ENT: Ear Problems 2 Flashcards

1
Q

What is tinnitus?

A

Tinnitus is the perception of sound in the absence of sound from the external environment. It may be described as a ringing, hissing, buzzing, sizzling, whistling, or humming, and can be constant or intermittent, and unilateral or bilateral

NOTE: thought to be due to cochlea producing a background sensory signal and the signal not being filtered out by central auditory system

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2
Q

What is primary tinnitus?

A
  • Tinnitus with no identifiable cause
  • Often occurs with sensorineural hearing loss
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3
Q

Secondary tinnitus refers to tinnitus with an identifiable cause; state some example causes

A

Example causes:

  • Impacted ear wax
  • Ear infection
  • Ménière’s disease
  • Presbyacusis
  • Noise exposure
  • Medications (e.g., loop diuretics, gentamicin and chemotherapy drugs such as cisplatin)
  • Acoustic neuroma
  • Multiple sclerosis
  • Trauma
  • Depression
  • TMJ disorders

Tinnitus may also be associated with systemic conditions:

  • Anaemia
  • Diabetes
  • Hypothyroidism or hyperthyroidism
  • Hyperlipidaemia
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4
Q

What is subjective tinnitus and what is objective tinnitus?

State some example causes of objective tinnitus

A
  • Subjective tinnitus (more common) if the perceived sound can only be heard by the affected individual. This is caused by abnormal activity in the inner ear or central nervous system.
  • Objective tinnitus (affecting 1% of people with tinnitus) if the sound can be heard by the affected individual and the examiner (by auscultating with a stethoscope around ear); This often originates from an identifiable and correctable source that produces sound near to, or within, the ear. Example causes:
    • Carotid artery stenosis (pulsatile carotid bruit)
    • Aortic stenosis (radiating pulsatile murmur sounds)
    • Arteriovenous malformations (pulsatile)
    • Eustachian tube dysfunction (popping or clicking noises)
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5
Q

When asking a pt about tinnitus, state some questions you should ask (focused around characteristics/pattern of symptoms)

A
  • Uni or bilateral
  • Frequency
  • Duration
  • Severity
  • Pulsatile or non-pulsatile
  • Additional symptoms such as hearing loss, dizziness, vertigo, balance problems, jaw pain or clicking, facial weakness, or sensitivity to loud noises

Then also ask:

  • Impact on life
  • PMH & past surgical history
  • Medications
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6
Q

What investigations may be done for someone with tinnitus?

A

NICE suggest:

  • Blood tests:
    • FBC (anaemia)
    • Glucose (diabetes)
    • TSH (thyroid disorders)
    • Lipids (hyperlipidaemia)
  • Audiology (assess hearing)
  • CT or MRI imaging (not often required but may be required to investigate e.g. acoustic neuroma)
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7
Q

State some tinnitus red flags that could indicate serious underlying pathology that needs specialist assessment

A
  • Unilateral tinnitus
  • Pulsatile tinnitus
  • Hyperacusis (hypersensitivity, pain or distress with environmental sounds)
  • Associated unilateral hearing loss
  • Associated sudden onset hearing loss
  • Associated vertigo or dizziness
  • Headaches or visual symptoms
  • Associated neurological symptoms or signs (e.g., facial nerve palsy or signs of stroke)
  • Suicidal ideation related to the tinnitus
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8
Q

Discuss the management of tinnitus

A
  • Reassure that it to tends to improve & resolve over time without intervention
  • Treat identifiable underlying causes e.g. wax
  • Measures to help improve & manage symptoms:
    • Hearing aids
    • Sound therapy (add background noise to mask tinnitus)
    • CBT
    • Support groups
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9
Q

What is vertigo?

A

A false sensation of movement (spinning or rotation) of the person or their surroundings in the absence of any actual physical movement.

