Ear Nose and Throat - The Offici - SFO UK - Compressed

Students and Foundation Trainees in Otolaryngology (SFO UK)
SFO UK
ENT UK t/a BACO & BAO-HNS
Royal College of Surgeons
35-43 Lincoln's Inn Field
London
WC2A 3PE
+442074058371
support@entuk.org
Ear, Nose and Throat: The Official Handbook for Medical

Students and Junior Doctors
By the Students and Foundation Doctors in Otolaryngology (SFO

UK)
Part of ENT UK
Authors and Editors
Alexander Yao
Michaella Cameron
Charlotte McIntyre
John Allen
Mamoona Khalid-Raja
Jayesh Doshi
Andrew Robson
Dheeraj Karamchandani
Roland Hettige
Eamon Shamil
Irfan Syed
Nimesh Patel
Contents
Introduction
Preface
Foreword
A Career in Ear, Nose and Throat Surgery
Further Information
Generic Skills in ENT

General ENT History
Ear Examination
Nasal Examination
Neck and thyroid status exam
Cranial Nerve Examination
Otology
Ear Anatomy
Dizziness and Vertigo
Hearing Loss
Tinnitus
Facial Nerve Palsy
Otalgia
Otorrhoea
Otitis Externa
Acute Otitis Media
Otitis Media with Effusion
Chronic Otitis Media
Cholesteatoma
Rhinology
Nasal Function and Anatomy
Epistaxis
Nasal obstruction
Fractured Nose
Septoplasty/Septorhinoplasty
Rhinitis and Rhinosinusitis
Allergic Rhinitis
Non-Allergic Rhinitis
Acute Rhinosinusitis
Chronic Rhinosinusitis
Nasal Polyps
Other Sinonasal Lesions
Cleft Lip and Palate
Head and Neck

Head and Neck Anatomy
Facial Muscles
Blood Supply to the Face and Neck
The Major Salivary Glands
Oral Cavity
Topography of the Neck
Fascial Layers of the Neck
Nervous Supply of the Head and Neck
Physiology of Swallowing
Taking History of a Neck Lump
Causes of Neck Lump
Branchial Cysts
Dysphagia
Dysphonia
Tonsillitis
Pharyngeal Pouch
Globus Pharyngeus
Thyroid Masses
Thyroglossal cyst or sinus
Multinodular goitre
Thyroid cancer
Benign and Malignant Neoplasms of the Salivary Glands
Carcinoma of the Oral Cavity
Carcinoma of the Pharynx
Carcinoma of the Nasopharynx
Carcinoma of the Oropharynx
Carcinoma of the Hypopharynx
Carcinoma of the Larynx
Laryngopharygeal reflux
Snoring and Obstructive Sleep Apnoea
ENT Emergencies
Acute Airways Obstruction
Epistaxis (Nose Bleed)
Foreign body in the nose
Nasal septum haematoma
Foreign body in the ear
Perforated tympanic membrane
FB in the pharynx or oesophagus
Deep neck space infections
Penetrating neck trauma
Medications in ENT
Antibiotics
Steroids
Antihistamines
Vestibular sedatives & Meniere’s disease
Practical Procedures in ENT

Nasal Cautery
Anterior Nasal Packing
Nasendoscopy
Oto-Microscopy and Foreign Body Removal
ENT Investigations
Pure Tone Audiometry
Audiogram Case Study 1
Tympanometry
Hearing Tests In Children
ENT Operations
Grommet Insertion
Middle ear and Mastoid surgery
Tonsillectomy
Adenoidectomy
Functional Endoscopic Sinus Surgery
Parotidectomy
Thyroidectomy
Neck Dissection
Tracheostomy
Introduction
Preface
ENT makes up a significant part of the clinical practice of general
practitioners, paediatricians and emergency doctors although
exposure to the specialty is often limited during undergraduate
training.
This “E-book” has been written to provide a practical guide to the

day-to-day management of common ENT conditions and will be
helpful to medical students and junior doctors as well as other
clinicians that have exposure to ENT as part of their practice. It has
been developed by the Students and Foundation Doctors in
Otolaryngology group (SFO UK), which is part of ENTUK. The group
aims to provide support for undergraduates in medicine and junior
doctors with an interest in ENT. The content is based on a Delphi
study that set out what the most important topics should be in an
undergraduate ENT curriculum taking in to consideration guidance
published in Tomorrow’s Doctors by the General Medical Council
guidance.
Congratulations to the authors and to my colleagues on the SFO UK

