Online learning module

Welcome to the asynchronous formal learning for Year 4 ORL/ENT teaching.

You have been allocated 4 hours to complete this online module. Some questions in your
exam will be sourced from this material.

The purpose of this online module is to give you a good overview of ORL conditions that
you are likely to encounter in your early clinical practice.

Otorhinolaryngology has four sub-specialties:

1. Head and Neck

2. Laryngology
3. Otology
4. Rhinology

On the left hand side you can navigate through the teaching materials under each of
these clinical topics.

Summary of objectives:
1. Spend a minimum of four hours learning from this module

2. Become comfortable with the principles in the basic sciences, diagnosis and
management of common ORL diseases

3. Enjoy the module!

Contents
Head and Neck – page 2

 Sore throat – page 2

 Deep neck space infection – page 7
 Neck lump - page 9

Rhinology – page 11

Laryngology – page 16

 Airway – page 16
 Voice – page 18
 Swallow – page 20

Otology – page 23

 Ear infections – page 23

 Cholesteatoma – page 27
 Hearing loss – page 29
 Vertigo and tinnitus – page 33

1
Head and Neck
Sore Throat
Differential diagnosis for a sore throat:

Tonsillitis

Peritonsillar abscess (Quinsy)

Supraglottitis / Epiglottitis

Deep neck space infections

-------

And the following that will be covered elsewhere in the curriculum:

Pharyngitis, common cold, foreign body, dental infections

Tonsillitis
Tonsillitis is inflammation of the pharyngeal tonsils. The inflammation usually extends to
the lingual tonsils and adenoids therefore pharyngotonsillitis and adenotonsillitis are
synonymous with tonsillitis

Aetiology

Most commonly viral - adenovirus, rhinovirus, RSV, EBV

15 - 30% are bacterial - mostly group A beta-hemolytic Streptococcus pyogenes

(GABHS).

Epidemiology

 Tonsillitis most often occurs in children; however, the condition rarely occurs in
children younger than 2 years.
 Tonsillitis caused by Streptococcus species typically occurs in children aged 5-15
years

History

 Fever
 Sore throat
 Halitosis (foul breath)
 Dysphagia (difficulty swallowing)
 Odynophagia (painful swallowing)
 Mild airway obstruction e.g. mouth breathing

2
Examination

1. Degree of respiratory distress

2. Full examination of oral cavity including the oral mucosa, dentition, salivary
ducts. In particular look for: tonsillar erythema, oedema +/- exudate (see pictures
above)
3. Tender cervical lymphadenopathy
4. Flexible nasoendoscopy - especially if severe to assess for degree of airway
obstruction

Possible complications of Streptococcal pharyngotonsillitis

Non-suppurative complications
Scarlet fever
Rheumatic fever
Post-streptococcal glomerulonephritis

Suppurative complications
Peritonsillar abscess (Quinsy)
Deep neck space infections
Cervical lymphadenitis

Management

1. ABC's

 Airway secured
 Fluid resuscitation

2. Antibiotics

 for acute inpatients - Penicillin IV 2MU Q6h

 for outpatients - Penicillin PO for 10 days

3. Steroids

 Reserved for inpatients - usually Dexamethasone either 8mg stat or 8mg TDS
for one day

4. Supportive therapy

 Anti-emetics
 Analgesia and antipyretics

3
EBV Tonsillitis

Consider infectious mononucleosis particularly when tonsillitis is accompanied by:

- tender lymph nodes

- splenomegaly
- severe lethargy
- white/gray membrane may cover tonsils that are infected with EBV (see image)

However, EBV diagnosis can only be confirmed via blood tests. The importance of this is
that EBV tonsillitis takes longer to resolve and patients should avoid contact sport

Peritonsillar Abscess (Quinsy)

Each tonsil is surrounded by a capsule. It is in the potential space (peritonsillar space)

between the tonsil and capsule that abscesses can form - a peritonsillar abscess, or in
layman's terms, quinsy

IMPORTANT: the peritonsillar space is contiguous with several deeper spaces and
infections can involve the parapharyngeal and retropharyngeal spaces (see deep neck
space infections)

Compare these pictures above with the pictures shown in the tonsillitis section. What are
the differences?

Note carefully the following:

 Uvula deviation to contralateral side

 Inferior and medial tonsil displacement
 Localised fluctuance (easier to appreciate when examining a patient than in
pictures)
 Swelling of supratonsillar fold/soft palate rather than tonsil itself

Aetiology

Tonsillitis can progress to cellulitis and then via tissue necrosis and pus formation to a
peritonsillar abscess
or starts via an infection of minor salivary glands

Microbiology:

 A polymicrobial flora is isolated from peritonsillar abscesses

 Predominant organisms are anaerobes
 Aerobic organisms present are commonly Strep, S aureus and H influenzae

Epidemiology

Peritonsillar abscess (PTA) usually occurs in teens or young adults but may present
earlier and occur in later adulthood

4
History

Symptoms are the same as for tonsillitis with a few other symptoms that are red flags
for PTA and deep neck space infections:

 Neck pain
 Throat pain, more severe on the affected side +/- referred ear pain
 Trismus (lock-jaw) - due to inflammation of chewing muscles
 Voice change - in PTA pharyngeal edema and trismus can cause a "hot-potato"
voice - as if the patient is struggling with a mouthful of hot food

Remember: nasty dental infections can mimic PTA therefore examine the oral cavity
carefully

Examination

As for tonsillitis.
Apart from the visual findings as noted above:

 Drooling
 Trismus
 More severe dehydration

Patients with quinsy should have a flexible nasoendoscopy/laryngoscopy performed to

rule out epiglottitis

Investigations for tonsillitis and PTA

General:
1. FBC, U+E (especially if dehydrated)
2. Monospot test/heterophile antibody test - to rule out infectious mononucleosis

With PTA or if you suspect deep neck space infections:

1. Lateral neck X-ray
If clinically concerned or X-ray suggestive then proceed to CT scan

Management

Always first think ABC's: In severe circumstances endotracheal intubation or a surgical

airway may be required.

The cornerstone of PTA treatment is: incision and drainage

In addition the treatment regime includes the same medication and considerations as for
tonsillitis.

