faint Giddy Imbalance Mental confusion
Can sometimes describe true giddiness.
What are some common causes of dizziness in the elderly?
Polypharmacy
Multifactorial disequilibrium of age (There is no apparent cause for the dizziness, just many factors along with the natural aging process).
Cerebral/cerebellar degeneration (causes can include cerebral vascular disease, stroke, hereditary etc).
What is vertigo?
Sensation between the Px and their environment.
May feel they are moving or the room is.
Often a horizontal spinning sensation.
Often associated with N+V, sweating and feeling generally unwell.
Can have either a peripheral or central cause.
What is BPPV?
Disorder of inner ear
Most common cause of vertigo
Gradual onset
Average age >55
Underlying pathophysiology is due to otoliths (crystals) in the semicircular canals (most commonly
posterior) causing abnormal stimulation of the hair cells giving a hallucination of movement.
What are some signs/symptoms of BPPV?
Vertigo triggered by change in head position
Associated nausea
Repeated episodes lasting 10-20 seconds
What are some investigations of BPPV?
Dix-Hallpike manoeuvre
- The patient is seated and positioned on an examination table such that the patient’s shoulders will come to rest on the top edge of the table when supine, with the head and neck extending over the edge
- The patient’s head is turned 45° towards the ear being tested
- The head is supported, and then the patient is quickly lowered into the supine position with the head extending about 30° below the horizontal while remaining turned 45° towards the ear being tested
- The head is held in this position and the physician checks for nystagmus (rotatory)
- To complete the manoeuvre, the patient is returned to a seated position and the eyes are again observed for reversal nystagmus
Consider audiogram in patients with hearing loss
Brain MRI to exclude CNS conditions eg multiple sclerosis.
How would you manage BPPV?
Wait for symptoms to settle
Patient education and reassurance
Epley manoeuvre
Ask patient to come back if not resolved in 4 weeks
Medication often prescribed (betahistine) but tends to be of limited value.
What are the central and peripheral causes of vertigo?
Central: o Stroke o Migraine o Neoplasms o Demyelination eg. MS o Drugs
Peripheral:
o BPPV
o Ménière’s disease
o Vestibular Neuronitis
What is a vestibular migraine?
Sudden or gradual onset
- Headache
- Vertigo
- Visual disturbances, photophobia
- Phonophobia
- Hearing loss (can overlap with Menieres)
How would you manage a vestibular migraine?
- Avoid triggers- such as dehydration, foods (chocolate, cheese), anxiety, poor sleep
- Keep symptom diary
What is Ménière’s Disease?
Disorder of inner ear, can affect balance and hearing
Unknown aetiology but may be associated with endolymphatic hydrops (raised endolymph pressure in the membranous labyrinth of the inner ear)
Suggested risk factors: autoimmunity, genetics, metabolic disturbances involving levels of Na + K in inner ear, vascular factors, viral infection, head trauma
- Natural history
-Symptoms resolve in the majority of patients after 5-
10 years
- The majority of patients will be left with a degree of
hearing loss
- Psychological distress is common
What are some signs/symptoms of Ménière’s Disease?
Tinnitus in affected ear
Episodic vertigo lasting minutes to hours with associated N+V
Fluctuating sensorineural hearing loss, which gradual becomes permanent
Aural fullness
Initially between attacks, Px will not experience any symptoms. With disease progression Px is more unsteady, with reduced vestibular function on affected side and progressive SNHL. Eventually disease burns out, so no more acute vertigo, but SNHL persists. Other ear can compensate for the vestibular system of affected ear but this takes longer in older people.
What investigations would you conduct in Ménière’s Disease?
Pure tone audiometry:
- Air and bone conduction are equal, indicating that the underlying pathology is in the cochlea or auditory nerve, not the outer and the middle ear
- Unilateral sensorineural hearing loss
- Usually low-frequency hearing loss is present in early stages of MD
- As disease progresses, middle and high frequencies are affected
How would you manage Ménière’s Disease medically?
- ENT referral to confirm diagnosis
- Self-care
- Reassure it is a LTC but vertigo usually significantly improves with treatment
- Advise that an acute attack of vertigo will normally settle within 24 hours in most people
- Reduce salt, chocolate, alcohol.
Medical:
- Acute attacks: oral or IM prochlorperazine (to help alleviate N&V, vertigo)- short course 1-2 weeks
- Reducing severity and frequency of attacks: betahistine and vestibular rehabilitation exercises
- If betahistine doesn’t provide clinical benefit; refer to ENT
- Patients should inform the DVLA. The current advice is to cease driving until satisfactory control of symptoms is achieved
How would you manage Ménière’s Disease surgically?
