ENT 469/11

Question 1

1. Muscle tension dysphonia- History

Answer 1

• common functional disorder of the larynx.
• clinical diagnosis with pointers in the history as well as findings on laryngoscopy.

History

• the onset of hoarseness
• whether hoarseness is constant (which tends to occur in structural lesions and traumatic injury) or intermittent (which tends to occur in muscle tension dysphonia, gastro-oesphageal reflux and postnasal drip)
• aggravating and relieving factors
• associated symptoms such as cough (as can occur in gastro-oesphageal reflux, allergies and as an effect of chronic laryngitis)
• risk factors for ‘throat cancer’
• determining each of the causes of hoarseness
  
  • voice abuse
  • symptoms such as heartburn and waterbrash
  • symptoms such as postnasal drip
  • symptoms associated with throat cancer
  • history of neck trauma
  • recent surgery
  • general state of health
• excluding causes of throat tightness

Question 2

1. Muscle tension dysphonia examination

Answer 2

Performed both to exclude other pathology and to demonstrate muscle tension dysphonia.

Question 3

1. Muscle tension dysphonia treatment

Answer 3

Muscle tension dysphonia usually responds well to voice therapy.

Question 4

1. Hoarseness

Answer 4

The majority of hoarseness in the community is due to viral laryngitis.

Hoarseness from viral laryngitis typically lasts up to 3 weeks.

If hoarseness persists beyond 3 weeks, referral for laryngoscopy should be considered to exclude other causes.

Question 5

1. Hoarseness- causes

Answer 5

Other diagnoses to consider as a cause for hoarseness include:

• structural lesions which can either be benign (eg. nodules, polyps and papillomas) or malignant (eg. carcinoma of the larynx)
• gastro-oesophageal reflux
• postnasal drip
• irritation from inhaled corticosteroids used to treat asthma
• irritation from fumes, dust or cigarette smoke
• autoimmune disease (eg. systemic lupus erythematosus, sarcoidosis and Wegener granulomatosis)
• infection (eg. Candida, or with Staphylococcus aureus)
• allergy
• traumatic injury.

Question 6

1. Throat tightness - history

Answer 6

Possible causes for throat tightness include:

• ischaemic heart disease – throat tightness may be atypical pain which could indicate underlying ischaemic heart disease. It is important to exclude ischaemic heart disease by appropriate investigations if this diagnosis is considered
• allergy – while allergy is a possible cause for throat tightness, in the absence of perioral swelling or rash, allergy is not likely
• asthma – asthma can present as throat tightness, though there are likely to be other symptoms such as cough, shortness of breath or wheeze present
• globus pharyngis – globus pharyngis is another condition which causes throat tightness but it usually presents with a sensation of a lump in the throat in the absence of signs.

Question 7

1. Hoarseness- management

Answer 7

• referral to ENT consultant for consideration of laryngoscopy.
• Antibiotics are unlikely to be helpful for muscle tension dysphonia hoarseness and, in general, are not helpful in most cases of hoarseness.
• There is no evidence that empirical use of corticosteroids is helpful for voice hoarseness.
• Corticosteroids could be helpful in previously diagnosed autoimmune conditions affecting the larynx, such as systemic lupus erythematosus, sarcoidosis and Wegener granulomatosis.
• Corticosteriods should be considered in airway inflammation and oedema, as can occur in emergency situations, and should transfer by ambulance to an appropriate hospital emergency department.

Question 8

1. Hoarseness and NSAIDS

Answer 8

It is possible that ibuprofen could exacerbate gastro-oesophageal reflux into the laryngopharynx or contribute to the formation of a haemorrhagic polyp, therefore contributing to voice hoarseness.

Question 9

1. Throat cancer signs and symptoms

Answer 9

‘Throat cancer’ is a nonspecific term and can mean cancer of the pharynx or larynx.

• The most common malignancy in the pharynx and larynx is squamous cell carcinoma and the main risk factors are smoking and heavy alcohol intake. Other less common risk factors include immunosuppression, exposure to asbestos and previous radiotherapy.

Some patients with squamous cell carcinoma of the head and neck region do not have the common risk factors. Symptoms and signs of concern include:

• dysphagia
• odynophagia
• loss of appetite or weight
• otalgia
• stridor or a neck mass.

If a patient has a persistently hoarse voice and risk factors for malignancy, or symptoms or signs of concern, an urgent referral to an ENT consultant should be made.

Question 10

1. Post op hoarseness

Answer 10

Voice hoarseness is not uncommon following surgery where an endotracheal tube or laryngeal mask has been used. The hoarseness is usually due to laryngeal oedema and resolves spontaneously over a period of up to 6 weeks.

Hoarseness can also be from a vocal cord granuloma or dislocation of the arytenoid cartilage resulting in an immobile vocal fold. It is important that the patient be referred to an ENT specialist for investigation with flexible laryngoscopy.

Voice hoarseness after surgery can also be due to trauma to the recurrent laryngeal nerve. Some surgical procedures are more likely to be associated with trauma to the recurrent laryngeal nerve. These include:

• cervical laminectomy via the anterior approach
• thyroid surgery
• carotid endarterectomy
• cardiac surgery
• surgery for oesophageal cancer.

Recurrent laryngeal nerve palsy could resolve and while awaiting recovery, voice therapy could improve function.

Treatment of vocal cord granuloma usually includes a combination of voice therapy, acid suppression and surgical excision.

Question 11

2. Acute hearing loss- examination

Answer 11

Weber’s tuning fork test

• will quickly differentiate between conductive deafness and sensorineural deafness.

An otoscopic examination should also be performed

Question 12

2. Weber test

Answer 12

The Weber test is performed using a tuning fork of 512 Hertz (middle C).

Strike the tuning fork and then place the stem firmly on the midpoint of the patient’s forehead. Ask the patient which ear the sound of the fork is louder in. The test is interpreted as follows:

• normal hearing – the sound is heard in the midline
• conductive deafness – the sound is heard in the deaf ear
• sensorineural deafness – the sound is heard in the nondeaf ear.

​If no tuning fork; can hum instead

Question 13

2. Idiopathic sudden sensorineural hearing loss

Answer 13

If the Weber test lateralises to the nondeaf ear, this suggests sensorineural hearing loss.

If it has been sudden, the most likely diagnosis is idiopathic sudden sensorineural hearing loss (ISSHL).

The next step would be to obtain
immediate advice from an ENT surgeon either by phone or by a referral that day.