Patients with PTA tend to be more toxic - therefore require more IV fluid resus (and
greater care)

5
Supraglottitis/Epiglottitis

Epiglottitis and supraglottitis are interchangeable terms meaning:

inflammation of structures above the insertion of the glottis in the oropharynx including
the epiglottis, vallecula, arytenoids and aryepiglottic folds (see picture below for
nasoendoscopic view of the larynx)

Aetiology

Haemophilus influenzae type b (Hib) used to be responsible for >90% of epiglottitis

cases
Due to vaccination the incidence has dropped markedly

Now other bacterial pathogens are responsible for the majority of cases including Strep,
Staph and a number of gram negative bacilli

A Danish study demonstrated an incidence of paediatric epiglottitis of 4.9 cases per

100,000 per year in the decade before Hib vaccination.

With the introduction of widespread Hib vaccination - 1996 to 2005 - an incidence of only
0.02 cases per 100,000 per year was seen. (1)

History

 Sore throat
 Odynophagia/dysphagia
 Muffled voice - "Hot potato voice"
 Adults may have had a preceding upper respiratory tract infection (URTI)

Always ask about vaccination if you suspect supraglottitis

Examination

 "Toxic" appearance of patient

 Sitting or leaning forward. Extreme = "Tripod position" - Sitting up on hands,
with the tongue out and the head forward
 Drooling/inability to handle secretions
 Irritability
 Stridor: A late finding indicating advanced airway obstruction

+ Muffled voice, cervical adenopathy, fever, respiratory distress, mild cough

Flexible laryngoscopy is required for diagnosis + assessment of airway (if patient will
tolerate it)

Remember: The progression of supraglottitis can be rapid (i.e. over hours!)

6
Investigation

1. Lateral Neck XR - may be useful (see image below)

Most adults are stable and may safely undergo imaging. When clarking patients with
possible epiglottitis, lateral neck XR can be a useful screening tool.

2. As mentioned above - judicious use of flexible nasoendoscopy

3. Blood cultures

This lateral neck X-ray demonstrates a classic radiographic finding in epiglottitis - the
"thumb sign"
- This is due to swelling of the epiglottis
- The swelling of the epiglottis on the X-ray is shown by the blue dotted line - the left
side is normal and the right has the abnormality

Management

1. Airway is the priority - ensure early ENT review. You should know where the surgical
airway (cricothyrotomy) kit is.
Unstable patients/severe respiratory distress may need immediate intubation or surgical
airway management.

If patient is stable they may still need monitoring in ICU.

Minimise distress - particularly important in paediatric patients.

2. Antibiotic - 1st choice is ceftriaxone

3. Supportive therapy
Analgesia, anti-emetics, IV fluid

Deep Neck Space Infections

The anatomy of the neck is complex. To understand the origin and spread of deep neck
space infections (DNSI) a basic understanding of the anatomy is required.

Summary of anatomical concepts:

 Spatial compartments in the neck are created by fascial planes

 These spatial compartments can communicate with each other -> spread of infection
 Anterior to the prevertebral fascia is the "danger space" that extends from the
skull base to the diaphragm - making mediastinitis a possible complication of
abscesses that spread into this space
 There are a number of important structures in this area including blood vessels,
nerves & bone that can become affected

Types of DNSI:
1. PTA/quinsy (see previous page)
2. Retropharyngeal
3. Parapharyngeal
4. Prevertebral
5. Submandibular (relatively superficial)

7
Challenge to diagnosis: DNSI may be covered by layers of unaffected tissues &
therefore is hard to visualise and palpate

Etiology

DNSI are most commonly complications of pharyngitis or dental infection

Other causes include: sialadenitis, IVDU, malignancy

Note: DNSI is often a complication of an inadequately treated pharyngitis, dental

abscess or tonsillitis

Important possible sequela of DNSI:

1. Internal jugular vein thrombophlebitis (Lemierre Syndrome) - causes septic emboli and sepsis
2. Mediastinitis - signalled by chest pain or widened mediastinum on CXR

Carotid artery rupture, meningitis and cavernous sinus thrombosis are rare.

History

 Sore throat, dysphagia, odynophagia, trismus

 Neck pain and pain on neck movement
 Can have painful neck mass

Examination

 Posterior pharynx erythema + swelling in retropharyngeal abscess

 Medial displacement of tonsil and lateral pharyngeal wall in parapharyngeal
abscess
 Torticollis (holds neck in rotated position)
 Tender lymphadenopathy

Findings suggesting complications:

- Neurological deficit - cranial nerves (eg. hoarseness from vocal cord paralysis with
carotid sheath and X/recurrent laryngeal nerve involvement)
- Horner syndrome from involvement of the cervical sympathetic chain

Investigations

1. Lateral neck X-rays +/- CT scan

2. FBC, U+E

3. Blood cultures

Management

1. ABC's As with PTA/Quinsy the airway is of paramount importance.

Followed by IV fluid resus for the "C"

2. Antibiotics

3. Surgery - incision and drainage

8
Neck Lump
The etiology of neck lumps are numerous and present a good opportunity to cover the
"surgical sieve".

The surgical sieve allows you to answer a "what are the causes of..." question (whether
on ward rounds or exams) in a systematic way. Using the VITAMIN CD acronym, for
neck lumps it can be constructed like this:

Vascular: AV malformation, aneurysm

Inflammatory:

Traumatic: Ranula, haematoma

Autoimmune/allergic: Thyroiditis

Metabolic: Goitre

Infective: Lymphadenitis, reactive lymphadenopathy

Neoplastic
Benign: Carotid body tumour/chemodectoma
Malignant: Squamous cell carcinoma, thyroid cancer, lymphoma, malignant
lymphadenopathy

Congenital: Branchial cleft cyst, thyroglossal duct cyst, dermoid cyst

Degenerative

-----------------------------------

Branchial cleft cyst

- These are congenital and present as an inflamed mass at the anterior border of the
sternocleidomastoid
- They occur due to the failure of branchial cleft obliteration during fetal development
- Like the thyroglossal duct cyst these remain asymptomatic until they become infected -
usually during an URTI

Goitre

- This is enlargement of the thyroid gland

- It may be diffuse or nodular and the patient may be euthyroid, hyper- and hypo-
thyroid
- The treatment varies with the type
Note: goitre is commonly more subtle than the one in this picture

9
Thyroglossal duct cyst
- They are congenital and are located in the midline of the anterior neck
- These cysts remain asymptomatic until they become infected - usually in the setting of
an URTI
- On examination they move with swallowing (like the thyroid) - but unlike the thyroid,
these cysts also move superiorly with protrusion of the tongue
- Treatment is with excision

History

Important points to cover when taking a neck lump history:

- Pain: chronic oral pain is suspicious of malignancy and referred unilateral otalgia
can be associated with tumours at the base of the tongue, larynx and hypopharynx (due
to CN IX and X innervating both the pharynx and the ear)

- Dysphagia: range of occasional "catching" to inability of swallowing solids. Tumours

generally cause gradual decline in ability to swallow food and weight loss. Nasal
regurgitation or aspiration suggests neurological cause.