committee for delivering an excellent and novel educational
resource. A number of individuals have been instrumental in
producing this E-book from conception to production.
These include Alex Yao, Michaella Cameron, Charlotte McIntyre,
John Lee Allen and Mamoona Khalid-Raja. I also wish to particularly
thank the section editors Andrew Robson, Dheeraj Karamchandani,
Roland Hettige, Eamon Shamil, Nimesh Patel & Irfan Syed as well
as James Tysome & Victoria Ward (Elf-ENT) for allowing us to use
many of their images.
Mr Jayesh Doshi
PhD FRCS (ORL-HNS) MMed
Consultant Otolaryngologist
Chairman of SFO UK committee (2018)
Foreword
Ear, Nose, and Throat (ENT), or otorhinolaryngology, is an important,
interesting and diverse specialty. It covers a wide range of areas
from the common, such as tonsillitis, to the highly specialised,
including cochlea implantation, congenital airway disease, voice
disorders, skull base and facial plastic surgery.
Whether you become a GP or an A&E doctor, you will encounter

ENT pathologies in abundance, some of which can be life
threatening. Yet, students have limited exposure to the specialty
within most undergraduate curricula.
This book complements the national ENT curriculum written by

ENTUK. Although not designed to be a comprehensive text, this
book aims to provide you with the most important topics that you
should know by the time you finish medical school and qualify as a
foundation doctor. The book will also prove useful for foundation
doctors wishing to refresh and review their ENT knowledge.
Topics are presented systematically in an easy-to-read format

suitable for short attachments. Students may also find it useful to use
as reference material chapters explaining common medicines,
investigations, procedures, and operations specific to ENT.
ENT is a very hands-on specialty and ENT doctors are generally

very approachable! So make the most of every opportunity to exude
enthusiasm, watch and participate during your attachment!
Professor Anthony Narula

Consultant Otolaryngologist
MA MB BChir FRCS FRCS (Ed)
President of ENTUK (2016)
A Career in Ear, Nose and Throat
Surgery
Ear Nose and Throat (ENT) surgery or Otorhinolaryngology offers an
exciting and varied surgical career option. It has been described as a
‘cradle to grave’ specialty with a caseload ranging from a baby with
hearing loss, teenager with allergic rhinitis to an elderly man with
throat cancer. As there is no separate medical companion, ENT
surgeons also manage the non-surgical care of their patients.
Furthermore, once at registrar level, on calls can be done from
home, which can be considered as particularly attractive.
Subspecialties
Head and Neck Surgery
Otology
Skull Base Surgery/Neuro-Otology
Thyroid and Parathyroid Surgery
Rhinology
Facial Plastic Surgery
Paediatrics
Laryngology
Typical working week

4 clinics a week
2 surgical sessions a week
Light emergency work
Multidisciplinary work with other specialties (audiology, speech and
language therapist, endocrinologist, oncologists, plastic surgeons,
maxillofacial surgeons and dermatologists)
Further Information
• Approach your local ENT team!
• ENT UK: www.entuk.org
• Student and Foundation Trainees in Otolaryngology (SFO UK):
http://sfo.entuk.org
• Association of Otolaryngologist in Training (AOT) :
www.aot.ac.uk
• Royal College of Surgeons of England: www.rcseng.ac.uk
• British Association of Paediatric Otolaryngology (BAPO):
www.bapo.org.uk
• British Rhinological Society (BRS) :
www.britishrhinologicalsociety.org.uk
• British Otolaryngology & Allied Sciences Research Society
(BOARS) https://www.entuk.org/boars-section
• Intercollegiate MRCS exams:
http://www.intercollegiatemrcsexams.org.uk/new
Generic Skills in ENT
General ENT History
Principles of history taking in ENT
Good history taking is an essential skill to be maintained throughout
your training. By building a good rapport, you will help the patient
feel more comfortable about discussing his/her symptoms. It
provides the opportunity to explore a patient’s concerns and
expectations. After completing a thorough history, you should have a
good idea of what the top differential diagnoses could be.
Before starting
• Wash your hands
• Introduce yourself and ensure the patient is comfortable
• Maintain good eye contact and remember the importance of
developing good rapport with the patient (and the parents if
present)
Structure of history taking