ISSHL:

• Incidence – this varies between 5–20/100 000 per annum
• Aetiology – there is ongoing debate about the cause. A viral theory is plausible, however, a microvascular event involving the cochlear-vestibular circulation may explain a proportion of presentations
• About 40% of cases report associated balance disturbance
• Approximately 10% of acoustic neuromata present with sudden sensorineural deafness therefore part of the diagnostic workup will involve a magnetic resonance imaging (MRI) scan
• ISSHL is an emergency needing immediate treatment
• There is consensus that immediate steroid treatment increases the chance of recovery. Prednisolone is used at a starting dose of 1 mg/kg and continued for 10 days; the dose is tapered after 3 days of maximum dose
• Antiviral medications have been advocated but there is no hard evidence that there is any significant benefit
• Between 20–30% of cases will improve spontaneously.

Question 14

2. Conductive hearing loss

Answer 14

If the Weber test lateralises to the deaf side, this indicates that there is a conductive deafness which can be caused by obstruction of the external ear canalor by pathology in the middle ear.

If pathology in the middle ear was the cause, the tympanic membrane would look abnormal due to the presence of middle ear fluid reflecting eustachian tube blockage secondary to upper respiratory inflammation.

If this is the case, treatment should be with nasal decongestants, either topical or systemic.

If otalgia was present, this might represent otitis media.

Question 15

2. Ramsey Hunt Syndrome

Answer 15

Another possible cause of sensorineural deafness is shown is Shingles.

An early herpes zoster vesicle can form on the ear drum.

The patient can present with the onset of severe otalgia and a sensorineural deafness before proceeding to develop a facial nerve palsy (Ramsay Hunt syndrome).

In this instance antiviral medication and steroids together are the first line treatments.

Question 16

3. AOM diagnosis

Answer 16

AOM without perforation

• The tympanic membrane is red and injected, and there is loss of the prominence of the anterior process of the malleus, consistent with pus under pressure.

AOM with perforation.

• The ear needs to be cleaned to assess the tympanic membrane.

The diagnosis of AOM may be difficult to make, especially in children younger than 3 years

• who have small external auditory canals,
• may not be cooperative and/or have wax obscuring the view.

In a comparison of doctors it was found that the accuracy in diagnosing whether or not there is middle ear fluid was: ENT surgeons – 74%; paediatricians – 51%; GPs – 46%.5

Using pneumatic otoscopy or a tympanogram can improve the diagnostic accuracy.

Question 17

3. Recurrent AOM

Answer 17

Recurrent AOM is defined as

• three or more episodes in 6 months, or
• four or more in 12 months.
• is an indication that a child is having more infections than would usually be expected.

Question 18

3. AOM- causative organisms

Answer 18

The organisms that commonly cause AOM are

• Streptococcus pneumoniae,
• Haemophilus influenzae – nontypeable, and
• Moraxella catarrhalis

Question 19

3. AOM History for treatment plan

Answer 19

Further questions to ask include the following.

• Is it first year of having a lot of contact with other children? (If he has not had previous exposure to infections through childcare then he is likely to continue having colds and ear infections)
• a past history of other infections, such as pneumonia, suggestive of an immune deficiency?
• Do they swim regularly in a swimming pool? (Although there is evidence that for Aboriginal children in remote communities in Western Australia, swimming in pools can reduce ear infections, this mainly relates to children with perforated tympanic membranes and chronic otorrhoea. Although swimming on the surface of the water is not usually associated with eustachian tube and middle ear problems, swimming more than 60 cm below the surface is sufficient to insufflate infected nasopharyngeal secretions into the middle ear during an upper respiratory infection. If child is having regular swimming lessons parents could try keeping them out of the pool for winter)
• Are there concerns about his hearing either at home or in school?

Question 20

3. AOM Rx

Answer 20

Treatment of AOM involves the following.

adequate analgesia

• Usually with an oral agent such as paracetamol.
• Topical anaesthetic drops such as amethocaine, benzocaine or lidocaine have some efficacy at 30 minutes after administration, but not more than paracetamol once they have been absorbed.
• Topical anaesthetic drops should not be administered when there is a perforation as they may enter the inner ear and cause vertigo.

antibiotic therapy

The current recommendations are that children older than 2 years who are not very ill (ie. no systemic features such as significant fever or vomiting) can be treated with observation only; the parents can
be given a prescription to be filled if the child is still in pain after 48 hours.

However, there are groups of children who should be treated:

• children 2 years of age or younger, because:
  
  • they are not able to describe their symptoms
  • they are more likely to have suppurative complications such as meningitis and mastoiditis
  • they are less likely to improve spontaneously
• children with severe illness with pain, or a tympanic membrane perforation (these imply a more virulent organism)
• a child with known immunodeficiency
• indigenous children, including Aboriginal, Torres Strait Islander and Maori and other Pacific Islander children
• children with a cochlear implant

Cleaning of ear with perforation;

• with suction if available, or
• with mopping with tissue spears.
• parent can continue with use of tissue spears at home as well

Question 21

3. AOM Antibiotic Rx

Answer 21

The usual antibiotic recommended is

• amoxycillin, 15 mg/kg up to 500 mg three times per day for 5 days.
• If the child has an allergy to penicillin (excluding immediate hypersensitivity), the alternative medication is cefuroxime in a dose of 10 mg/kg up to 500 mg twice per day for 5 days, or ceflacor in a dose of 10 mg/kg up to 250 mg three times per day for 5 days. The efficacy of ceflacor is thought to be similar to that of amoxycillin but it may be less as it penetrates middle ear mucosa less efficiently.

With a perforation of the eardrum, topical antibiotic drops are useful both to treat the middle ear and also to treat secondary otitis externa if present.

• The recommended antibiotics are quinolones such as ciprofloxacin with or without steroid, which are not ototoxic when there is a tympanic membrane perforation.
• If the tympanic membrane is intact there is no advantage in treatin with topical antibiotics.

If perforated this ear should be kept dry.

If there is infection and fluid in both his ears, child may not be hearing well.

Parents should be warned of this and asked to notify the teachers at school to report concerns about his hearing or behavioural changes which could suggest hearing difficulties.

Question 22

3. Recurrent AOM- risk factors

Answer 22

Risk of recurrent otitis media depends on the presence of recognised risk factors for otitis media. These are:

• age – especially 6–11 months
• race – eg. Indigenous Australian children. There are differences in the eustachian tube and immunological response, but socioeconomic factors are also important
• craniofacial abnormalities – including cleft palate and those caused by Down syndrome
• genetic – both anatomical and immunological
• birth order – children with older siblings are more likely to have infections than the first born.