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10
Q

Remind yourself of the 3 sensory inputs for maintaining balance and posture

A
  • Vision
  • Proprioception
  • Signals from vestibular system
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11
Q

Remind yourself of the structure of the vestibular system and how it works to maintain balance and posture

A

Structure

  • Vestibular apparatus in inner ear
  • Made up of the semi-circular canals, utricle and saccule
    • Stereocilia in utricle & saccule respond to linear acceleration and static pull of gravity
    • Stereocilia in semicicrucular canals respond to rotational acceleration in 3 different planes
  • Semi-circular canals filled with endolymph and are orientated in different directions to detect various head movements
  • When head moves, fluid in the canals moves
  • Fluid movement is detected by stereocilia
  • Stereocilia generate action potential
  • Signal carried, by vestibular nerve, to the vestibular nucleus in brainstem and to the cerebellum
  • Vestibular nucleus sends signals to oculomotor, trochlear and abducens nuclei that control eye movements and also to the thalamus, spinal cord and cerebellum
  • Cerebellum helps coordinate movement throughout the body
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12
Q

Vertigo can be caused by a peripheral or a central problem; explain what we mean by each

A
  • Peripheral: due to problem with vestibular system
  • Central: due to problem with brainstem or cerebellum
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13
Q

State some peripheral causes of vertigo (highlighting the 4 most common)

A

Four most common

  • Benign paroxysmal positional vertigo
  • Ménière’s disease
  • Vestibular neuronitis
  • Labyrinthitis

Others

  • Trauma to the vestibular nerve
  • Vestibular nerve tumours (acoustic neuromas)
  • Otosclerosis
  • Hyperviscosity syndromes
  • Herpes zoster infection (often with facial nerve weakness and vesicles around the ear – Ramsay Hunt syndrome)
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14
Q

State some central causes of vertigo

A

Central problems disrupt signals from vestibular system and cause sustained, non-positional vertigo.

Most common causes

  • Posterior circulation infarction (stroke)
  • Tumour
  • Multiple sclerosis
  • Vestibular migraine
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15
Q

What is the first thing you must establish in a patient presenting with ‘dizziness’?

A

Whether it is vertigo (rotatory or spinning symptoms) or a non-rotatory dizziness e.g. light-headedness, off-balance

**NICE states to consider asking:

  • ‘When you have dizzy spells, do you feel light-headed or do you see the world spin around you as if you had just got off a playground roundabout?’
  • If the person has nystagmus it is likely that their dizziness is vertigo.
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16
Q

Discuss how you can distinguish between peripheral and central vertigo based on:

  • Onset
  • Duration
  • Hearing loss
  • Tinnitus
  • Coordination
  • Nausea
A
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17
Q

Alongside features of vertigo, there are other things you can enquire about in history to try and determine cause; state these

A
  • Recent viral illness (labyrinthitis or vestibular neuronitis)
  • Headache (vestibular migraine, cerebrovascular accident or brain tumour)
  • Typical triggers (vestibular migraine)
  • Ear symptoms, such as pain or discharge (infection)
  • Acute onset neurological symptoms (stroke)
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18
Q

If a pt presents with vertigo, what examinations must you do? (5)

A
  • Ear examination including otoscopy & hearing tests (infection or other pathology)
  • Neurological examination (assess for central causes)
  • Cardiovascular examination (assess for cardiovascular causes of dizziness)
  • Cerebellar examination
  • Special tests:
    • Romberg’s test (looks for sensory ataxia)
    • Dix-Hallpike manoeuvre (diagnose BPPV)
    • HINTS examination
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19
Q

What is the HINTS examination used for?

What does it involve?

A

Used to distinguish between central and peripheral vertigo. It stands for:

  • HIHead Impulse
  • NNystagmus
  • TSTest of Skew
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20
Q

Explain how to perform the head impulse test and explain what the results mean

A

How to perform

  • Sit pt upright and ask to look at examiners nose (and continue looking at it throughout)
  • Examiner holds pt’s head and rapidly jerks it 10-20 degrees in one direction
  • Slowly return head back to centre and repeat in opposite direction

Results

  • Normal vestibular system: eyes remain fixed on examiners nose
  • Abnormal vestibular system/peripheral cause of vertigo: eyes will make a corrective saccade before eventually fixating back on examiners nose
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21
Q

Explain how to check for nystagmus and what the results mean

A

How to perform

  • Get pt to look to the left or right and hold the gaze
  • Observe eye movements

Results

  • Unilateral/unidirectional horizontal nystagmus: more likely peripheral
  • Bilateral horizontal or vertical nystagmus: more likely central
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22
Q