- Stridor: inspiratory sounds - caused by airflow blockage at or above the vocal cords
i.e. is a symptom of upper respiratory obstruction.

- Hoarseness: suggests laryngeal disease - needs referral to ORL

- Constitutional symptoms: weight loss, night sweats, anorexia, chills/fevers - suggestive

of malignancy

- Social factors: smoking and alcohol - highly associated with head and neck cancers.

Examination

1. A thorough neck examination includes the thyroid, lymph nodes, parotid &
submandibular glands (including CN VII) - Note: the neck is examined from behind the
patient after initial inspection

Lumps should be assessed for:

Position
Size
Contour - smooth, craggy
Texture - soft, firm, hard or fluctuant
Mobility
Tenderness

2. Look for signs of hypo- or hyper- thyroidism

3. In Australia and New Zealand adults neck lumps are commonly metastatic SCC
therefore check the skin and oral cavity for a possible primary tumour

10
Investigations

1. Imaging: Ultrasound, CT or MRI

2. Cytology/histology: Fine needle aspiration (FNA) or biopsy

3. Blood tests
FBC - useful if haematological condition suspected
Thyroid function tests - useful in thyroid disease

Rhinology
Sinusitis
The terms rhinosinusitis and sinusitis are synonymous as inflammation of the sinuses is
always accompanied by inflammation of the nasal cavity

Acute and chronic rhinosinusitis are independent clinical entities with different underlying
pathophysiological mechanisms

Examination (this is identical for all types of sinusitis)

1. Anterior rhinoscopy - can be performed with otoscope

- look for mucopurulence, oedema, erythema and polyps
2. Flexible fibreoptic endoscopy

11
Acute Rhinosinusitis

Up to 4 weeks of purulent nasal discharge accompanied by nasal obstruction, facial pain,

facial pressure or fullness

Aetiology and History

Both viral and bacterial RS are preceded by an URTI

Viral:
Symptoms of acute rhinosinusitis are present less than 10 days
Symptoms do not worsen

Bacterial:
10 days+ beyond onset of URTI symptoms
Symptoms worsen within 10 days after initial improvement
Common bacteria that cause sinusitis are the same as for otitis media:

 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis

Purulent rhinorrhea, facial pain/pressure and nasal obstruction strongly suggest a

bacterial cause

Management

Antibiotics - amoxicillin + clavulanate for 7 days

Further investigation and surgery may be indicated for recurrent or persistent sinusitis
and complications

Chronic Rhinosinusitis

Aetiology

The pathophysiology of CRS is multifactorial and forms a large part of the research that
the University of Auckland ORL department performs
Factors include:

1. Immunology - intramucosal B and T cells

2. Microbiology - intramucosal S. aureus
3. Anatomy - sinus ostia obstruction (outlet of sinus)

12
History and Diagnosis

12 weeks or longer of 2+ of the following:

Mucopurulent discharge (anterior, posterior or both)
Nasal obstruction (congestion)
Facial pain/pressure/fullness
Decreased sense of smell

and inflammation as seen by:

Purulent mucus or oedema in the middle meatus or ethmoid region
Polyps
Imaging - CT

Management

1. Antibiotics
- ideally culture-directed; duration 3-4 weeks

2. Anti-inflammatory
- intranasal or oral steroids
- allergy management (if previous allergy known)

3. Mechanical
- nasal saline irrigation

4. Surgery - performed if symptoms remain despite maximal medical therapy for 4 - 6

weeks
- Functonal endoscopic sinus surgery (FESS)

Complications

Complications of sinusitis are rare in the antibiotic era

Orbital infection
This represents a progression of the infection"

1. Periorbital oedema
2. Orbital cellulitis
3. Subperiosteal abscess
4. Orbital abscess
5. Cavernous sinus thrombosis

Intracranial complications
Meningitis
Epidural abscess
Pott Puffy tumour (osteomyelitis of frontal bone with subperiosteal abscess)

13
Allergic Rhinosinusitis

This is one of the most common ENT diseases and a differential diagnosis for sinusitis

It is the inflammation of the nasal mucous membranes caused by an IgE-mediated

reaction to one or more allergens

History

Patients may be atopic and complain of:

- clear and watery nasal discharge

- itching of nose, eyes and throat
- nasal congestion

Seasonal symptoms may include exposure to pollen or cats

Management

Mainstay:
1. Antihistamines
2. Intranasal corticosteroids

Others:
3. Systemic corticosteroids - if intractable symptoms
4. Decongestants - be aware of rebound effects

Epistaxis

Epistaxis is bleeding from the nose

Aetiology

Bleeding occurs when the mucosa erodes and the vessels become exposed. Can be due
to the following:
- infections e.g. cold
- trauma e.g. nose picking, foreign body, inhalation of dry air (on an aeroplane for
example)
- medications e.g. anticoagulants, topical nasal meds, illicit drugs
- rare: systemic conditions e.g. coagulopathy, sarcoidosis, Wegener's granulomatosis +
tumours
but often idiopathic
>95% of bleeds are from Little's area (Kiesselbach's plexus) in the anterior septum
Very small number are posterior nose bleeds (NB these are more difficult to manage &
there is a larger chance of airway compromise)

Epidemiology
Very common - only small percentage of patients present for medical assessment

Epistaxis in children is often due to nose picking or URTI

14
History

- Did bleeding being unilaterally or bilaterally? -> anterior bleeds start unilaterally and
become bilateral whereas posterior bleeds are bilateral from the beginning

- Foreign body? -> very important to ascertain in young children

- General medical history -> particularly systemic conditions, medications

(anticoagulants!) and smoking

- History of easy bruising, prolonged bleeding or recurrent epistaxis -> consider systemic
conditions

- Family history of bleeding disorders

Examination

Before starting make sure you have all equipment prepared including cautery, packing
and topical meds