• Presenting complaint (PC) ‘How may I help you today?’
• History of presenting complaint (HPC) ‘ When did this problem
begin’
• Enquire about the relevant risk factors and other specific
questions relating to the presenting complaint. Do have a
targeted list of questions for PCs related to “Ear”, “Nose”, and
“Throat/Head Neck” (For targeted histories, go to the relevant
sub sections of this booklet)
• Previous episodes - Severity, response to previous treatment
and hospitalisation
• Past medical history (PMH)
• Birth History – Particularly important for ear conditions in
children
• Drug history (DH) - Including over the counter medication and
vaccinations
• Allergies
• Family History
• Social history (SH) - Do not forget to enquire about the impact
that the presenting complaint has had on quality of life
• Systems review - Also enquire on any tendency to bruise or
bleed easily
At the end of the history

• Summarise the patient’s history to them. Clarify that you
understood them correctly and whether there is anything else
that they would like to mention.
Ear examination
Before starting
• Gel/wash your hands
• Introduce yourself and ensure the patient is comfortable
• Ask about any pain or tenderness
• The patient should be positioned on the chair and you should
place yourself to the side of the patient. In children, positioning
is even more important. Children should be sat across the
parent/nurses lap, with the side of the head held to the chest by
the carer’s hand (See Figure 1) Flailing arms can be secured
with the carer’s other hand. Ideally, aim to examine children as
opportunistically as possible and incorporate play as part of the
examination.
Figure 1: Correct positioning of a child for ear exam
Inspection
From the front: note the size, assess symmetry of the pinna. Are
there differing degrees of protrusion? Is there an obviously
abnormal pinna? For example, see Figure 2.
Figure 2: Congenital Microtia of the External Auditory Canal
Inspect each ear individually - Start with the normal ear

Pre-auricular - Inspect for scars (previous parotidectomy or
middle ear surgery), swelling (infection, parotid tumour),
erythema (infection/ inflammation), sinuses, pits, fistulae
Pinna - Note any signs of erythema, swelling (infection,
haematoma) or tenderness
Post-auricular - Move pinna anteriorly to inspect behind the
pinna. Note any post-auricular scars. Acute and/ or painful
swelling here suggests infection (mastoiditis or lymphadenitis)
Examine the other ear. Note any difference.
Otoscopy
Ensure the otoscope has good magnification and illumination.
Use the largest speculum that will fit comfortable in the external
auditory canal (EAC)
Start with the “normal” ear
Gently pull the pinna upwards and backwards to straighten the
ear canal to best visualise the tympanic membrane. In children,
pulling the pinna downwards and backwards may provide better
visualisation
Hold the otoscope like a pencil and use your little finger as a
fulcrum against the cheek to avoid injury should the patient
move suddenly
Inspect systematically
Figure 3: Normal right tympanic membrane
External auditory canal: Wax or discharge, erythema, swelling

(infection, trauma)
Tympanic membrane (See Figure 3): Is there a normal light

reflex in the anteroinferior quadrant? Colour of drum - Normal is
greyish & translucent. Pink/red colouring can mean
infection/inflammation and white plaques can indicate
tympanosclerosis. Position of drum - Retracted (cholesteatoma,
infection), bulging (infection), perforation
Ossicles: The malleus, incus and stapes can be seen
sometimes through the tympanic membrane especially if there is
a perforation.
Pneumatic otoscopy can also be used to assess tympanic
membrane mobility – this modified otoscope has an air-tight seal
when placed in the ear canal and a rubber bulb (similar to that of
a sphygmomanometer) which the user can squeeze which
alters the pressure within the ear canal
Hearing tests
These tests include the Pure Tone Audiogram (see Chapter:
ENT Investigations - Pure Tone Audiogram).
Examine a patient’s response grossly to your greeting. Can they
hear you? Is there a hearing aid being used?
(i) Free field speech testing
Free field testing is a good screening tool for hearing loss