Explain how to perform the test of skew (also know as alternate cover test) and explain what the results mean

A

How to perform

  • Sit pt upright and ask pt to fixate/look at examiners nose
  • Examiner covers one eye at a time, alternating between the two eyes

Results

  • Eyes should remain fixed on examiners nose
  • If there is vertical correction when eye is uncovered (meaning eye has drifted up or down when covered so needs to move vertically to re-fixate on nose) = indicates central cause of vertigo
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23
Q

Summarise HITT examination findings in peripheral and central causes of vertigo

A
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24
Q

Remind yourself of features of cerebellar disease (and hence what to assess in cerebellar examination)

A
  • DDysdiadochokinesia
  • AAtaxic gait (ask the patient to walk heel-to-toe)
  • NNystagmus (see below for more detail)
  • IIntention tremor
  • SSpeech (slurred)
  • HHeel-shin test
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25
Q

Discuss the management of vertigo (brief overview)

A
  • May need further investigations to establish underlying cause
  • Symptom control in peripheral vertigo:
    • Prochlorperazine
    • Antihistamines (e.g. cyclizine, cinnirazine)
  • Treat underlying cause:
    • Ménière’s disease: betahistine to reduce attacks
    • BPPV: Epley manouevre
    • Vestibular migraine: avoid triggers, triptans for acute symptoms, betablockers/amitriptyline/topiramate for prophylaxis
    • MS: medications
    • Tumours: surgical removal
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26
Q

What is BPPV?

A

Benign paroxysmal positional vertigo

Get recurrent episodes of sudden onset vertigo triggered by head movement

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27
Q

Describe pathophysiology of BPPV

A
  • Otoconia (crystals of calcium carbonate) are usually found in utricle & saccule above the stereocilia; they are displaced in response to movement and cause depolarisation of hair cells- which is perceived as movement
  • In BPPV, otoconia get into the semicircular canals (most commonly in the posterior semicircular canal)
  • Displacement/movement into semicircular canals may be caused by viral infection, head trauma, ageing or idiopathically
  • Crystals disrupt normal flow of endolymph in canals; they can continue to stimulate hair cells even after head movement has ceased leading to vertigo
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28
Q

Describe typical presentation of BPPV

A

Average age of onset is 55yrs:

  • Vertigo triggered by head movements (commonly by turning over in bed or looking up)
  • Episodes last 10-20 seconds
  • Associated nausea
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29
Q

What test can be done to diagnose BPPV?

Explain how it is done

What is a positive results?

A

Dix-Hallpike test

Head movements move the endolymph through semicircular canals and triggers vertigo in pts with BPPV.

  • The patient sits upright on a flat examination couch with their head turned 45 degrees to one side (turned to the right to test the right ear and left to test the left ear)
  • Support the patient’s head to stay in the 45 degree position while rapidly lowering the patient backwards until their head is hanging off the end of the couch, extended 20-30 degrees
  • Hold the patient’s head still, turned 45 degrees to one side and extended 20-30 degrees below the level of the couch
  • Watch the eyes closely for 30-60 seconds, looking for nystagmus
  • Repeat the test with the head turned 45 degrees in the other direction

In patients with BPPV, the Dix-Hallpike manoeuvre will trigger rotational nystagmus and symptoms of vertigo. The eye will have rotational beats of nystagmus towards the affected ear (clockwise with left ear and anti-clockwise for right ear BPPV).

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30
Q

Discuss the management of BPPV

A

Usually resolves spontaneously within a few weeks to months hence pt has option of waiting; however, there are a couple options to relieve symptoms:

  • Epley manoeuvre (sucessful in ~80%)
  • Brandt-Daroff exercises
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31
Q

Describe how to perform the Epley manoeuvre

A

Idea is to move otoconia in the semicircular canals to a position that doesn’t cause symptoms. Maintain each head position for at least 30 seconds and wait for any nystagmus or vertigo to settle

  • Start with the person sitting upright with their head turned 45 degrees to the affected side, then lie them back (with their head still turned 45 degrees) until the head is dependent 30 degrees over the edge of the couch (as if performing the Dix-Hallpike manoeuvre)
  • With the face upwards, but still tilted backwards by 30 degrees, rotate the head through 90 degrees to the opposite side.
  • Hold the head in this position for about 20 seconds and ask the person to roll onto the same side as they are facing.
  • Rotate the person’s head so that they are facing obliquely downward with their nose 45 degrees below the horizontal.
  • Sit the person up sideways while the head remains rotated and tilted to the side.
  • Rotate the head to the central position and move the chin downwards by 45 degrees.
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32
Q