First you should spray local anaesthetic into both sides

If bleeding is obviously from one side - soak a small cotton ball with a mixture of
transexamic acid and local anaesthetic with adrenaline then examine 15 minutes later -
this will provide anaesthesia and may stop bleeding allowing better examination

Use the following:

- headlight: allows two free hands
- nasal speculum
- may need gentle suctioning of blood or clot to allow better view

Inspect both sides - if packing does not stop bleeding then a posterior bleed is possible
and flexible naso-endoscopy needs to be performed

Batteries can cause an alkali burn that can cause tissue necrosis

Investigations

1. FBC - to assess severity of haemorrhage via the Hb

2. Coagulation screen - especially if on warfarin
3. X-rays if FB suspected (paediatric population) - see below

15
Laryngology
Airway
Stridor

Stridor is a harsh noise produced by turbulent airflow through a partially obstructed

upper airway

It is commonly inspiratory indicating an obstruction at the larynx

Note: expiratory and biphasic stridor are rarer and imply obstruction at the level of the
trachea and subglottis

Stridor is a symptom more commonly encountered in children and therefore we will

focus on paediatric presentations of stridor

Aetiology

In a child the differential diagnosis is (using a surgical sieve):

Traumatic: Foreign body

Autoimmune/allergic: Anaphylaxis

Infective: Laryngotracheobronchitis (croup), tracheitis, supraglottitis/epiglottitis, DNSI

(see head and neck section)

Neoplastic
- Benign: respiratory papillomatosis/vocal fold papilloma, vocal fold cysts & nodules (see
hoarseness section)

Congenital: Laryngomalacia, laryngeal web, vocal cord paralysis, subglottic stenosis (can
be secondary to prolonged intubation)

Stridor should be treated as a medical emergency

In adults the following are the most common causes of stridor:

 Anaphylaxis
 Foreign body
 Trauma e.g. laryngeal fracture
 DNSI
 Malignancy: laryngeal or mediastinal
 Benign external compression e.g. goitre

Chronic stridor in an adult should raise concern and malignancy needs to be excluded

16
Laryngomalacia

 Stridor occurs as a result of prolapse of the supraglottic structures into the

laryngeal inlet on inspiration
 Most common cause of stridor in infants and most common congenital laryngeal
abnormality
 Majority of infants can be managed conservatively. ~10% require surgery

Picture of flexible nasolaryngoscopic examination of a patient with

laryngomalacia
- The epiglottis is omega-shaped and folded upon itself to that the lateral margins lie
close to one another
- The aryepiglottic folds are foreshortened and thin
- The arytenoids are large with redundant mucosa
- Mucosal oedema from vibratory trauma to the supraglottic area exacerbates the
symptoms

Laryngeal web

 Congenital condition that presents with an abnormal cry and stridor

 Arises from the failure of the recanalization of the larynx in the embryo
 Treatment is with incision for thinner webs; thicker webs may require stenting

Subglottic stenosis

 This is the partial or complete narrowing of the subglottic area - which is the
narrowest portion of the airway in children
 Congenital - present with stridor at birth or intermittent stridor if mild stenosis
e.g. only with URTI or
Acquired - commonly secondary to prolonged endotracheal intubation (~90% of
cases)
 Lateral neck X-ray can show stenosis
 Treatment is dictated by age of patient, grade and type of stenosis
Procedures range from observation for mild cases to laryngotracheal
reconstruction for severe cases

Tracheostomy

This is an operative technique that creates a surgical airway in the cervical trachea - it is
formed by anastomosing the proximal tracheal stump to the skin surface

Indications - can be elective or acute:

1. Relieve upper airway obstruction - e.g. congenital deformity, trauma, infection,
neoplasm
2. Prophylactically in head and neck surgery (temporary airway)

Laryngeal fracture

 Caused by trauma
 Symptoms: hoarseness, pain, crepitus, loss of normal midline neck landmarks
 Investigations: CT and fibreoptic laryngoscopy for diagnosis
 Management:
- If airway stable and minimal displacement then treatment is conservative with
antibiotics if mucosal tears present +/- steroids for the oedema
- If airway compromised or large amount of displacement then surgery is advised

17
Voice
Hoarseness or Voice Change

Voice change or dysphonia (including hoarseness) is a symptom of primary laryngeal

disease although rarely it can be due to other diseases e.g. lung cancer or
hypothyroidism

The function of the larynx is primarily phonation and airway protection

Aetiology

Every patient that presents with dysphonia needs to have malignancy excluded

The common causes of dysphonia are (remember the surgical sieve):

Trauma - phonotrauma - voice abuse & misuse leads to trauma of the vocal cords.
Repetitive phonotrauma leads to a local inflammatory response which can progress to
nodules and polyps

Neoplasm
Benign lesions: Vocal fold nodule, vocal fold polyp, vocal fold papilloma, laryngeal cysts
Malignant neoplasms: Laryngeal SCC (>90% of laryngeal cancer)

Multiple underlying pathological mechanisms: vocal cord paralysis or recurrent laryngeal

nerve paralysis

Recurrent respiratory papillomatosis

Bimodal distribution:
Juvenile onset - ages 2 to 4 due to infection with HPV during pregnancy or birth
Adult onset - ages 30 to 50 due to HPV infection in adulthood

Treatment is with CO2 laser resection or cold steel resection. Recurrence is very common

Vocal cord polyp

Associated with smoking and voice abuse

Treatment is excision to exclude malignancy and provide resolution

Vocal fold cyst

Formed by mucous glands that are found throughout the larynx

Treatment depends on location

18
Vocal fold nodule

Commonly affects professional voice user and are the most common cause of persistent dysphona in children
(they shout a lot)

Usually bilateral & mainstay of treatment is speech therapy

History

 The onset, duration and progression of any voice change

 Preceding upper respiratory tract infections, direct or vocal trauma and
endotracheal intubation
 Social factors: particularly smoking and alcohol
Occupation - professional voice users have higher rates of benign laryngeal
disease as they have higher rates of voice misuse and abuse - therefore a careful
history of voice use is needed
 Systemic enquiry should include symptoms of hypothyroidism and gastro-
oesophageal reflux disease (GORD)

Age is very important:

- Adults have a greater incidence of malignant disease
- In children the main differential diagnosis is vocal cord nodules and laryngeal
papillomatosis

Persistent and progressive dysphonia in a person with a smoking history is a red flag for
laryngeal malignancy - especially if associated with dysphagia or odynophagia