Use of masking improves the accuracy of testing: Rub the
tragus of the contralateral ear whilst performing this to prevent
sound being heard in the contralateral non-test ear
Use polysyllabic phrase (number or letter) e.g. ‘C5’, ‘37’ or
motivational phrases in children e.g. ball, sweets, crisps
Test normal ear first. Perform, in order of intensity at 60cm
(arms length) and 15cm: whisper, conversational speech, loud
voice. Patient should be able to repeat >50% of the
letters/numbers correctly.
If he/she can repeat:

Whisper at 60cm – Hearing better than 30dB
Whisper at 15cm – Hearing better than 35dB
Conversational voice at 15cm - Hearing better than 55dB
Loud voice at 60cm – Hearing worse than 75-90dB
ii) Weber’s and Rinne’s tests
These tests assess air conduction (AC) and bone conduction (BC)
and are used to help delineate whether hearing loss is sensorineural
(SNHL)or conductive (CHL) in origin.
Weber’s test
Figure 4: Weber’s test
Vibrating 512Hz tuning fork applied firmly to the midline of the

forehead, apex of head (see Figure 4)
Ask the patient if he/she can hear a tone in the right ear, left ear
or centre of the head
The “louder” ear may be due to conductive hearing loss in that
ear (sound travels through the bone), or sensorineural hearing
loss in the other ear
You can work out which this is by performing Rinne’s test.
Rinne’s test
Figure 5: Rinne’s test
Place vibrating tuning fork with base on mastoid process

(position 1, testing bone conduction). See Figure 5
Then move the tuning fork so its prongs are adjacent to (but not
touching) the external auditory meatus (position 2, testing air
conduction).
Ask patient to tell you which is louder, when the fork is placed
behind the ear or in front of the ear
Position 2 is louder than position 1 in the normal ear (Positive
Rinne), as an intact hearing apparatus of the external and
middle ear amplifies sound. When position 2 is quieter than
position 1, (Negative Rinne), this indicates external or middle
ear disease affecting the air conduction
Interpretation of Weber’s and Rinne’s test

(AC= Air conduction, BC= Bone conduction, SNHL= Sensorineural
hearing loss, CHL= Conductive hearing loss)
Facial Nerve Examination

See “Cranial Nerves Examination” section.
Concluding
Thank patient
Wash hands
In an exam setting, summarise findings to the examiner and
mention extra tests that you may wish to perform: Rigid
nasendoscopy - Useful to identifying nasopharyngeal pathology
e.g. adenoids, carcinoma, Pure tone audiometry and
tympanometry.
Nasal Examination
Before Starting
Gel/wash your hands
Introduce yourself, ask for permission to examine the patient
and ensure they are comfortable. Ensure the examination area
is well lit.
Ask about any pain or tenderness
Ask if they have had any previous surgery
Inspection
From the front: shape change, deviation from the midline,
symmetry of one side to another, scars, skin changes
It is often easier to split the nose into thirds when describing
shape or deviations, (see Figure 6 and Figure 7).
Figure 6: Separation of the nose into bony pyramid, cartilaginous

pyramid and lobule. The upper third mostly composed of bony vault,
middle third made up of dorsal septum and upper lateral cartilages,
and lower third or nasal tip composed primarily of lower lateral
cartilages, septum and soft tissue)
Figure 7: Upper, middle and lower thirds of the nose.
From the side (the side or dorsal profile of the nose): can
comment on shape, hump (protruding bump) or collapse
(sunken in), projection (how far the nose sticks out from the
face) and rotation of the tip (whether the tip of the nose is
pointing up or drooping down). When performing advanced
assessment of the nose, e.g for cosmetic analysis, then angles
and measurements of the nose in relation to the surrounding
face become more important.
From below – look for symmetry, deviations and scars of
previous surgery.
Palpation
Skin envelope – feel the thickness of nasal skin (thinnest over
bone, thicker sebaceous skin over lower nose)
Tip Recoil – the tip of the nose is pushed in and the degree of
resistance is assessed- lack of recoil may indicate lack of tip
support
Anterior rhinoscopy
Examine the anterior internal nose with a Thudicum’s speculum and
headlight (see Figure 8).
How to hold a Thudicum’s speculum
Figure 8: How to perform anterior rhinoscopy with a Thudicum’s

speculum.
The speculum is held from the tip of the index finger of the left hand
with the tines facing the patient. The middle finger goes in the front
and the ring finger behind, with the thumb pressed firmly on top to
support the speculum. The hand is then twisted, and pressure is
then used between the middle and ring fingers to open and close the
speculum.
The speculum is held like this so the rest of your hand does not
obscure your view into the nose. Your contralateral dominant hand is
then free to use instruments in the nose should you need to. It is
important to ensure your light source is lined up with the nasal cavity.
Look especially for these common pathological findings:
Septal deviations (see Figure 9)