Briefly outline what Brandt-Daroff exercises involve

A

Brandt-Daroff exercises can be performed by the patient at home to improve the symptoms of BPPV. These involve sitting on the end of a bed and lying sideways, from one side to the other, while rotating the head slightly to face the ceiling. The exercises are repeated several times a day until symptoms improve.

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33
Q

Discuss the prognosis of BPPV

A
  • Usually resolves spontaneously after few weeks to months
  • ~50% get recurrence 3-5yrs later
34
Q

What is vestibular neuronitis?

What causes vestibular neuronitis?

A

Inflammation of the vestibular nerve- usually due to a viral infection. Inflammation of the nerve distorts signals travelling from vestibular system to the brain resulting in episodes of vertigo.

35
Q

Describe typical presentation of vestibular neuronitis

A
  • Hx of recent viral URTI
  • Acute onset of vertigo
    • Most severe in first few days (may be constant at first but then reduce to being triggered by head movement)
  • Associated nausea and vomiting (can be severe)
36
Q

Discuss the management of vestibular neuronitis

A
  • Treatments for symptom relief- can be used for up to 3 days:
    • Prochlorperazine (can be given IM or buccal in severe, PO in mild)
    • Antihistamines (e.g. cyclizine, cinnirazine, promethazine)
  • Admit pts if they are becoming dehydrated due to severe nausea & vomiting
  • Refer to ENT if symptoms not improved after 1/52 or resolved after 6/52 (may need further investigation or vestibular rehabilitation therapy which involves tailored exercises specific to pt)
37
Q

Discuss the prognosis of vestibular neuronitis

A
  • Symptoms most severe in first few days; usually resolves within 6 weeks
  • Recurrence is rare
38
Q

What is labyrinthitis?

What is it usually caused by?

A
  • Inflammation of inner ear (semicircular canals, vestibule [utricle & saccule] and cochlea)
  • Usually caused by viral URTI however can be rarely caused by bacterial infection (usually secondary to otitis media or meningitis)
39
Q

Describe typical presentation of labyrinthitis

A
  • Hx of viral URTI
  • Acute onset vertigo
  • Hearing loss
  • Tinnitus
  • Nausea and vomiting
40
Q

Discuss the management of labyrinthitis

A

Management similar to vestibular neuronitis & like vestibular neuronitis it usually resolves in a few weeks

  • Treatments for symptom relief- can be used for up to 3 days:
    • Prochlorperazine (can be given IM or buccal in severe, PO in mild)
    • Antihistamines (e.g. cyclizine, cinnirazine, promethazine)
  • If chronic, refer to ENT as may benefit from vestibular rehabilitation therapy
41
Q

Compare vestibular neuronitis and labyrinthitis

A
  • Vestibular neuritis is used to define cases in which only the vestibular nerve is involved, hence there is no hearing impairment
  • Labyrinthitis is used when both the vestibular nerve and the labyrinth are involved, usually resulting in both vertigo and hearing impairment.
42
Q

What is Ménière’s disease?

What is the classic triad of features?

A
  • Meniere’s disease is a long term disorder affecting the inner ear, of unknown cause, which can affect balance and hearing.
  • It is a clinical syndrome characterized by episodes of vertigo, fluctuating hearing loss, and tinnitus and is associated with a feeling of fullness in the affected ear.
43
Q

Describe the pathophysiology of Ménière’s disease

A
  • Excess endolymph within labyrinth of inner ear
  • Causes increased pressures (increased pressure of endolymph called endolymphatic hydrops)
  • Which
44
Q

Describe the typical presentation of Ménière’s disease (include typical age of presentation)

A

Typically a 40-50yr old patient with:

Classic triad

  • Vertigo (episodes last 20mins-hours. Can come in clusters and then be followed by prolonged periods without symptoms. Not triggered by movement or posture)
  • Unilateral hearing loss (typically fluctuates at first but then gradually becomes more permanent, low frequencies affected first, may become gradual over time)
  • Unilateral tinnitus (usually occurs with vertigo episodes before becoming permanent, may become gradual over time)

Other symptoms

  • Sensation of fullness in ear
  • Unexplained falls (drop attacks) without loss of consciousness
  • Imbalance can persist after vertigo
  • Unilateral nystagmus during an attack
45
Q

How is Ménière’s disease diagnosed?