Examination

1. A full ear, nose and throat exam

2. A neck exam - particularly looking for lymphadenopathy

3. Flexible nasoendoscopy with particular focus on laryngoscopy

4. Video stroboscopy - allows visualisation of the mucosal wave and has an appearance
of a "slow motion" film. It is useful in diagnosis, monitoring rehabilitation and speech
therapy

19
Treatment of Laryngeal Cancer

Treatment strategy depends on histology type, grade, tumour stage and overall health of
the patient

Like most major cancers, this requires an MDT approach involving:

 Surgeon
 Speech language therapist
 Specialist nurses e.g. tracheostomy nurse
 Dietician
 Radiologist
 Radiation oncologist
 Medical oncologist
 Pathologist

The mainstay of treatment involves:

1. Surgery - partial or total laryngectomy (the latter requiring a tracheostomy)

+/- reconstruction using surgical flaps
2. Radiotherapy - primary or adjuvant
3. Chemotherapy in some cases

Swallow
Dysphagia is difficulty eating due to disruption of the swallowing process

Differential diagnosis:

Vascular - Stroke
Inflammatory - GORD
Trauma
Autoimmune/allergy - Eosinophilic oesophagitis, scleroderma
Metabolic
Infective
Neoplastic - Barret's oesophagus, oesopheageal cancer, brainstem tumours
Congenital
Degenerative - Achalasia, Zenker diverticulum

Chronic Cough
Cough that lasts more than 8 weeks

Aetiology

3 conditions account for ~95% of chronic cough:

1. Postnasal drip syndrome/upper airway cough syndrome (UACS)

2. Asthma
3. GORD

20
Be aware that a number of other conditions make up the remainder e.g. ACE inhibitor
therapy, smoking, CHF, non-asthmatic eosinophilic bronchitis etc.

UACS - most common cause - secretions containing inflammatory mediators stimulate

pharyngeal and laryngeal sites -> cough

GORD - either via:

1. Distal oesophageal acid exposure that stimulates an oesophageal-tracheobronchial
cough reflex via CN X
2. Microaspiration of acid to the larynx/trachea (laryngopharyngeal reflux) this is most
often silent i.e. patients do not get heartburn

Investigation and Management

For this presentation history has very little yield for diagnosis

UACS
Treat any underlying sinusitis, avoid allergens
Hallmark of this syndrome is the lack of pathognomonic findings - diagnosis made by
response to:
1. Antihistamines
2. Decongestants
NB: response may take weeks to months

Non-asthmatic eosinophilic bronchitis

Diagnosis made by induced sputum showing increased eosinophils
Highly responsive to inhaled corticosteroids

GORD
Treated with PPI

Therefore investigation should proceed with:

1. Stop smoking and other factors e.g. ACE inhibitor therapy (response may take
one month)
2. Chest XR - to rule out pulmonary lesions
3. Trial of UACS treatment
4. Induced sputum
5. 24 hour pH monitoring
6. If the above show no yield then more extensive investigation required: sputum
for TB, HRCT, bronchoscopy

21
Globus

Globus is a persistent or intermittent painless sensation of a lump or foreign body in the

throat

Aetiology

1. GORD - accounts for ~25 to 50% of patients

.
2. Non-specific oesophageal motility disorder
.
3. Malignancy
.
4. Psychological/stress
.
5. Others: retroverted epiglottis, thyroid disease, TMJ dysfunction etc

Investigation and Management

Like with chronic cough, the history is low yield but should be used to evaluate for
malignancy, reflux & psychological factors

1. Full ENT exam including laryngoscopy - to exclude malignancy + other causes

2. 3 month trial of PPI therapy (e.g. omeprazole)
3. If unresponsive to PPI then further Ix: 24 hour pH monitoring, endoscopy and
barium swallow
4. If above negative consider: psychiatry input

If suspicious findings on history, exam or laryngoscopy then more aggressive

investigation is needed

Pharyngoesophageal diverticulum
The herniation of the posterior pharyngeal/oesophageal mucosa and submucosa due to
increased intraluminal pressure. Either due to lack of coordination of musculature or a
hypertensive upper oesophageal sphincter

History
Dysphagia
Regurgitation of undigested food from the pouch - with risk of aspiration
Halitosis

Investigation

Barium swallow
Fibreoptic endoscopic evaluation of swallow
+/- pH monitoring to assess for associated GORD

Management

The management of this condition is increasingly being handled by

otorhinolaryngologists (c.f. general surgeons previously)

Transoral endoscopic treatment with CO2 laser or electrocautery is becoming standard

22
Otology
Ear infections
Types of ear infections:

 Otitis externa
 Acute otitis media (AOM)
 Otitis media with effusion (OME) or glue ear

A large study performed in South Auckland found that over 25% of Pacific Island
children have OME (2)
NZ Maori and Pacific Island children suffer from a high burden of OME

Otitis externa

Otitis externa is an inflammatory and infectious process of the external auditory canal
(EAC) +/- auricle

Predisposing factors include:

 Heat
 Humiditiy
 Trauma (e.g. cotton bud)
 Exposure to water (e.g. swimming)
-> swimmers are particularly prone to it because repetitive swimming results in
removal of cerumen & drying up of the EAC

Aetiology

Most common pathogens: Pseudomonas aeruginosa, S. aureus

Less commonly: S. epidermidis, Proteus spp., E. coli, diphteroids

History

 Otalgia (ear pain)

 Otorrhoea (ear discharge)
 Aural fullness
 Pruritis (itchiness)
 Tenderness
 Hearing loss (due to oedema and debris obstructing EAC)
 If advanced there may be oedema and erythema of the auricle/pinna

23
Examination

Using an otoscope: EAC erythema, oedema + otorrhoea

+/- Pain on distraction of the pinna
+/- Advanced: periauricular and cervical lymphadenopathy

Management

1. Antibiotic drops - Sofradex (framycetin sulphate/gramicidin/dexamethasone) or

Ciproxin (ciprofloxacin)

2. Earwick insertion to stent open the EAC if there is occlusion (occlusion shown in right-
most picture above)
- this is important in order to allow the antibiotic to reach the infected tissues

3. Aural suctioning (atraumatic debridement) with the use of a microscope - if

experienced enough

4. Analgesia

5. If exostoses (surfer's ear) present: may need surgical management to stop recurrence
of otitis externa

Note: the steroid component in the ear drops helps with decreasing ear canal oedema