Evidence of swelling (rhinitis causing enlarged inferior
turbinates, oedema and clear rhinorrhoea- Figure 10)
Septal perforations (holes in the cartilage – see Figure 11)
Prominent blood vessels (see Figure 12)
Polyps in middle meatus/nasal airway (see Figure 13)
Figure 9: Septal deviation to the right

Figure 10: Right Inferior Turbinate swelling due to allergic rhinitis
Figure 11: Septal perforation when viewed through the right nasal
airway.
Figure 12: Prominent blood vessels overlying right Little’s area
(anterior septum)
Figure 13: Left-sided inflammatory nasal polyp
Other nasal tests

Nasal misting
Perform nasal misting with a Lack’s cold metal tongue depressor
(see Figure 14)
Figure 14: Cold spatula misting test. The humidified expired air
creates a mist on the cold metal tongue depressor. Due to its
simplicity and lack of invasiveness, it is especially useful to assess
bilateral nasal patency in paediatric patients.
Cottles & Modified Cottles Test

Perform Cottle’s & Modified Cottle’s Test using a Jobson-Horne
probe/ear curette for external/internal nasal valve patency +/- alar
collapse (Figure 15).
Figure 15: Modified Cottle’s test
Modified Cottle’s Test which involves placing a Jobson Horne probe

under the lower end of the upper lateral cartilage and opening out
the internal nasal valve (the narrowest point of the nasal airway)
which can be narrowed by septal deviations, enlarged inferior
turbinates or collapsed nasal cartilages. The original Cottle’s
maneuver described pulling the side of the face outwards to try and
relieve the nasal obstruction, but this was not always deemed a
reliable method of assessment.
Examine the oropharynx

Examine oropharynx with a tongue depressor. Look for posterior
cobble-stoning associated with chronic inflammation or infection/post
nasal drip or large antro-choanal polyp.
Perform Flexible Nasendoscopy (FNE)

The use of modern flexible endoscopes allows a thorough
assessment of the nasal cavity and drainage pathways of the
paranasal sinuses. One can also pass the endoscope beyond the
post nasal space to assess the oropharynx, larynx and hypopharynx.
However, in this section, we will concentrate on the examination of
the nasal cavity.
There main areas of examination are as follows:

Figure 16: Endoscopic view of the right anterior nasal cavity.
Figure 17: Endoscopic view of the right middle metal region

Figure 18: Endoscopic view of the right post-nasal space. The
Eustachian tube orifice is where the middle ear drains down into the
nasal cavity. The Fossa of Rosenmueller is an important place to
check for pathology such as nasopharyngeal carcinoma.
Neck and thyroid status exam
Before Starting
Wash your hands
Introduce yourself and ensure the patient is comfortable
Ask about any tenderness (does their voice sound normal?)
Expose the neck adequately (ideally to the clavicles)
Ensure that you are able to move around the patient. If not, the
patient should be repositioned
Inspection
Assess from the front and both sides of the patient
Note any neck asymmetry or obvious masses. Be able to
describe gross features of the mass (size, neck level, overlying
skin involvement and obvious pulsatility)
Scars from previous radiotherapy changes, thyroid surgery,
parathyroid surgery, neck dissection, tracheostomy
Palpation
Figure 19: Correct hand position for thyroid examination
You should examine the patient from behind. You may be able
to note proptosis of the eyes (Graves’ disease)
Fingers are more sensitive than thumbs so use your fingertips to
palpate neck, rolling tissues and compressing them gently
(Figure 19)
Ask the patient to swallow a sip of water. If the mass moves
upwards with swallowing it suggests thyroid origin
Ask the patient to stick out their tongue- a midline lump moving
up suggests a thyroglossal cyst
When noting any lump during palpation, describe the presence of the
following signs:
Tender (infection, inflammation i.e. thyroiditis) /non-tender