Grommet insertion
- Dexamethasone middle ear injection
- Endolymphatic sac decompression
- Vestibular destruction using middle ear injection of gentamicin
- Surgical labyrinthectomy – very rarely required
What is vestibular neuronitis?
Inflammation of the inner ear causing severe vertigo lasting several days with associated nausea and vomiting. During the attack Px will have horizontal nystagmus.
How would you manage vestibular neuronitis?
Vestibular sedatives (i.e. prochlorperazine) during the acute attack, and IV fluids if needed. Often post attack Px may still experience long term vestibular deficit- unsteadiness lasting a number of weeks whilst the brain tries to compensate. Px should engage in rehabilitation exercises e.g. Cawthorne-Cooksey exercises. Do not take vestibular sedatives after the attack as this can delay recovery.
What is 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
How is labyrinthitis investigated and managed?
Investigated with the head impulse test.
Managed with vestibular suppressant/anti-emetic- promethazine, cyclizine
What is the head impulse test?
Diagnose peripheral vertigo.
Pt sits upright and focuses on examiner’s nose, hold patients head and rapidly jerk it 10-20 degrees in one direction whilst pt continues to focus on your nose, head is slowly moved back to centre before repeating in opposite direction
Ask about neck pain beforehand
Observe for eyes rapidly moving back and forth
What is Unteberger’s 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
What is the difference between the length of vertigo experienced in BPPV, Meniere’s and vestibular neuronitis?
BPPV- Seconds
Meniere’s- Minutes
Vestibular neuronitis- Days
What is tinnitus?
Persistent sound which is not present in the environment.
Ringing in ears, buzzing, hissing or humming
What are some causes of tinitus?
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
What is otitis externa?
What are the different types?
What are the causes of otitis externa?
Inflammation of the external ear canal.
Acute <3 weeks
Chronic >3 months
Diffuse- through the entire external ear canal.
Localised- to one hair follicle.
Malignant- Spread to the temporal and mastoid bone; needs urgent treatment. This is common in diabetics, immunocompromised. Presents with chronic discharge, ear pain and may have some CN palsies.
What are the causes of otitis externa?
Infection (bacterial- staph aureus or fungal; bacterial more common)
Non infectious dermatological causes (seborrhoeic dermatitis or allergic dermatitis).
N.B Always consider OME as a cause, where otitis externa is secondary to otorrhea.
What are the RF for developing OE?
Frequent water contact i.e. swimmers Local trauma i.e. ear buds Ear eczema/psoriasis Diabetic/Immunocompromised Humid environment Ear polyps
What are the signs and symptoms of otitis externa?
Ottorhoea
Otalgia
Ear discomfort- Ranging from pruritis to severe pain worsened by motion of ear eg chewing
Feeling of fullness in ear + loss of hearing
Px may have tender ear canal, can become swollen and closed, have pus/discharge. Px may have some lymphadenopathy.
How is otitis externa investigated?
Hx is usually enough for a diagnosis.
Can take a swab if persistent for MSC.
How is otitis externa managed?
Protect 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 a
Abx may suggest fungal cause- topical fungal treatment eg clotrimazole drops.
May require swelling to reduce swelling and allow better penetration of the Abx.
Analgesia
If affecting a single hair follicle or cellulitis then requires oral Abx; flucloxacillin or clarithromycin if penicillin allergy.
Diabetes- the likely organism is pseudomonas therefore use ciprofloxacin.
If non resolving then urgent ENT referral for malignant otitis externa.
Malignant OE- Aggressive IV Abx and topical ear drops to eradicate infection.
What are the complications of otitis externa?
What are the associated RF?
Significant risk factors: Diabetes mellitus Age > 65 Recurrent AOE Chemo or radiotherapy or immunocompromised in another way
Complications:
=>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
=>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).
What is the most likely causative agent of Malignant otitis externa?
How would you act to manage it?
Pseudomonas aeruginosa
Ix- microbiology/ swabs of discharge, IV access, FBC, U&Es, serum glucose, CRP, ESR
Blood cultures if pyrexial
Sepsis 6
CT scan: thickening & enhancement of soft tissue, opacification of mastoid air cells & abscess formation.
Mx- Aggressive IV Abx as well as topical treatment required to eradicate infection
6wks
What is acute otitis media?
What are the causes of acute otitis media?
Common acute onset inflammation of the middle ear with effusion.
Commonly caused by a preceding viral URTI but can have bacterial causes; strep or H.influenza.
Increased risk in young males, +ve FHx, previoius viral URTI.