A
  • Clinical diagnosis made by ENT (hence need to refer to ENT in primary care)
  • Audiometry needed to assess hearing
46
Q

Discuss the management of Ménière’s disease

A
  • Symptomatic relief during attack:
    • Prochlorperazine
    • Antihistamines (cyclizine, cinnarizine, promethazine)
  • Prophylaxis:
    • Betahistine
  • If symptoms are severe enough, people may require hospital admission for intravenous (IV) labyrinthine sedatives and fluids to maintain hydration and nutrition
47
Q

What is the law in regards to vertigo and driving?

A
  • Must not drive on presentation and must notify DVLA.

When satisfactory control of symptoms has been achieved, relicensing may be considered for restoration of the ’til 70 licence.

48
Q

What is otitis media?

What is it often preceded by?

A

Infection of middle ear

Often preceded by viral URTI

49
Q

Who is otitis media common in?

A

Children <4yrs

(especially those who are subject to passive smoking, attend daycare or nursery, are formula-fed, or have craniofacial abnormalities)

50
Q

State most common causative organisms of otitis media

A

Although often preceded by viral URTI, acute otitis media usually caused by bacterial infection.

  • Most common= Streptococcus pneumoniae
  • Others:
    • Haemophilus influenza
    • Moraxella catarrhalis
    • Staphylococcus aureus
51
Q

Describe typical presentation of otitis media

A
  • Ear pain
  • Reduced hearing in affected ear
  • Feeling generally unwell (e.g. fever)
  • Hx of or current symptoms or URTI (cough, coryzal symptoms, sore throat)
  • Discharge from ear if tympanic perforation
52
Q

What might you find on otoscopy in otitis media?

A
  • Bulging, red tympanic membrane (like a doughnut)
  • May see perforation in tympanic membrane
53
Q

Discuss the management of otitis media

A

Antibiotics

Most cases resolve without abx in around 3-7 days. Hence, antibiotics are not always needed. Antibiotics can be given as an immediate or delayed prescription.

Indications for immediate antibiotics include:

  • 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

Indications for delayed antibiotics (to be used after 3 days) include:

  • No improvement or worsening of symptoms
  • More likely to benefit (e.g. <2yrs with bilateral symptoms, otorrhea)
  • Helpful strategy in pts pressing for abx

Antibiotic choice:

  • First line= amoxicillin 5-7 days
  • If penicillin allergy= clarithromycin
  • If penicillin allergic & pregnant= erythromycin

Other aspects of management:

  • Safety netting
  • Simple analgesia
54
Q

Which children with AOM would you admit to hospital?

A

Admit for immediate specialist assessment:

  • People with a severe systemic infection
  • People with suspected acute complications of acute otitis media (AOM), such as meningitis, mastoiditis, intracranial abscess, sinus thrombosis, or facial nerve paralysis
  • Children younger than 3 months of age with a temperature of 38°C or more
55
Q

State some potential complications of otitis media

A
  • Otitis media with effusion
  • Hearing loss (usually temporary)
  • Perforated tympanic membrane (with pain, reduced hearing and discharge)
  • Labyrinthitis (causing dizziness or vertigo)
  • Mastoiditis (rare)
  • Abscess (rare)
  • Facial nerve palsy (rare)
  • Meningitis (rare)
56
Q

What is otitis externa?

A

Inflammation of external ear canal; may also involve tympanic membrane and pinna

57
Q

What do we mean by:

  • Acute otitis externa
  • Chronic otitis externa
A
  • Acute otitis externa is inflammation of less than 6 weeks duration, typically caused by bacterial infection with Pseudomonas aeruginosa or Staphylococcus aureus.
  • Chronic otitis externa is inflammation which has lasted longer than 3 months, and may be caused by fungal infection with Aspergillus species or Candida albicans.
58
Q

State some risk factors for otitis externa

A
  • Swimming (often called swimmers ear)
  • Trauma (e.g. from cotton buds or earplugs)
  • Removal of ear wax (ear wax is protective)
  • Eczema
  • Seborrheic dermatitis
  • Psoriasis
  • Contact dermatitis
59
Q

What are the two most common causative organisms of otitis externa?