Acute otitis media

AOM is the inflammation and infection of the middle ear

Aetiology

Normal function of the pharyngotympanic tube (PT tube) is:

1. Middle ear aeration to allow pressure equilibration between the atmosphere and
the middle ear
2. Mucociliary clearance of the middle ear space
3. While doing above it prevents aspiration from nasopharynx to the middle ear

Underlying pathogenesis is pharyngotympanic (Eustachian) tube dysfunction - leading to

pathogens passing from the nasopharynx into the middle ear

AOM is usually preceded by a viral URTI - causes PT tube inflammation & therefore
dysfunction
The most common pathogens are:

 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis


Epidemiology

24
Peak incidence is is in children aged 3 to 18 months with incidence tapering as a child
approaches adolescence

History

 Otalgia
 Fever
 Hearing loss
 Otorrhoea (if ear drum perforation)
 Can have decreased appetite and a concurrent URTI

Note: AOM in children can present with fussiness and irritability and therefore an
otoscopic examination should be part of a general paediatric assessment

Examination

On otoscopy a bulging tympanic membrane (TM) with erythema can be seen

Management

1. Reassurance with analgesia and watchful waiting is appropriate for the majority of
children as 80% will have spontaneous resolution within 2 to 14 days. In certain cases
antibiotics are appropriate 1st line treatment e.g. severe illness, <6 months of age and
not improved within 48 hours of watchful waiting

2. Oral antibiotics:
1st line: Amoxicillin
2nd line: Erythromycin or co-trimoxazole

In paediatrics:
Drug doses are often given in ranges (e.g. 50 - 100 mg/kg/dose) - always give
maximum dosage for their weight
Underdosing, by using lower end of range dosing, is one of the primary causes of failure
of treatment

3. Analgesia:
Paracetamol is 1st line
Ibuprofen if no contraindications

Otitis media with effusion

Aetiology

 Like AOM the pathogenesis includes PT tube dysfunction

 Usually follows AOM

A number of hypotheses exist to explain the above findings but the following two are
most often quoted:
1. PT tube dysfunction leads to loss of pressure equilibration of the middle ear with the
astmosphere

25
- nitrogen is absorbed by the middle ear mucosa leading to the middle ear having a
relatively negative pressure
- this elicits a transudate secretion by the middle ear mucosa and increased passage of
pathogens into the middle ear
- this leads to chronic inflammation and effusion

2. The initial trigger is inflammation of the middle ear (via AOM and/or ongoing reflux
from the nasopharynx into the middle ear via PT tube dysfunction)
- the inflammation induces a mucin-rich transudate

In both of these hypotheses the transudate also acts as a further culture medium for
bacteria

The following risk factors are thought to worsen PT tube dysfunction:

 Parental smoking
 Absence of breast feeding
 Adenoid hypertrophy
 Day care attendance (increased exposure to pathogens)

Epidemiology

Most common in children up to the age of 15

Prevalence much higher in Maori and Pacific Island children compared to European (see
blue box above)

History

 Often asymptomatic
 Commonest complaint = decreased hearing (usually noticed by parent)
 Recent AOM or URTI common
 Parents notice poor sleep in child (likely due to sensation of pressure)

Examination

Otoscopy (include pneumatic otoscopy):

Dull grey or yellowish immobile TM
If the TM is clear air-fluid levels can occasionally be seen

In adults flexible nasoendoscopy should be performed to exclude a nasopharyngeal

tumour

Investigation

Tympanometry - allows testing of TM mobility and middle ear function (abnormal in

OME)

Audiology - conductive hearing loss in OME

Management

Firstly patients are categorised into two groups:

26
1. High risk group: children at risk for speech, language or learning problems
This includes suspected hearing loss, language delay, autism, developmental delay or
uncorrectable visual impairment

2. Low risk group: children with no suspicion of above problems

The low risk group can be managed via "watchful waiting":

- Review 3 months after diagnosis. If still has OME -> audiology testing
- If hearing normal review again in 3 months time -> if OME persists (i.e. 6 months)
needs ORL review
- A 10 day course of oral amoxicillin can be trialled but evidence base is small

The high risk group needs ORL review

ORL review
The surgeon will consider placement of tympanostomy tubes (grommets) - see pictures
below
Adenoidectomy will be considered in children with repeat need for grommets

Cholesteatoma
A destructive lesion of the skull base and middle ear formed by trapped
squamous epithelium

Aetiology

The trapped squamous epithelium forms a sac with keratin debris

Chronic inflammation and infection ensue leading to:
- growth and migration of the squamous epithelium
- osteoclastic activity
- causes PT tube dysfunction and oedema; providing a culture medium for bacteria

Can be congenital or acquired

- secondary to retraction of TM (primary acquired)
- squamous epithelium migration during surgery e.g. grommet placement (secondary
acquired)

History

 persistent or recurrent purulent otorrhoea

 hearing loss
 tinnitus
 rarely: vertigo, ataxia, facial nerve paresis (from invasion)

Hallmark symptom is painless otorrhoea

27
Examination

If due to retractions (primary acquired):

 retraction of parts of the TM

 purulent otorrhoea, polyps and granulation tissue
 ossicular erosion

If due to TM perforation (secondary acquired):

 debris visible through the perforation

If perforation has healed or occured secondary to surgery (also secondary acquired)

 TM can appear normal

 once cholesteatoma is large - it may be able to be seen through the TM

Cranial nerve function especially facial nerve should be checked in all patients

Investigations

CT scan
Audiometry
MRI if facial nerve, labyrinth or intracranial involvement suspected

Management

The mainstay of treatment is surgical - mastoidectomy and the extent of the operation
will depend on the location of the cholesteatoma

Medical adjunctive therapy:

 microscopic removal of debris from EAC

 keep all water out of ears - prevent contamination
 topical antibiotics

Complications

 bone erosion - including ossicular chain

 sensorineural hearing loss, dizziness
 facial nerve injury
 infection including: mastoiditis, intracranial abscess, sigmoid sinus thrombosis,
meningitis

Hearing Loss
28
Aetiology

Hearing loss can be divided into two types:

Conductive hearing loss (CHL) - anything that decreases the transmission of sound to
the cochlea

1. cerumen impaction
2. middle ear effusion including OME
3. otosclerosis
4. cholesteatoma

Sensorineural hearing loss (SNHL) -anything that stops transmission from the cochlea
onwards