Question 23

3. Recurrent AOM; environmental factors

Answer 23

There are recognised environmental factors, and parents can help control these by implementing the following:

• reduce contact with people with upper respiratory infections, especially large group childcare centres
• avoid tobacco smoke both during and after pregnancy. Children exposed to passive smoking are more likely to have recurrent otitis media and have middle ear effusions that persist for longer
• breastfeed for at least 6 months, preferably 12 months. If bottle fed, prop the baby up as milk can reflux into the ear if lying flat, causing inflammation
• avoid pacifiers/dummies – this possibly increases the risk of AOM by inadvertent sharing in childcare centres
• vaccination with the polyvalent pneumococcal vaccine reduces the incidence of AOM by 8%.

Question 24

3. AOM clinical follow up

Answer 24

• should be reviewed in 2 days if not better.
• At that stage, if the AOM has not resolved, institute change to an antibiotic such as amoxycillin/clavulanate.
• should also be reviewed at the 2 week mark to ensure that the perforation of the tympanic membrane has healed.

Note that at 2 weeks following an episode of AOM, 70% of children will still have a middle ear effusion but most perforations will have healed.

Question 25

3. Recurrent AOM Rx

Answer 25

Further ear infections and ongoing middle ear effusion. These factors are likely to affect hearing and school work.

Management could involve:

• use of amoxycillin/clavulanate in case child had a resistant Pneumococcus as he has had a recent infection treated with amoxycillin
• referral for audiology
• treating his nose – saline sprays help to clear the mucus, and steroid sprays help to reduce the size of the adenoids, but there is no evidence that either will improve the eustachian tube function and clear fluid from the middle ear.

Question 26

3. Chronic OM- grommets indication

Answer 26

Indications include

• chronic otitis media with effusion for 4 months or longer with conductive hearing loss. The level of hearing that is significant is not known, and probably differs for each child
• significant hearing loss
• known language delay
• learning/intellectual problems
• visual impairment in addition to hearing loss from chronic otitis media with effusion
• damage to the tympanic membrane with retraction pockets to prevent permanent ossicular erosion.
• Middle ear ventilation tubes are also effective in preventing recurrent acute otitis media, and for the treatment of complications of acute otitis media such as facial nerve paresis and meningitis.

Question 27

3. Chronic OM - prophylactic Abx

Answer 27

Treatment with prophylactic antibiotics

• (usually a single daily dose of amoxycillin 20 mg/kg)

has some efficacy, however, due to concerns about antibiotic resistance, prophylactic antibiotics are reserved for children under special circumstances.

• children who are a poor risk for general anaesthesia, or
• those who have had tubes inserted and have persistent infections.

Question 28

3. Recurrent OM and adenoidectomy

Answer 28

It is usually recommended that adenoidectomy be performed if the child needs a second set of ventilation tubes, unless there is significant nasal obstruction, in which case it may be performed earlier.

Adenoidectomy has not been shown to be effective in preventing recurrent AOM

Question 29

4. Vestibular Neuritis

Answer 29

Acute vestibular syndrome is a description of a clinical syndrome which usually implies an acute peripheral vestibulopathy, however, occasionally a central disturbance can mimic this syndrome.

The presumptive cause of acute vestibular syndrome is vestibular neuritis, otherwise known as vestibular neuronitis or viral neurolabyrinthitis.

This clinical syndrome is commonly thought to be related to reactivation of herpes simplex virus infection of vestibular nerve ganglion (also known as Scarpa ganglion).

Question 30

4. Differential DIagnosis- Migraine

Answer 30

migraine

• Migraine can cause acute vertigo, however, usually there are no clinical signs and there is usually, but not invariably, significant headache present.
• Consider a diagnosis of migraine where there is a past or family history of migraine. Like Meniere disease, recurrent episodes are required before a diagnosis of vestibular migraine can be made.
• The criteria for diagnosing migrainous vertigo are listed in Table 2.

Question 31

4. DDx Meniere’s Disease

Answer 31

meniere disease

While Meniere disease, which is frequently overdiagnosed, can cause acute vertigo, it is not the likely cause in this case because:

usually the vertigo of acute Meniere disease attacks would not last as long as 5 hours, though the after effects of nausea, disequilibrium and ear symptoms may last hours to days

recurrent episodes are required to make the diagnosis associated ear symptoms (eg. fluctuating low frequency sensorineural hearing loss, aural fullness and tinnitus) while not invariably, are often present – Table 1 outlines the diagnostic criteria for Meniere disease.

Question 32

4. DDx Stroke

Answer 32

stroke

The vestibular pseudoneuritis syndrome can appear very similar to vestibular neuritis. Vestibular pseudoneuritis is due to brainstem/cerebellar ischaemia (ie. ischaemia in the posterior inferior cerebellar artery or anterior inferior cerebellar artery territories).

Stroke should be considered when there are vascular risk factors, the presence of any one of the red flags or abnormal signs on examination of the cranial nerves.

A careful ocular motor examination can help distinguish central vestibular pseudoneuritis and vestibular neuritis. The clinical signs in this case synopsis do not suggest a stroke syndrome. There are a number of red flags to consider in patients presenting with vertigo and nausea that could indicate stroke

Any one of the following red flags suggests the possibility of a stroke or other central lesion:

• acute unaccustomed headache
• inability to stand or walk
• the presence of spontaneous direction changing nystagmus • spontaneous vertical nystagmus
• a normal head impulse
• the presence of additional focal neurological signs.

Question 33

4. DDx BPPV

Answer 33

benign paroxysmal positional vertigo

Episodes of vertigo in benign paroxysmal positional vertigo (BPPV) are usually:

provoked by a change in position of the head or change in posture

brief and not accompanied by vomiting and not associated with spontaneous nystagmus before provocation.

Question 34

4. Examination- Head impulse test

Answer 34

The head impulse test is performed by rapidly rotating the patient’s head while the patient is instructed to fixate on a central object such as the examiner’s nose.

When the vestibulo-ocular reflex is intact, an equal and opposite eye movement keeps the eyes stationary in space.

An abnormal result is indicated by failure to maintain fixation. In this case, movement of the eyes occurs then the patient will suddenly perform corrective refixation back to focus on the central object.