A
  • Pseudomonas aeruginosa
  • Staphylococcus aureus

TOM TIP: It is worth remembering Pseudomonas aeruginosa. It is a gram-negative aerobic rod-shaped bacteria. It likes to grow in moist, oxygenated environments. Other than causing otitis externa, an important exam-related point to remember is that it can colonise the lungs in patients with cystic fibrosis, significantly increasing their morbidity and mortality. It is naturally resistant to many antibiotics, making it very difficult to treat in children with cystic fibrosis. It can be treated with aminoglycosides (e.g., gentamicin) or quinolones (e.g., ciprofloxacin).

60
Q

Describe typical presentation of otitis externa

A
  • Ear pain
  • Discharge
  • Itchiness
  • Conductive hearing loss (if the ear becomes blocked)
  • Tenderness when press tragus
61
Q

What might you see on otoscopy of pt with otitis externa?

A
  • Red, swollen canal
  • Eczematous canal
62
Q

How is otitis externa diagnosed?

A
  • Clinical diagnosis
  • Ear swab not usually required
63
Q

Discuss the management of otitis externa

A

Main aspects of management:

  • Advice to all: keep ear clean & dry, aural toilet, simple analgesia
  • Mild otitis externa: acetic acid 2% (can buy OTC. Has antifungal & antibacterial effects)
  • Moderate otitis externa: topical abx (usually aminoglycosides or quinolones) & steroid for 7-14 days
    • E.g. neomycin, dexamethasone & acetic acid (Otomize spray)
    • Other combinations of: gentamicin, ciprofloxacin, hydrocortisone, betamethasone
      • Aminoglycosides: neomycin, gentamicin
      • Quinolines: ciprofloxacin
  • Severe or systemic symptoms or immunocompromised: oral abx (e.g. flucloxacillin or clarithromycin)

Other aspects of management:

  • Fungal infections: can use clotrimazole drops
  • Ear wick may be used if canal is very swollen and treatment with drops or sprays will be difficult (w**icks are inserted into the ear canal and left there for a period of time (e.g., 48 hours). Contain topical treatments. As the swelling and inflammation settle, the ear wick can be removed, and treatment can continue with drops or spray)
64
Q

When are aminoglycosides NOT used in otitis externa?

A

Do not use if tympanic perforation (hence MUST exclude before prescribing); can cause hearing loss.

65
Q

When would you refer a pt with otitis externa to ENT?

A
  • Symptoms persist despite optimal management in primary care
  • There is external ear canal occlusion due to ear discharge, swelling, or debris which is stopping topical treatment working effectively
    • Specialist ‘aural toilet’ including microsuction, ear wick insertion, or use of systemic antibiotics may be needed.
  • Cellulitis extending beyond the external ear canal which cannot be managed in primary care
66
Q

What is malignant otitis externa?

A

Potentially life-threatening progressive infection of the external ear canal causing osteomyelitis of the temporal bone and adjacent structures.

67
Q

State some risk factors for malignant otitis externa

A

Malignant otitis externa is usually related to underlying risk factors for severe infection, such as:

  • Diabetes
  • Immunosuppressant medications (e.g., chemotherapy)
  • HIV
68
Q

Describe typical presentation of otitis externa

A
  • Similar, but more severe, to those of otitis externa with additional features such as headache, severe pain, fever
  • Granulation tissue at junction between bone & cartilage in ear canal (~ ½ way along)= key finding
69
Q

Discuss the management of malignant otitis externa

A

Emergency admission to hospital under ENT for:

  • IV abx (that cover pseudomonas)
  • Imaging (CT or MRI head) to assess extent infection
70
Q

State some potential complications of malignant otitis externa

A
  • Facial nerve damage and palsy
  • Other cranial nerve involvement (e.g., glossopharyngeal, vagus or accessory nerves)
  • Meningitis
  • Intracranial thrombosis
  • Death
71
Q