What are the signs and symptoms of acute otitis media?
What are the complications?
Otalgia
Discharge- TM rupture- pus from middle ear- pain stops at this point
Reduced hearing in affected ear
Symptoms of URTI- cough, coryzal symptoms, sore throat
Fever, feeling generally unwell
Complications include:
Recurrence of infection
Hearing loss
Tympanic membrane perforation
Rarely; mastoiditis, meningitis, intracranial abscess, sinus thrombosis, and facial nerve paralysis
How is acute otitis media investigated?
Use an otoscope-
- TM is distinctly red, yellow, or cloudy and may be bulging
- Perforation with purulent otorrhoea
- Looks like a donut- evidence of positive pressure
- Otoscopy appearance of a bulging, erythematous tympanic membrane and absent landmarks
How is acute otitis media managed?
- Self-limiting- Pain & fever- paracetamol, ibuprofen. Advise the normal course is 3-7 days.
- Admit child under 6 months
- If need Abx: 5-7 days amoxicillin is first-line (For penicillin allergy- clarithromycin or erythromycin {in pregnant})
Abx needed if;- Symptoms not improving within 4 days
- Have otorrhoea - perforation
- Bilateral otitis media in child <2 years of age
- People who are systemically very unwell
- People who have symptoms and signs of a more serious illness or condition
- People who have a high risk of complications
- If unresponsive to Abx or severe pain: tympanocentesis
- Relieves pressure in the middle ear space and provide relief of otalgia
- Risks of trauma to the TM and middle ear structures and risk of anaesthesia.
- Preventing recurrent infection
- In children — avoiding exposure to passive smoking, use of dummies, and flat, supine feeding; and ensuring that children have had a complete course of pneumococcal vaccinations as part of the routine childhood immunization schedule
- In adults — avoiding smoking and/or passive smoking.
What is otitis media with effusion?
What are the causes?
This is a non infectious cause of glue ear, i.e. effusion of the ear.
The exact cause is unknown but may be due to a impaired eustachian tube i.e. impaired pressure balance in the ear.
More likely if the Px has Downs syndrome, cleft palate etc.
What are the signs and symptoms of otitis media with effusion?
Commonly present with hearing loss
Ottorhoea- where if persistent/foul smelling need urgent referral
Recurrent URTI or ear infections
How is otitis media with effusion investigated?
Tympanometry: assesses ability of eardrum to react to sound, may be used to improve accuracy of OME diagnosis
Audiometry to determine level of hearing loss
Otoscopy- retracted TM, abnormal colour/opacification of TM, signs of inflammation are not seen.
How is otitis media with effusion managed?
Common to have spontaneous resolution- active observation for 12 weeks.
Abx, antihistamines, mucolytic, decongestants, corticosteroids are all NOT recommended
- Hearing aids
- Auto-inflation
- Surgery: myringotomy and insertion of grommets (ventilation tubes)
What are the complications of otitis media with effusion?
Chronic TM damage
Problems with speech and language development
Conductive hearing loss
What is otosclerosis?
How is it investigated?
How is it managed?
Remodelling of small bones in the ear- to spongy bones. The stapes fixes onto the oval window. Get progressive conductive hearing loss. May also get tinnitus. Autosomal dominant inheritance. Affecting 20-40yrs old.
High resolution CT is used to identify changes.
Manage conservatively with hearing aids.
or
Surgically with:
Stapedectomy- Remove stapes and replace with prosthesis.
Stapedotomy- Remove part of stapes, allowing some attached to the OW. A prosthesis is inserted then through a hole in the stapes.
What is cholesteatoma?
- Abnormal sac of keratinising squamous epithelium + accumulation of keratin within middle ear/ mastoid air cell spaces
- Benign but can become infected or erode nearby structures, nerves and middle ear cavity; predisposes to severe infections.
- Common age 10-20
Although aetiology is unknown, suspected dysfunctional ET creates a -ve pressure, retracting the TM and creating a pocket for keratin to accumulate.
What are the signs and symptoms of cholesteatoma?
- Foul-smelling, non-resolving discharge
- Hearing loss
- Local invasion: vertigo, facial nerve palsy, altered taste, cerebellopontine angle syndrome.
How would you investigate a cholesteatoma?
- Otoscopy: attic crust seen in upper part of ear drum; retraction pocket in attic
- If infected- signs of otitis externa (redness, swelling, narrow ear canal, debris + discharge)- this has to be treated before diagnosis as ear drum becomes hard to see.
How is a cholesteatoma managed?
- Semi-urgent ENT referral
- They will investigate further including CT scan to assess local invasion.