An abnormal test suggests an acute vestibular syndrome due to vestibular neuritis and a normal test usually suggests the symptoms are due to a central lesion such as stroke, though this is not always the case and must be interpreted in context

Question 35

4. Examination

Answer 35

Further examination could consist of the following:

Romberg test – to perform this test, the patient stands erect with their feet close together and eyes closed and is observed for 1 minute. Romberg sign is said to be positive if the patient becomes unsteady in this position

bedside assessment of hearing

assessment of gait and preponderance to veer to one or other side

Hallpike manoeuvre –

• take care with the manoeuvre in patients who have neck disease and avoid performing the manoeuvre in patients with major cervical spine instability. After explaining to the patient what you are going to do, the patient sits upright with the head rotated 30–45 degrees laterally.
• The patient is then rapidly moved into a supine position on the examination couch with the head hanging over the end of the couch or a pillow placed behind the shoulders.
• The patient’s head is supported either by the examineror by the couch if a pillow is placed behind the shoulders. The examiner then observes the patient for nystagmus and asks about vertigo. Then the test is repeated with the patient’s head turned to the opposite side.
• The test may then be repeated to assess for fatigability of the response

A positive Hallpike test has the following characteristics and suggests a diagnosis of BPPV:

• brief latency – in BPPV, there is usually a brief latency of several seconds before the onset of nystagmus and it usually lasts 10–20 seconds
• nystagmus – usually torsional (rotational around the anteroposterior axis of the eye globe) but may be horizontal. In BPPV, on performing the Hallpike manoeuvre, there is usually upbeating, torsional nystagmus arising from otolithic debris in the ipsilateral posterior semicircular canal. Horizontal nystagmus on positioning suggests that the lateral canal is affected. Downbeating, torsional nystagmus which occurs on positioning indicates that the ipsilateral anterior semicircular canal is affected
• reversal – upon sitting after a positive manoeuvre, the direction of nystagmus is reversed for a brief period of time
• fatigability – repetition of the test will result in less nystagmus each time.
  ​

The presence of a positive Romberg test (a Romberg sign) indicates loss of proprioceptive or vestibular input,, is supportive of a diagnosis of vestibular neuritis.

On the other hand, when a central lesion is present where the cerebellum
is affected, such as in the case of a stroke, while the patient is also unstable at rest, they are not made more unstable when performing a Romberg test (this constitutes a negative Romberg test).

In cases of acute vestibular syndrome, there is spontaneous horizontal nystagmus before performing the Hallpike manoeuvre, which suggests a peripheral cause of vertigo other than BPPV.

In acute vestibular syndrome caused by vestibular neuritis, nystagmus is often noted while performing the Hallpike manoeuvre as well as it being present before performing the maneouvre.

• In these cases the Hallpike manoeuvre will not result in latency, reversal and fatigability in vestibular neuritis as it tends to in cases of BPPV.

In cerebrovascular causes of vertigo, spontaneous nystagmus can occur and it will usually be vertical or direction changing. On performing the Hallpike manoeuvre, there is upbeating, downbeating or direction changing nystagmus but no latency, reversibility or fatigability.

Question 36

4. Acute Vestibular Neuritis Treatment

Answer 36

Once a diagnosis of acute vestibular neuritis is made, treatment could consist of the following:

• symptomatic treatment with antiemetics and fluids for rehydration if necessary
• benzodiazepines may be useful in reducing the intensity of vertigo for the first 24–48 hours but should be used sparingly after this time period
• steroids – a course of steroids similar to that given for Bell palsy should be considered
• antiviral therapy – there is controversy over the use of antiviral therapy in this situation, although the existing evidence does not support its routine use.

Following a bout of vestibular neuritis, recovery usually begins after a few days, although the patient may be rendered bedbound or housebound for up to 1 week.

As the patient recovers from the acute disturbance, vestibular adaptation exercises or even formal vestibular physiotherapy should be considered to aid further recovery over the ensuing weeks or months.

Question 37

4. Investigations

Answer 37

Computed tomography (CT) or MRI brain would not be considered absolutely necessary.

Patients could be referred to hospital for imaging to look for evidence of stroke if there is in any doubt about the diagnosis, or for rehydration if his vomiting is severe.

If there is significant suspicion of a stroke, then the patient ought to be admitted for observation and investigation.

The presence of any one of the red flags for stroke with the presence of vascular risk factors suggest a possible stroke, in which case a neuroimaging study, preferably MRI, needs to be ordered.

Frequently a CT brain is ordered in this situation, however, a CT scan is not sufficient to rule out a stroke in the posterior fossa. A CT brain scan may reveal a large cerebellar hemisphere infarct or a posterior fossa haemorrhage.

Usually the CT brain in the clinical scenario described above is normal. Certainly if there is no, or limited, access to MRI, then it would be reasonable to get a CT brain and consider transfer to another institution with MRI access.

If there is doubt about the diagnosis, admission for observation would be wise.

Question 38

4. Causes Recurrent Vertigo

Answer 38

Postvestibular neuritis benign positional vertigo

• The recurrence of vertigo after a few weeks most likely indicates postvestibular neuritis benign positional vertigo.
• Vestibular neuritis frequently involves the superior division of the vestibular nerve resulting in damage/dysfunction to the afferents from the superior and lateral semicircular canals and sparing the posterior semicircular canal afferents. Therefore any otolithic debris dislodged by the acute vestibular insult may accumulate in the posterior semicircular canal and give rise to benign positional vertigo.
• This diagnosis may be confirmed by performing a Hallpike manoeuvre, which will be positive. It is treated satisfactorily with a particle repositioning manoeuvre such as the Epley (see Resources) or Semont manoeuvre.

decompensation

• After initial improvement from vestibular neuritis, decompensation can occur and the reasons are often not clear. Formal vestibular investigations and vestibular physiotherapy may be useful in clarifying this clinical scenario.
• If the original bout of acute vertigo lasts less than 24 hours, and the Hallpike manoeuvre is repeatedly negative, then other possible diagnoses such as vestibular migraine, Meniere disease or even ‘recurrent vestibulopathy’ (a term used for recurrent unexplained vertigo) may explain recurrent symptoms.

migraine

• With migraine, vertigo may occur with or without headache.

meniere disease

• Additional clinical features such as those outlined in Table 1 and 2 should sort out whether migraine or Meniere disease is most likely.

recurrent vestibulopathy

• A term used for recurrent unexplained vertigo.

recurrent vestibular neuritis

• may occur but is uncommon.

vascular vertigo

• (vertigo due to cerebrovascular disease) might be suspected with the occurrence of recurrent vertigo, particularly in the presence of vascular risk factors. Usually the recurrent symptoms would be brief, lasting seconds to minutes, and would not ordinarily continue beyond 6–8 weeks without other transient ischaemic attack manifestations or permanent posterior circulation territory infarction.

perilymph fistula or autoimmune inner ear disease

• would be other much less common causes of recurrent vertigo and would usually be associated with hearing loss.

