Primary Care - Common ENT conditions Flashcards
1
Q
What is benign paroxysmal positional vertigo (BPPV)?
A
-
episodic vertigo (lasting < 1 minute) that is triggered by sudden changes in the position of the head
- e.g. suddenly standing up, bending forwards
- it is the most common cause of peripheral vertigo
2
Q
What causes BPPV?
A
- it is caused by otoconia dislodging and migrating into one of the semicircular canals, where it disrupts the endolymph dynamics
- most commonly the posterior semicircular canal
- the exact aetiology is unknown
3
Q
What are the risk factors for BPPV?
A
- female sex
- increased age
- low vitamin D levels
- osteopenia or osteoporosis
- patients with both osteoporosis and BPPV are at increased risk of fall-related fractures
4
Q
What are the clinical features of BPPV?
What other symptoms is it associated with?
A
-
episodic vertigo which is sudden and recurrent
- patient describes the feeling of the room spinning
- vertigo lasts for several seconds and is triggered by sudden head movements
- associated with nystagmus, N&V and risk of falling
- risk of N&V lower than other types of vertigo due to short duration
- does NOT typically cause cochlear (hearing loss / tinnutis) or neurological symptoms
5
Q
What manoeuvre is used to diagnose posterior canal BPPV?
A
Dix-Hallpike manoeuver
- patient sits upright on examination bed and keeps eyes open
- rotate head by 45o towards the affected side
- keeping the neck rotated, quickly lay the patient in a supine position with the neck slightly extended and the affected ear facing downwards
- their head should hang slightly off the side of the table
- hold this position for 20-30 seconds are examine eyes for nystagmus
- slowly reposition the patient into an upright posture and observe for reversal of nystagmus
- if negative, repeat the test with the head turned to the unaffected side
6
Q
What is the first-line treatment for BPPV?
A
Epley manoeuvre
- starts the same as the Dix-Hallpike manouevre
- once the patient is lying supine and affected ear is facing down, hold the position for 30 secs or until nystagmus stops
- turn patient’s head by 90o toward unaffected side and hold this position for 30 seconds
- turn patient’s head and body by 90o towards unaffected side so they are now lying on their side with their face turned towards the ground
- hold this position for 30 seconds
- bring them back to a seated upright position and ask them to stay there for 15 minutes
7
Q
When might vestibular suppressants be given to patients with BPPV?
What should the patients be warned about?
A
- they are not routinely indicated due to adverse side effects
- e.g. falls, cognitive dysfunction, drowsiness
- they should only be used in intractable BPPV or patients who refuse to undergo canalith repositioning manoeuvres
- chronic use is contraindicated as it can exacerbate chronic gait and postural instability
8
Q
What is Wernicke encephalopathy?
What usually causes it and what can it progress to?
A
- an acute, reversible condition caused by severe thiamine (vitamin B1) deficiency often due to chronic alcohol abuse
- it can also be caused by inadequate intake, impaired absorption or increased excretion of thiamine
- chronic thiamine deficiency can progress to Korsakoff syndrome
9
Q
What is the classical triad of symptoms associated with Wernicke encephalopathy?
A
- confusion
-
oculomotor dysfunction
- gaze-induced horizontal / vertical nystagmus
- diplopia
- conjugate gaze palsy (impaired ability of eyes to move in a single direction)
- gait ataxia - wide-based, small steps
10
Q
What are the typical symptoms of Korsakoff syndrome?
A
- this occurs in patients with persistent vitamin B1 deficiency, usually due to chronic alcohol abuse
- confabulation - patients produce fabricated memories to fill in lapses of memory
- anterograde and retrograde amnesia (long-term memory is usually preserved)
- personality changes - apathy, indifference, decrease in executive function
- hallucinations
- disorientation to time, place and person
11
Q
What is the treatment for Wernicke encephalopathy in the acute phase?
A
- immediate IV administration of high-dose thiamine (e.g. Pabrinex) until symptoms recede
- in patients with loss of consciousness, IV glucose is administered
- thiamine must be administered before glucose as glucose increases thiamine demand, so will worsen encephalopathy
12
Q
What are the long-term treatments for Wernicke encephalopathy?
A
- long-term oral replacement of vitamins B1, B6, B12 and folic acid
- this is continued until patient has adopted a balanced diet and successfully abstained from alcohol
- abstinence from alcohol
13
Q
What is vestibular neuritis?
A
- inflammation of the vestibular nerve
- typically manifests with features of vestibular hypofunction:
- nausea
- vomiting
- vertigo
- gait instability
- there is usually no hearing loss
14
Q
What is labyrinthitis?
A
- all the features of vestibular neuritis with ipsilateral sensorineural hearing loss
- this is caused by a viral (sometimes bacterial) infection affecting the inner ear
- both branches of the vestibulocochlear nerve are inflamed, resulting in hearing changes and vertigo
15
Q
What is Meniere disease?
Who tends to be affected?
A
- a disorder of the inner ear caused by impaired endolymph resorption
- exact aetiology unknown but linked to viral infections, autoimmunity and allergies
- tends to affect adults between 40-50 years of age
17
Q
How does hearing loss in Meniere disease change over time?
What tests can be used to identify this?
A
- starts as low to mid-frequency hearing loss that progressively worsens with each episode
- it can progress to deafness over several years
- tuning fork tests can be used:
Weber test - lateralisation to the healthy ear indicating SNHL in opposite ear
Rinne test - bilaterally positive as they have normal conductive hearing