1. congenital
- syndromic e.g. Usher syndrome
- non-syndromic - 80% is autosomal recessive
2. perinatal causes e.g. low birth weight or sepsis
3. infections
- prenatal e.g. CMV, rubella, toxoplasmosis, varicella
- postnatal e.g. OM, mumps, meningitis or HIV
4. trauma
5. ototoxic drugs e.g. aminoglycoside
6. presbycusis/age-associated
7. neoplasms - acoustic neuroma, cerebellopontine angle tumours

History

- include: duration, nature of onset, progression and which side(s) affected

- presence or absence of: tinnitus, vertigo, imbalance, otorrhoea, headache, facial

nerve dysfunction

- and: head trauma, ototoxic exposure, occupational or recreational noise exposure

and a family history of hearing impairment

Examination

- Otoscopy - assess TM for retraction & with insufflation for TM mobility +

compliance

- Nose, nasopharynx and oral exam +/- flexible nasoendoscopy to assess for
neoplasm

- Cranial nerve examination with special focus on V, VII and VIII

- Rinne and Weber tuning fork tests

Investigations

29
 1. Audiometry

2. Imaging

- CT if conductive (look for ossicular and other bone abnormality)

- MRI if asymmetric or unilateral SNHL (look for neural lesions)

Management

1. Environment
- reduce back ground noise
- ensure good lighting on speaker's face etc.

2. Amplification
- hearing aids
- bone anchored hearing aid (BAHA)

3. Cochlear implants

Otosclerosis

Otosclerosis is a disease of the temporal bone - nearly exclusively of the otic capsule. It
is characterised by abnormal removal of mature bone and replacement with thicker
woven bone

This disease process has a predilection for the bone of the oval window and stapes
footplate

In 80 - 90% of patients the disease is limited to the oval window and stapes footplate

Aetiology

Normal bone turnover that happens in other bones of the body does not occur in the
healthy otic capsule after initial development
In otosclerosis increased osteo-clastic and -blastic activity leads to fixation of the stapes
(causing CHL) and rarely extend into the inner ear (causing SNHL)

Thought to be due to genetic and environmental factors:

- often there is a family history (autosomal dominant with incomplete penetrance)
- associated with Measles virus (? activates responsible gene)
- fluoridation of water thought to be contributing to decreased incidence now

Epidemiology

~10% Caucasian population affected (clinical disease only ~0.5%)

Asians and Africans have much lower rate

History

30
  Slowly progressive hearing loss - usually bilateral and asymmetric (~30%
unilateral)
 Tinnitus common
 Usually present between the age of 20 and 35

Examination

1. Otoscopy - usually normal but done to help exclude other causes of CHL e.g.
cholesteatoma, OME etc
2. Rinne and Weber tests - CHL findings

Sometimes patients will talk quietly as they perceive their voices to be loud due bone
conduction

Investigations

Given normal examination findings, investigations are important

1. Imaging - CT diagnostic
2. Audiometry - demonstrates CHL
3. Tympanometry - middle ear not affected therefore normal in early and mid stages.
Abnormal once stapes fixation severe

Management

Management strategy depends on severity of disease and symptoms

Options are:

1. Observation with yearly follow up

2. Medication - occasionally sodium fluoride and bisphosphonates
3. Hearing aid
4. Surgery - stapedectomy (total or partial) with prosthesis placement

Presbycusis

Presbycusis is otherwise unexplained SNHL in the elderly - usually bilateral &

symmetrical

Aetiology

1. Genetic predisposition
2. Noise trauma
3. Diet, nutrition, ototoxin exposure
4. Multifactorial age-associated changes:
- Central pathology: decreased cell population in auditory cortex with increased
synaptic and information processing time
- Cochlear pathology: loss of hair cells and supporting cells
- CNVIII fibre loss

History

31
Progressive hearing loss - particularly worse with ambient noise

Ask about:
- occupation especially military, industry (high noise jobs)
- family history

Examination usually normal but performed to exclude other diagnoses

Investigations

Audiometry is diagnostic
Consider other tests e.g. imaging if suspect other diagnosis (e.g. unilateral hearing loss)

Management

Options:

1. Hearing aid
2. Assistive devices e.g. telephone amplifier, headsets for TV
3. Cochlear implant (reserved for profound hearing loss)

Investigations

Audiometry

Pure-tone audiometry is the most common test of hearing

The patient is asked to respond to sounds of decreasing intensity across the frequency
range
Both air conduction and bone conduction can be tested

Tympanometry

A tympanometer presents a low frequency sound to the ear and measures the sound
energy reflected from the eardrum

The eardrum is most floppy when the pressure on both sides of it is equal. If fluid is
present in the middle ear, the eardrum is unresponsive to changes in pressure of the
external ear canal and a flat tracing is observed

Tympanometry does not depend on major patient co-operation, so the test is quite
useful in testing children for "glue ear" (otitis media with effusion)

Vertigo and Tinnitus

32
Tinnitus is the perception of sound in the head or the ears.

Vertigo is defined as perception of movement in the absence of movement. It is caused

by asymmetry in the baseline input into the vetibular centres, which causes the vertigo
but also nystagmus and vomiting.

It is very important to differentiate this symptom from other symptoms that patients
may complain of Typically patients will describe "dizzines", "light-headedness" etc. These
are not specific and must be explored further by the doctor and differentiated into:
- pre-syncope
- syncope
- vertigo
- weakness
- unsteadiness or imbalance

Differential Diagnosis

Central

1. Ischaemia: TIA, stroke, vertebrobasilar insufficiency + migraine

2. Neoplastic: Acoustic neuroma (usually presents with unilateral progressive
hearing loss)
3. MS

Peripheral (the first 4 diagnoses are in order of incidence)

1. Benign paroxysmal positional vertigo (BPPV)

2. Meniere disease
3. Vestibular neuronitis
4. Labyrinthitis
5. Others: otitis media, sinusitis

Note: vertigo that doesn't start to improve within 48 hours may indicate a central cause

History

- As above, ensure you understand exactly which symptomatic entity the patient is
describing i.e. is the patient truly describing vertigo?
- Timing: how long does it last?
- Onset: is it sudden?
- Vertigo association: do certain postures bring it about?
- Presence of tinnitus, hearing loss, otalgia, otorrhoea, aural fullness
- Preceding URTI
- Smoking and other medications or herbal remedies

- Review of systems:
- associated gait problems or ataxia (suggest a neurological cause)
- head trauma
- other medical problems
- other ENT diseases