Question 39

5. Epistaxis- predisposing factors

Answer 39

There are various local and systemic conditions which can predispose to epistaxis. These include:

local conditions – conditions such as

• trauma,
• structural abnormalities (eg. septal deviation/perforation);
• inflammatory diseases (eg. infection, allergy, granulomatous disorders);
• tumours and
• vascular malformations

environmental conditions –

• the decrease in ambient humidity during winter causes a drying effect of the nasal mucosa that impairs wound healing and enhances crust formation.
• This encourages local digital trauma, and a vicious cycle of trauma and inflammation ensues

medications – such as

• intranasal steroids used for allergic rhinitis,
• aspirin,
• anti-inflammatories,
• clopidogrel and
• warfarin, and
• drugs such as cocaine used on a long term basis, may predispose to epistaxis

systemic factors – such as

• deficiencies in coagulation,
• vascular diseases and
• cardiac/pulmonary diseases (the latter, as a result of the combination of increased intravascular pressure and medically-induced coagulopathy) have been associated with more severe epistaxis (as well as higher risk for posterior nasal bleeds).

Investigation for coagulation disorders should be considered in recurrent and multifocal bleeds.

The association between hypertension and severe epistaxis is still debateable.

Question 40

5. Epistaxis history

Answer 40

History

• the initial laterality,
• duration and
• amount of blood loss and
• whether he has had nose bleeds before.

It is also important to ask him questions directed at establishing the cause of his nosebleed, such as

• a recent common cold,
• nasal blockage,
• discharge or crusts,
• local digital trauma,
• use of medications,
• intake of alcohol and drugs,
• past history of allergic rhinitis and
• systemic disease and whether he has had any bleeding elsewhere.

It is also important to ask him questions directed at identifying the source of bleeding, namely whether it is from an anterior nasal source or posterior nasal source.

To elicit this, ask where the bulk of the bleeding seems to be presenting (into the throat or out through the nose),

as well as about triggers and response to any first aid applied.

Question 41

5. Epistaxis examination

Answer 41

Important features on examination include

• assessment of haemodynamic status and
• examination of nose to identify the source of the bleeding.

The rest of the examination depends on features elicited in the history.

In cases of significant bleeding, history, examination and treatment will proceed concurrently.

Question 42

5. Epistaxis anterior vs posterior bleed

Answer 42

There are some factors in the history that will guide you in identifying the source of the bleeding as being either anterior or posterior. These are outlined in Table 3.

The source of the bleeding can be differentiated by two means on examination.

Response to first aid – this includes pinching the nostrils together, or response to a properly applied anterior nasal pack. More than 90% of nasal bleeding arises from the ‘Little area’ in the anterior nasal septum. Anterior epistaxis usually responds to pressure from pinching the nostrils together or a properly applied anterior nasal pack. If the bleeding arises from another source, such as the branches of the sphenopalatine artery posteriorly, these manoeuvres will be ineffective. If a patient continues to bleed, particularly with the blood running down the pharynx despite a properly applied anterior pack, and coagulation defects have been ruled out or corrected, a posterior bleed must be suspected

Inspection of the nasal cavity – this requires a good light source, a nasal speculum and suction equipment if available, and even this allows examination of only the anterior nasal cavity.

Locating the source of bleeding is often difficult, especially when confronted with a profusely bleeding patient

The source of the bleeding can also be indentified with endoscopy. In a well anaesthetised and decongested nose endoscopic evaluation will often allow definite source identification.

Question 43

5. Hereditary Haemorrhagic Telangiectasia

Answer 43

In patients with recurrent, profuse nosebleeds who have mucocutaneous telangiectasias, a possible diagnosis of hereditary haemorrhagic telangiectasia (HHT – Osler disease) should be considered. It has an incidence of 2–4 /100 000 and is an inherited disorder through an autosomally dominant gene. The disease is characterised by mucocutaneous telangiectasia and arteriovenous malformations brought about by the absence of smooth muscle and elastic tissue in the vascular endothelium.

Epistaxis is the most common presentation of HHT.

Question 44

5. Recurrent Epistaxis

Answer 44

Recurrent epistaxis associated with persistent nasal obstruction should be further evaluated for neoplastic causes.

Clinical signs of skull base tumours (eg. cranial nerve palsies), intracranial spread and neck node metastases can suggest malignancy and should be referred immediately for imaging and consult with an otolaryngologist or neurosurgeon.

A young, male patient with reoccurring significant nosebleeds should be investigated for juvenile angiofibroma.

Question 45

5. Epistaxis- Treatment

Answer 45

Most cases of epistaxis are self limiting and patients rarely seek medical help. Patients with spontaneously resolving epistaxis are advised to avoid local trauma and avoid nose blowing, hot drinks and alcohol for 12 hours and are instructed on first aid for epistaxis should it recur. Measures to improve nasal hydration such as topical antibiotic/antiseptic ointments and air humidifiers may be helpful.

Below is a stepwise treatment of epistaxis in the office setting:

• first aid in mild cases where an anterior epistaxis is suspected – this involves pinching the nostrils together, between the patient’s thumb and index finger, with pressure applied toward the face. This is performed in a position with the patient’s head slightly forward for a total of 5 minutes continuously. In addition, someone else can apply an ice pack to the bridge of the nose
• patients with persistent bleeding should be assessed for the need for resuscitation and the usual ‘ABCs’ must be performed when necessary. The attending health providers should always protect themselves by using the ‘three Gs’ – gowns, goggles and gloves.