Temperature- heat may indicate inflammation or infection
Firm/soft
Smooth/craggy. Can you feel multiple nodules?
Fixity to the overlying skin or underlying tissues.
Site of lump. Is it in the anterior or posterior triangle?
Size of lump; often comparing the size of a lump to common
fruits (eg grape, plum, bean) is helpful
Examine the lymph nodes in the neck (anterior & posterior triangles)
Begin in midline with submental lymph nodes. Progress on to
submandibular nodes, pre/ post-auricular nodes, occipital
nodes, anterior/posterior cervical chain
Do not forget the supra- clavicular area
Auscultation
Auscultate the thyroid. A bruit is a sign of increased blood flow and
may indicate hyperthyroidism
Percussion
Tap the superior part of the sternum for a large goitre extending
retrosternally with percussions sounding stony dull.
Thyroid status examination

General
Appropriately dressed
Look sweaty?
Hands and arms
Examine for tremor (hyperthyroidism) by asking patient to put

arms outstretched
Inspect the nails for thyroid acropachy (similar to clubbing,
hyperthyroid- see Figure 20), and palmar erythema
(hyperthyroid)
Feel the temperature of hands and presence of sweating
(hyperthyroid)
Take the pulse. Atrial fibrillation, tachycardia (hyperthyroid),
bradycardia (hypothyroid)
Figure 20: Thyroid acropachy.
Face
“Peaches and cream” complexion of hypothyroidism.

Loss of outer 1/3 of eye brows (hypothyroidism)
Graves’ ophthalmopathy (see Figure 21), proptosis, chemosis,
and injection of sclera in severe disease
Examine the eye movements for dysconjugate gaze (indicator of
severe disease)
Examine for lid lag (sympathomimetic effect of thyrotoxicosis)
Figure 21: Proptosis secondary to thyroid eye disease
Legs
Inspect for pre-tibial myxedema which is present in

hypothyroidism
Check the ankle reflexes- brisk in hyperthyroidism, and the
opposite in hypothyroidism
Pemberton’s test
Pemberton’s test is a test for a retrosternal goitre that may obstruct
the thoracic outlet and superior vena cava. A positive sign is
congestion of facial/neck veins and hoarse voice upon raising the
arms.
Concluding
Thank the patient
Wash your hands
Summarise your findings to examiner
Cranial Nerves Examination
Before starting
Introduce yourself and obtain consent
Wash your hands
Ask about tenderness
CN I: Olfactory nerve
Informal: Ask about changes in smell sensation
Formal smelling set test e.g. The University of Pennsylvania
Smell Identification Test (UPSIT)
CN II, III, IV, VI: Optic nerve,

Oculomotor, Trochlear, Abducens
Inspect for normal colour vision and normal eye movements as
these functions can be affected by skull base tumours and
orbital infections. Gradenigo’s syndrome is a complication of
acute otitis media resulting in a triad of periorbital unilateral pain,
diplopia secondary to VI nerve palsy, & petrositis.
CNV: Trigeminal nerve

Motor component
Patient to clench teeth whilst you palpate the tone of the
masseter and temporalis muscles.
Open mouth- look for deviation. Tests the pterygoids
Sensory component
Ask the patient to close their eyes, and say ‘yes’ when they feel
you touching them with cotton wool
Touch the patient’s face on the left then right of the forehead,
cheeks and mandible in turn to test the 3 somatic sensory
divisions of the trigeminal: ophthalmic, maxillary and mandibular
divisions respectively. Rarely tested in practice are the
temperature and pain sensations in these distributions
Both motor and sensory
Corneal reflex. The afferent limb of this reflex is mediated by

CNV. The efferent limb is mediated by CNVII
Jaw jerk. Minimal or absent is normal. Brisk is pathological but
may be present in younger patients
CNVII: Facial nerve