- Definitive treatment: surgical removal
- Commonly canal wall up mastoidectomy, allowing removal of cholesteatoma and canal wall left intact.
Need a second-look procedure 9-12 months later to ensure no residue.
- Commonly canal wall up mastoidectomy, allowing removal of cholesteatoma and canal wall left intact.
What are the different types of hearing loss?
Conductive- Pathology of the external and middle ear.
Sensorineural- Pathology of the inner ear or the CNVIII.
Mixed- Conductive and sensorineural.
How is mastoiditis diagnosed?
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
What are the causes of sensorineural hearing loss?
Presbycusis- Most common cause Noise exposure (also a common cause) Labyrinthitis Trauma to head/ear Malignancy i.e. nasopharyngeal tumour Vestibular Schwannoma Ototoxic drugs Meniere's Neurological i.e. MS, stroke Sudden SNHL
What are the causes of conductive hearing loss?
Impacted ear wax Foreign body i.e cotton bud SCC of the external canal Cholesteatoma Ear infection Otosclerosis Middle ear effusion TM perforation
What is presbycusis?
Age related sensorineural hearing loss.
- Slow, gradual hearing loss, usually bilateral
- Speech becoming difficult to understand
- Need for increased volume on the television or radio
- Difficulty using the telephone
- Loss of directionality of sound
- Worsening of symptoms in noisy environments
- Hyperacusis: Heightened sensitivity to certain frequencies of sound (Less common)
- Tinnitus (Uncommon)
Why does presbycusis occur?
Loss of hair cells in cochlea
Loss of neurones in cochlea
Atrophy of stria vascularis
Reduced endolymphatic potential
What are the RF for presbycusis?
Age Male FHx Loud noise exposure Diabetes HTN Ototoxic medications Smoking
How is presbycusis investigated?
Rule out otosclerosis, cholesteatoma or conductive hearing loss (due to foreign body/impacted wax) with otoscopy.
Weber’s test lateralises to least affected side.
Audiometry- bilateral hearing loss of high frequency.
How is presbycusis managed?
Reassure that this is normal for their age
Assisted hearing devices
Hearing aids
If hearing aids ineffective then may consider cochlear implants
What is sudden SNHL?
Sudden hearing loss
Almost always unilateral
Many go to bed fine and awaken with deafness
May be associated tinnitus or vertigo
No significant otalgia, discharge, or other neuro signs eg nystagmus
What are the causes of sudden SNHL?
90% of 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)
What are the diagnostic criteria for sudden SNHL?
Rule of 3:
Sensorineural loss worse than 30dB
In 3 consecutive frequencies
Within 3 days (72hrs)
How is sudden SNHL managed?
Oral steroid eg 60mg prednisolone reducing over 10 days
Gastric protection
MRI IAM (internal auditory meati) as a routine outpatient
Assess in next ENT clinic with Audiology support
Hearing recovers spontaneously 66% of the time
Presence of vertigo = poor prognostic sign
Intra-tympanic steroid injections if no hearing improvement within 1-3 weeks
Persistent hearing loss- consider hearing aids
What are the consequences of impacted ear wax?
Conductive hearing loss Discomfort in ear Feeling of fullness Pain Tinnitus
How is a build up of earwax managed?
Ear drops- olive oil or sodium bicarbonate 5%
Ear irrigation- squirting water in ears to clean away wax- performed by GP, contraindications: perforated TM, infection
Microsuction- to suck out the wax, performed by ENT specialist
What are the 4 levels of hearing loss?
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)
What are types of hearing aids are available?
1) Behind the ear hearing aids- most common type
2) In the ear hearing aids
3) Completely in canal
What are the types of hearing implants?
1) Bone conduction hearing aids
Conductive hearing loss
Mixed hearing loss
Bone conduction > 65
2) Middle ear implant
3) Cochlear implants
4) Auditory brainstem implant
Bilateral acoustic neuroma (neurofibromatosis II)
What are the indications for a cochlear 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
What are the contraindications for a cochlear implant?
Lesions of cranial nerve VIII or the brainstem causing deafness
Chronic infective otitis media, mastoid cavity or tympanic membrane perforation
Cochlear aplasia
What is the difference between a cochlear implant and bone anchored hearing aid (BAHA)?
Cochlear implant: implanted surgically with electrodes so directly stimulates the auditory nerve with electrodes
BAHA: sound is transmitted to the cochlear via bone conduction
Which medications cause SNHL?
Loop diuretics eg furosemide
Aminoglycoside abx eg gentamicin
Chemotherapy drugs eg cisplatin