Epistaxis can potentially deteriorate from a mild bleed to an uncontrollable exsanguination

• nasal toilet and evacuation of clots if a suction device with appropriate suction tips is available
• decongestion and anaesthesia of nasal mucosa with cophenylcaine (lignocaine hydrochloride plus phenylephrine) helps to control low flow minor bleeds, and permits a thorough inspection of the nasal cavity to determine the specific site of the bleeding vessel. Cophenylcaine soaked in ribbon gauze is introduced into the nasal cavity. Pay attention to recommended doses for lignocaine, especially when dealing with children and older patients
• for anterior epistaxis – you can perform chemical cauterisation with silver nitrate sticks or electrocautery. Chemical cauterisation is safely performed after the nose has been toileted, decongested and anaesthetised. Do not cauterise blindly, and avoid cauterising both sides of the septum simultaneously (Figure 12)
• nasal packing – anterior with or without posterior packing

In the case of refractory epistaxis refer the patient to a hospital emergency department or ENT specialist.

Question 46

5. Epistaxis- packing materials

Answer 46

Packing materials include absorbable or nonabsorbable types.

Absorbable materials include oxidised regenerated cellulose (Surgicel®) and gelatin foams (Gelfoam®).

The mechanism of action is not well described but oxidised regenerated cellulose is believed to form a scaffold for platelets to attach to. The effect of gelatin foams on the other hand is thought to be physical rather than an alteration of clotting mechanism.

Nonabsorbable packs include polyvinyl acetyl sponge (Merocel®), impregnated ribbon gauze (BIPP Gauze®), calcium alginate (Kaltostat®) or inflatable balloon catheters (Rapid Rhino®, Foley Catheter®).

Once the nose has been adequately decongested and anaesthetised with cophenylcaine (lignocaine hydrochloride plus phenylephrine), most of these packs are easy to introduce with forceps.

Packs are generally left in situ for 1–5 days depending on the patient’s risk factors, coagulation state and severity of bleed.

Consider antibiotic cover for S. aureus to minimise the risk for toxic shock syndrome.

Question 47

5. Epistaxis- referral to ED

Answer 47

Situations that would prompt you to send a patient with epistaxis to a hospital emergency department include:

• signs of haemodynamic shock (eg. pallor, tachycardia, hypotension, tachypnoea, vasovagal reflex)
• persistent bleeding despite adequate first aid measures
• suspicion of posterior nasal bleed
• recurrent anterior epistaxis not responding to cauterisation
• patients with medical comorbidities requiring close observation
• epistaxis secondary to severe coagulation deficits requiring reversal or blood transfusion
• bleeding from a suspected nasal mass or vascular malformation
• significant bleeding after nasal, sinus or anterior skull base surgery.

Question 48

6. Rhinitis

Answer 48

If Symptoms are occurring on most days of the week (more than 4) and for more than 4 consecutive weeks, they are termed persistent.

Previously, terminology classified rhinitis as seasonal or perennial. However, the terms

• intermittent and
• persistent are now favoured.

Symptoms may then be also subclassified as

• allergic or nonallergic and as
• mild, moderate or severe.

Question 49

6. Rhinitis history

Answer 49

History supportive of a diagnosis of allergic rhinitis include:

• symptoms are seasonal
• children also have symptoms, suggesting a possible genetic predisposition
• profession eg as a cleaner, and therefore exposure to chemicals in cleaning products.

Taking further history should aim to help establish the initial diagnosis of allergic rhinitis and rule out alternative contributory factors such as medications.

Further history should include enquiries about:

• atopy – personal history of atopy including the presenceof eczema and asthma and precipitation or exacerbation of symptoms with the presence of pets at home
• family history of rhinitis – similar symptoms is relevant because genetic factors within the human leukocyte antigen system have been identified in allergic rhinitic patients.
  
  • However, the causes for allergic rhinitis are multifactorial and environmental factors play a significant part
• asthma – symptoms suggestive of asthma. Take a full respiratory history and, if possible, assess airway function before and after bronchodilator use, owing to the potential of individuals with persistent rhinitis to have undiagnosed asthma or bronchial hyper-reactivity.
  
  • Additionally, rhinitic patients with asthma have been shown to experience more hospital admissions and visits to GPs, which supports the idea of the unified airway and that rhinitis and asthma represent a continuum of disease at differing locales along the respiratory tract
• occupational – profession may also be a source of her symptoms either through exposure to an increased allergen load while cleaning or due to sensitivity to cleaning chemicals
• medications – a wide range of medications including nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin coverting enzyme (commonly known as ACE) inhibitors, beta-blockers and oral contraceptives can generate nasal symptoms.
  
  • In particular, intranasal vasoconstrictors may cause rebound rhinitic symptoms following extended use, a condition termed ‘rhinitis medicamentosa’.

Question 50

6. Rhinitis examination

Answer 50

Examination is secondary in the diagnostic process in this condition.

Examination should aim to exclude alternate pathology such as septal deflection (septal deviation) or nasal polyposis.

However, features such as hypertrophied inferior turbinates and the ‘allergic salute’ which results in a crease on the nose due to the patient repeatedly rubbing the nose upwards, would further lend weight to a rhinitic aetiology.

Question 51

6. Rhinitis investigations

Answer 51

A number of modalities exist to investigate allergic aetiologies.

However, skin prick testing (SPT) has been shown to provide favourable sensitivity when performed by trained practitioners in patients who have been correctly counselled before testing, ie. to avoid medications that would suppress the wheal and flare response before testing.

Blood tests in the form of immunoglobulin E specific, radioallergosorbent (RAST) tests provide lower sensitivity but higher specificity and do not expose the patient to the risk of anaphylaxis.

However, the relationship between allergen identified on testing and symptoms is less certain with RAST testing than with SPT.

A common allergy test battery would assess sensitivity to

• house dust mites (the most common being dermatophagoides pteronyssinus and farinae),
• grasses,
• pollens,
• fungi,
• cats and dogs.

Question 52

6. Rhinitis- management

Answer 52

Conservative advice

If SPT was positive to specific allergens, allergen avoidance advice would be appropriate.

Measures to combat dust mites include the reduction of soft furnishings, regular cleaning with a vacuum cleaner which has a high efficiency particulate air filter (commonly known as HEPA filter) and the use of protective bedding. Dust mites thrive in areas of high humidity (>80%) and high temperature (>20°C). Therefore, closed environments using central heating may contribute to their proliferation. Humidity levels <50% cause dust mite death. A Cochrane Review has suggested that measures to reduce dust mites result in some minimal improvement in symptoms but the studies were generally small and of poor methodological stature.

Broadly speaking, initial medical therapeutic options fall into the drug categories outlined below.