Examination

33
- Vital signs including orthostatic BP
- Full ENT exam (particularly for signs of infection, hearing loss etc.)
- Thorough neurological exam is mandatory with specific focus on cranial nerves, gait
and cerebellar function

Special tests:
- Dix Hallpike test
- Romberg and tandem gait
- Head thrust
- Caloric testing

Investigations

A range of specialist vestibular reflex testing exist

Imaging with MRI is indicated where there is asymmetric hearing loss an (acoustic
neuroma may be suspected)

Baseline bloods should be performed e.g. FBC, U+E, Glucose

BPPV

Aetiology

BPPV is defined as vertigo that is elicted by certain head positions. The positions trigger
nystagmus.
The cause of this is unknown but is postulated to be due to 2 pathological mechanisms:

1. Canalithiasis: This is due to otoliths that have become detached from the otolithic
organs and are free-floating; exerting a force on the cupula mechanism within the
semicircular canals
(analogy is: pebbles in a tyre - when the tyre turns the pebbles tumble down due to
gravity; this tumbling triggers the nerves inappropriately)

2. Cupulolithiasis: This is due to deposits of otoliths on the cupula themselves; rendering

the cupula more sensitive to gravitational force with certain head positions
(analogy is: heavy object placed on a skinny pole; extra weight makes pole unstable and
harder to keep in upright position - pole easily clunks from one side to another and tends
to keep tilted position)

History

Onset of vertigo is sudden and severe - lasting ~30 seconds

Typically occur when moving the head in certain positions e.g. from lying to sitting
May be associated with nausea and vomiting

Examination

Diagnosis is made by Dix-Hallpike test

Remainder of examination should be normal

34
Management

1. Canalith repositioning via Modified Epley Maneuver

2. In the acute setting vestibulosuppresants can be tried for symptomatic relief:

- Promethazine
- Benzodiazepines e.g. lorazepam
- Scopolamine

Surgery reserved for severe intractable cases

Meniere Disease

Aetiology

Also known as endolymphatic hydrops (hydrops is another term for oedema)

The cause is thought to be due to impaired reabsorption of the endolymphatic fluid

The precipitent factors is still unknown but postulated to be infectious, immunologic or
allergic

History

Meniere disease occurs as attacks lasting for hours. The four symptoms are:

1. Unilateral fluctuating SNHL

2. Vertigo lasting minutes to hours
3. Constant or intermittent tinnitus - typically increasing in intensity during vertiginous
attack
4. Aural fullness

The attack is associated with nausea and vomiting - followed by feeling lethargic for a
few days

Investigation

Meniere disease is a clinical diagnosis - based on history and normal examination

Audiometry is used to confirm SNHL

The following are performed to help rule out differential diagnoses:

- Syphilis as this can perfectly mimic Meniere disease
- As noted before if hearing loss is asymmetric then MRI needs to be performed

35
Management

Acutely:
1. Vestibular suppresants - promethazine, benzodiazepines, scopolamine
2. Betahistine

Long term suppression

1. Dietary restriction of salt
2. Thiazide diuretic
3. Betahistine
4. Aminoglycoside injection into middle ear
5. Surgery reserved for severe and intractable cases

Vestibular neuronitis

Aetiology

This is an acute, sustained dysfunction of the peripheral vestibular system causing

vertigo, nausea and vomiting

The most likely cause is reactivation of HSV in the vestibular ganglion and nerve - other
viruses e.g. adenovirus are also potential pathogens (note: do not confuse this with
Herpes Zoster Oticus - which is a Varicella Zoster virus mediated disease)

Epidemiology

Commonly in 4th to 6th decades

History

Commonly have preceding URTI

Sudden and acute vertigo, nausea and vomiting without hearing loss
Lasts for days -> cannot work or do usual activities

Examination

Should have normal hearing and neurological exam (otherwise suspect something more
sinister)

Nystagmus will be present with slow phase towards injured ear

Management

1. Vestibular suppressants
2. Corticosteroids for 3 weeks (decreases chances of long term vestibular function loss)

36
Labyrinthitis

Aetiology

This is inflammation of the labyrinthine structures including the vestibular and cochlear
components

This may be caused by viral or bacterial pathogens

Viral
Rubella and CMV - can cause prenatal SNHL
Mumps and measles - can cause postnatal SNHL
Other viruses e.g. adenovirus, parainfluenza virus etc.
VZV can cause a special kind of labyrinthitis - Herpes Zoster Oticus - and if the facial
nerve is involved it is called Ramsay Hunt Syndrome

Bacterial
Occurs secondary to otitis media or meningitis

Rarely, labyrinthitis can also be autoimmune

History

The key difference between labyrinthitis and vestibular neuronitis is that you get SNHL in
labyrinthitis

Viral
Sudden loss of unilateral loss of vestibular function and hearing
Bedridden for days to weeks - some unsteadiness can last for months
Preceding URTI common

In HZV oticus Sx are deep, burning auricular pain followed by eruption of vesicular rash
in EAC and concha

Bacterial
Can have symptoms of AOM, meningitis and cholesteatoma in addition to the above

Examination

A full examination as outlined in the "Overview" bar

In addition consider looking for signs of meningitis

Investigation

Baseline blood tests

Audiometry
Consider CSF in suspected meningitis

37
Management

Viral
As per vestibular neuronitis

Bacterial
IV antibiotics

If OM -> myringotomy with effusion evacuation

Mastoiditis and cholesteatoma will need surgery
Neurosurgery if intracranial abscess

References
1. Guldfred LA, Lyhne D, Becker BC. Acute epiglottitis: epidemiology, clinical
presentation, management and outcome. J Laryngol Otol. 2008;122(8):818-23

2. Paterson JE, Carter S, Wallace J, Ahmad Z, Garrett N, Silva PA. Pacific Islands families
study: The prevalence of chronic middle ear disease in 2-year-old Pacific children living
in New Zealand. International Journal of Pediatric Otorhinolaryngology. 2006:10;771-8

The globus section was helped greatly by:

Lee BE, Kim GH. Globus pharyngeus: a review of its etiology, diagnosis and treatment.
World J Gastroenterol. 2012. 18(20): 2462-71

Bibliography

Lalwani, AK. Current Diagnosis & Treatment in Otolaryngology - Head and Neck Surgery.
3rd Ed. 2012. McGraw Hill Medical

Please see the online version for full copyright/references list

38