Remind yourself of the components of earwax (2)

A

Cerumen + discarded/dead skin cells

72
Q

State some symptoms of impacted ear wax

A

Ear wax can build up and become impacted and stuck to the tympanic membrane. This can result in:

  • Conductive hearing loss
  • Discomfort in the ear
  • A feeling of fullness
  • Pain
  • Tinnitus
73
Q

Discuss the management of excess/impacted ear wax

A

Most cases doesn’t require treatment. Pts should be advised to avoid inserting cotton buds into ear. Methods to remove ear wax include:

  • Ear drops: olive oil or sodium bicarbonate
  • Ear irrigation: squirting water into ear to clean wax away. Perforation is a contraindication.
  • Microsuction
74
Q

What is glue ear?

Who is it common in?

A
  • Also called otitis media with effusion; collection of fluid in middle ear without signs of acute inflammation (hence NOT an infection)
  • Most common in winter in children aged 6 months to 4 years
    • It is the most common cause of hearing impairment in children
75
Q

Describe the pathophysiology of glue ear/otitis media with effusion

A
  • Negative pressure builds up inside ear, often due to dysfunction of Eustachian tube, causing build up of fluid in middle ear
  • Decreases motility of tympanic membrane and ossicles hence decreases hearing
76
Q

State some risk factors for glue ear/otitis media with effusion

A
  • Recent acute otitis media (50% follow on from AOM)
  • Parental smoking
  • Siblings with OME
  • Allergy
  • Reflux disease
  • Other conditions:
    • Down’s syndrome
    • Primary ciliary dyskinesia
    • Cystic fibrosis
    • Allergic rhinitis
77
Q

Describe typical presentation of glue ear/otitis media with effusion

A
  • Hearing loss is usually presenting feature
  • May see secondary problems such as speech & language delay, behavioural problems, balance problems
78
Q

Discuss the management of glue ear

A

Non-surgical

  • Active observation for 3 months (should have audiology assessments and assess impact on life)
  • Auto inflation using nasal balloon or Valsalva manoeuvre (useful in older children- may do in the active observation period)
  • Hearing aids (if surgery not suitable or acceptable)

Surgical

  • Grommets: allow air to pass into middle ear and hence do the job normally done by Eustachian tube. Majority stop functioning after 10 months & fall out on their own in time
  • Adenoidectomy: if adenoids obstructing Eustachian tube
79
Q

For chronic suppurative otitis media, discuss:

  • What it is
  • Presentation
  • Management (in primary care)
A
  • Chronic inflammation of the middle ear and mastoid cavity, which presents with recurrent ear discharge (otorrhoea) through a tympanic perforation. (WHO says after 2/52 of discharge but some experts say >6/62 discharge)
  • Presentation:
    • Ottorhea >2/6 weeks without pain or fever
    • Hearing loss
    • Hx of AOM, trauma, grommet insertion, OME
  • Otoscopy findings: perforated tympanic membrane
  • Refer to ENT (don’t swab or initiate treatment)
80
Q

For Ramsey Hunt syndrome, discuss:

  • What it is
  • What else it is called
  • Cause
  • Features/presentation
  • Management
A
  • Peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth
  • Also called herpes zoster oticus
  • Caused by reactivation of varicella zoster virus in the geniculate ganglion of CNVII
  • Features:
    • Auricular pain
    • Facial nerve palsy
    • Vesicular rash around ear on affected side (can extend to anterior ⅔ of tongue and hard palate)
    • Vertigo
    • Tinnitus
  • Management:
    • PO aciclovir and corticosteroids
    • Lubricating eydrops
81
Q

For perichondritis, discuss:

  • What it is
  • Presentation
  • Management
A
  • Infection of perichondrium (tissue that covers cartilage) in ear
  • Presentation:
    • Erythema
    • Pain
    • Swelling
  • Management:
    • Antibiotics & corticosteroids
    • If abscess, incision & drainage
    • Simple analgesia
  • Complications:
    • Cauliflower ear
82
Q

State some common causes of hearing loss in children

A
  • Acute otitis media (most common)
  • Glue ear
  • Other infections e.g. mumps, meningitis
  • Ear wax blockage
  • Foreign body
  • Genetics