• Decongestants – these are generally alpha-agonists and achieve symptom control through vasoconstrictive mechanisms. They should not be used for more than 3 days in a row owing to the risk of leading to rhinitis medicamentosa
• Antihistamines – the previous generation of sedating H1-blockers has given way to the second generation of nonsedating antihistamines which can provide excellent symptom control
• Intranasal corticosteroids – intranasal corticosteroids are also excellent at controlling nasal symptoms but do not have an immediate onset of action. Their method of delivery and low dose results in minimal risks owing to low systemic absorption but can cause dryness, bleeding and nasal irritation/stinging. While effective for nasal symptoms, the presence of ocular symptoms may require additional therapy directed at the eye
• Intranasal anticholinergics – these can be very effective in the control of rhinorrhoea and while not being a first line choice in allergic rhinitis, can be helpful in vasomotor rhinitis in the elderly
• Cromone – again, while effective at symptom control in a subgroup of people, their regimen requires frequent and continued administration that can affect compliance
• Leukotriene antagonists – these have been found to be beneficial in treating symptoms of allergic rhinitis on par with H1-blockers but inferior to corticosteroids.

When symptoms are mild, any of the above groups may be used in symptom control but when moderate or severe, intranasal corticosteroids would be preferred.

Question 53

6. Persistent Rhinitis Management

Answer 53

If symptoms persisted despite treatment, referral to a specialist should be considered.

At that stage, associated anatomical abnormalities would be assessed and perhaps a short course of oral steroids trialled.

Failure of medical therapy to control symptoms may then prompt consideration of surgical intervention in the form of inferior turbinoplasties to improve symptoms of nasal congestion/ obstruction.

However, such intervention would be an adjunctive therapeutic modality as the underlying allergic aetiology would not have been dealt with.

Alternatively, referral to an immunologist for consideration of immunotherapy may be considered. However, while current regimens can provide excellent rates of control, patients should be counselled regarding prolonged therapeutic times, the potential for anaphylaxis and failure of treatment.

Question 54

7. Chronic Rhinosinusitis

Answer 54

Symptoms suggestive of this diagnosis that you would enquire about include

• nasal congestion/blockage/obstruction, anterior nasal discharge and postnasal drip.
• Symptoms such as halitosis and mouth breathing may occur secondary to either nasal obstruction or nasal discharge.
• Additionally, symptoms of facial pressure or pain or
• reduction or loss of sense of smell may be present.

When these symptoms are present for

• more than 12 weeks in 1 year, they are termed chronic (persistent) rhinosinusitis and
• acute (intermittent) when they occur for fewer than 12 weeks in 1 year.

The history should be completed with enquiries into the presence of

• nasal bleeding,
• crusting,
• cacosmia (perception of a foul odour when none exists), and unilateral symptoms.

The presence of nasal bleeding, cacosmia or unilateral symptoms or the presence of neurological, visual or systemic symptoms would merit urgent referral to an ENT specialist.

Question 55

7. Chronic rhinosinusitis- examination

Answer 55

Examination of the anterior portion of the nasal cavity (anterior rhinoscopy) involves

• inspection with the naked eye and
• then inspection with a headlight, nasal speculum or otoscope to identify the presence of any signs of infection such as mucopus or obstructive lesions such as a septal deflection, nasal polyposis or turbinate hypertrophy.

Question 56

7. Chronic Rhinosinusitis- Inx

Answer 56

Investigations such as X-ray and CT scanning are not helpful at this presentation.

X-ray and CT scans are not usually necessary when managing uncomplicated sinonasal disease in general practice

Plain radiograph correlation with CRS is poor although CT can be useful in surgical planning to identify anatomical features.

Magnetic resonance imaging is not indicated for the diagnosis or management of CRS but may be useful in combination with CT for the differentiation of fungal and neoplastic disease.

If the history and/or examination suggested sinister pathology, investigations targeted towards the suspected pathology should be considered.

Question 57

7. Chronic Rhinosinusitis Management

Answer 57

Treatment with a topical steroid spray together
with nasal douching is appropriate.

• Nasal douching has potential beneficial effects through mechanical cleansing of nasal mucous and also improvement in mucociliary transport.
• Nasal douching can be administered using commercial preparations or may be made up by adding 1 teaspoon of salt (non-iodised with no caking ingredients) and 1 teaspoon of baking soda to a pint of water that has been boiled and cooled. This can then be sniffed in from a cupped hand to the postnasal space and then spat out.
• The side effect profile for topical steroid sprays is minimal and mainly includes initial stinging sensation, nasal dryness and epistaxis.
  
  • The initial stinging sensation usually settles after a few days of use but may be reduced through the use of aqueous based intranasal corticosteroid preparations.
  • The side effect of dryness may be helped through douching, and epistaxis helped through instilling the nasal spray such that it is not always directed medially toward the nasal septum. Systemic absorption and influence upon the hypothalamic pituitary axis are minimal owing to the relatively low concentration dose and local nature of application and should therefore not discourage prescription of topical nasal steroids.

If symptoms are controlled at the 1 month mark, the treatment regimen with intranasal steroids and nasal douching should be continued to the 3 month mark followed by a period of cessation with recommencement should symptoms recur.

Question 58

7. Chronic Rhinosinusitis management if persistent

Answer 58

If symptoms are not controlled after 1 month saline and nasal steroids referral to an ENT specialist is advised.

An ENT specialist will often investigate infective components and comorbidities, including allergies, and consider further trials with topical and oral steroids. Additionally, a 3 month trial of macrolide therapy may also be prescribed. The use of macrolides in this manner is related to their anti-inflammatory properties and has been shown to have good efficacy.

A desensitisation injection regimen may be appropriate where a specific allergy has been identified on skin prick testing.

Surgery may be considered in specific cases if medical therapy fails.

Question 59

7. Unilateral nasal obstruction

Answer 59

A benign inflammatory polyp is the most common cause of persistent unilateral obstruction if anatomical deformities such as septal deflection are excluded.

A benign inflammatory polyp can appear as a uniform, slightly translucent swelling usually arising from beneath the middle turbinate. If large, a polyp may occlude the entire nasal passage and even present at the nares (nostrils).

Hypertrophy of the inferior turbinate may appear similar to a nasal polyp and be misinterpreted as such.

However, hypertrophied inferior turbinates appear more opaque, arise from the lateral wall and are very sensitive if touched by a probe. Further, application of a decongestant spray can reduce the turbinates to clarify their nature but will not alter the size of true nasal polyps.

However if history suggests unilateral symptoms, it is important to consider the possibility of an antrochoanal polyp, inverted papilloma, or other sinonasal inflammatory or neoplastic aetiologies.

The initial presentation of unilateral signs and symptoms should always prompt caution and consequently the next management step would
be to refer to a specialist to exclude sinister pathologies.

A specialist is likely to perform formal nasendoscopy to assess for sinister pathologies and identify the presence of further polyps on the contralateral side.

Question 60

7. Nasal polyposis special considerations

Answer 60

History that prompts special consideration.

• smoking and other atmospheric pollutants have been shown to affect nasal mucosa in vitro, however, population based data has not supported this
• asthma in coexistence with nasal polyposis, the literature presents evidence that control of nasal polyposis through surgical measures may have beneficial effects on pulmonary function
• aspirin** **sensitivity** is important when combined with **nasal polyposis and asthma.This symptom complex has been termedSamter triad. Patients with Samter triad are notoriously difficult to manage owing to their recalcitrant disease process despite medical and surgical therapy and may require frequent courses of oral steroids and nasal polypectomy procedures. Consequently, a multidisciplinary approach including a chest physician, ENT surgeon, endocrinologist and immunologist may be appropriate.

Question 61

7. Nasal discharge/obstruction/sinus pathology Red Flags

Answer 61

Red flag symptoms that are important to ask about include:

• unilateral nasal obstruction or discharge
• symptoms due to extension of pathology into the nearby orbit – these symptoms include epiphoria (watery eyes), particularly if it is unilateral, diplopia and reduced vision. Owing to the proximity of the orbit to the nose and paranasal sinuses, pathologies within the latter region may cause obstruction of the nasolacrimal duct resulting in tearing. Expansion may result in globe displacement with invasion, possibly causing ophthalmoplegia and/or visual loss. The coexistence of such findings would merit urgent specialist referral

symptoms which may indicate serious underlying pathologies. These include:

– blood in the saliva or in the nasal discharge. This could suggest neoplasm

– constitutional symptoms such as weight loss and anorexia could suggest neoplasm or an inflammatory disorder

– respiratory symptoms such as cough and shortness of breath or recurrent respiratory infections could suggest cystic fibrosis or Kartagener syndrome in the paediatric population.

Question 62

8. Otitis externa

Answer 62

An infection involving the skin of the external auditory canal.

In your initial history, it is important to ask about

• recent upper respiratory tract infections as this could guide your diagnosis toward otitis media rather than otitis externa.
• Also, ask about predisposing factors for otitis externa
  
  • including water exposure (eg. regular swimming),
  • trauma from cotton buds or fingernails,
  • known narrow ear canals and
  • past history of exostoses.
• Ask about symptoms of itchiness and skin scaling from the ear canals. This could suggest underlying skin conditions such as eczema, seborrhoeic dermatitis or psoriasis which may predispose to refractory otitis externa.

Question 63

8. Bacterial otitis externa.

Answer 63

The common bacteria involved are Pseudomonas aeruginosa and S. aureus.

Rx

• ear canal debridement (for discharging otitis externa). Thorough ear canal debridement (ear toileting). Referral to an ENT service is often required for this. Debridement is performed using a head light and fine suction
• If suction is not available, a dental brooch with a small piece of cotton wool wound around the tip can be used, under direct vision and with care. This procedure requires skill and training, as the ear is often exquisitely painful in otitis externa and trauma to the canal wall or tympanic membrane can occur with this technique.
• Ear toileting may need to be repeated after several days to ensure the drops are effective. It is important to debride sufficiently to visualise the tympanic membrane before coming to a definitive diagnosis of otitis externa. Otitis media with a discharging perforation may mimic otitis externa.
• ear drops
  
  • Bacterial otitis externa can be treated with either framycetin sulphate/gramicidin/dexamethasone ear drops or ciproxin hydrocortisone ear drops. Treatment is usually continued for 7–10 days. If there is concern about a perforated tympanic membrane, ciproxin drops should be used without the steroid component, which may cause stinging.
• An otowick is inserted if there is marked canal oedema. The wick helps to reduce oedema, delivering the topical antibiotic and steroid preparation deep in the canal.
  
  • It is normally removed after 48 hours and further ear toileting performed.
• oral analgesia
  
  • Moderately strong analgesia may be required for several days.
• Treatment of underlying skin conditions
  
  • such as eczema and psoriasis, should be treated

Oral antibiotics are not normally required unless there is associated perichondritis (in which case a course of oral ciprofloxacin is given), concurrent otitis media or systemic illness.

Microbiologic swabs are not normally necessary to direct treatment unless the patient is not responding to the above treatments or malignant otitis externa is suspected.

Question 64

8. Fungal Otitis externa

Answer 64

Commonly caused by

• Aspergillus or
• Candida albicans, though this results in different otoscopic findings.

Rx:

Fungal otitis externa may be treated with either

• flumethasone pivalate/cliquinol drops for 2 weeks or alternatively,
• the ear canal may be filled with otocomb ointment for 1 week, followed by flumethasone pivalate/cliquinol for 1 week.

Question 65

8. Otitis Externa- prevention

Answer 65

• should keep ears dry for 2 weeks after this infection has resolved.
• When showering should use cotton wool coated in petroleum jelly to prevent water entering his ears.
• If a swimmer, could consider custom made ear plugs for swimming and the use of an over-the-counter preparation containing alcohol and acetic acid after swimming.
• Use of cotton buds should be avoided.
• Any underlying skin conditions should be treated.

Question 66

8. Malignant Otitis Externa

Answer 66

A diagnosis that is important not to miss is malignant otitis externa (or skull base osteitis).

Malignant otitis externa is a potentially life threatening infection of the external ear and skull base. This most commonly presents in

• elderly patients,
• diabetic patients and the
• immunocompromised (eg. HIV-infected patients and postchemotherapy patients).

It usually presents with unrelenting otalgia over several weeks.

On examination there is ear discharge, with granulation tissue visible in the floor of the external ear canal. There may be facial nerve or other lower cranial nerve involvement.

Investigations include:

• CT scan of the temporal bones to document the extent of disease
• bone scan to document osteomyelitis
• gallium scan to document and track active disease.

Malignant otitis externa is treated with a prolonged course of intravenous and oral antibiotics in consultation with an infectious disease unit.

A high index of suspicion is needed for early diagnosis in high risk populations as the condition has a significant mortality.

Urgent referral is indicated.