Inspect for facial tone- asymmetry
Motor. Testing the branches emanating from the parotid
Raise eyebrows. Note forehead wrinkles and whether this is
forehead sparing or not. If there is no forehead sparing, this
likely suggests a lower motor neuron palsy
Screw up eyes tight.
Puff out cheeks.
Smile.
Show teeth/grimace.
Hyperacusis- due to loss of the dampening effect of nerve to
stapedius.
Loss of taste- due to loss of chorda tympani.
Loss of these modalities depend of the location of facial nerve
lesion.
CNVIII: Vestibulocochlear nerve
See “ear examination” section for further details:
Free field testing / whisper voice tests
Weber’s and Rinne’s test
CNIX, and CNX: Glossopharyngeal

and Vagus nerve
Open mouth, say “ahhhhh”. Uvula will deviate away from the
side of the lesion.
Assess voice (hoarseness) and quality of cough. Is there a
bovine sounding coughing? Think recurrent laryngeal nerve
palsy if abnormal (CNX)
Swallowing.
Gag reflex
CNXI: Accessory nerve

Shrug against resistance- testing trapezius
Turn head- tests the sternocleidomastoid of the contralateral
side.
CNXII: Hypoglossal nerve

Look for tongue atrophy
Ask patient to move the tongue side to side.
Protrude tongue- tongue tip deviates towards the side of the
lesion
Conclusion
Thank the patient
Wash your hands
Summarise your findings to the examiner
Otology
Ear Anatomy
The ear is subdivided into 3 main parts: 1) the external ear 2) the
middle ear 3) the inner ear (Figure 22).
Figure 22: External auditory canal and middle ear (Elf-ENT)
The External Ear

The external ear canal consists of the pinna (auricle) and the external
auditory canal.
Pinna (auricle)
The pinna consists of elastic cartilage, thrown into folds (see

Figure 23), and a fibrofatty lobule.
It is supplied by the greater auricular nerve, lesser occipital and
facial nerve.
Figure 23: Anatomy of the pinna (reproduced with permission from
Otolaryngology Houston, www.ghoryeb.com)
Nerve supply of the pinna

Lateral
Anterosuperior – Auriculotemporal nerve (V3)

Anteroinferior – Great auricular nerve (C2/3)
Posterior – Lesser occipital nerve (C2)
Conchal bowl and ear canal – Auricular branch of vagus nerve
Medial
Greater auricular nerve (C2/3) and lesser occipital nerve (C2)
External Auditory Canal (EAC)

It is an oblique tube - 3 cm in length. The outer 1/3 is cartilage,
and inner 2/3 is bony
Ceruminous glands only exist in the outer 1/3. These glands
secrete wax
The tympanic membrane forms the medial boundary of the
canal.
Clinical important point: Examining the EAC

In adults, the outer third of the canal is directed superiorly and
posteriorly as it runs medially. The inner two thirds of the canal is
directed inferiorly and anteriorly. When examining the ear canal, you
must pull the auricle superiorly and posteriorly to align the two
portions. (In infants, pull the pinna (gently!) posteriorly)
Blood supply of the external ear
Auriculotemporal branch of superficial temporal artery

Posterior auricular branch of the external carotid artery
Clinically important point: Cauliflower ear

The cartilage derives its nutritional support from the overlying
perichondrium. Separation of the two layers (with blood, infection or
inflammation often following trauma) may result in cartilage necrosis
resulting in a cauliflower ear (see Figure 24)
Figure 24: Cauliflower ear (reproduced with permission from
Nerve supply of the external ear canal

The auriculotemporal nerve and the auricular branch of the vagus
nerve
The Middle Ear

The middle ear is an air-containing cavity held within the
temporal bone and it is lined with mucous membrane. It also
communicates with the nasopharynx via the Eustachian tube.
The function of the middle ear is mainly to amplify and transmit
sound energy.
The tympanic membrane forms the lateral boundary of the
middle ear cavity. It is a circular shape and roughly 1cm in
greatest diameter. It is innervated on the outer surface by the
auriculotemporal nerve and the auricular branch of the vagus.
Figure 25 illustrates the component of the tympanic membrane.
The membrane is normally greyish/ pinkish in colour. When the
membrane is examined with an otoscope, the concavity of the
structure produces a cone reflex in the anteroinferior quadrant.
The tip of the handle of malleus forms the deepest concavity of
the membrane called the umbo, which is where the cone of light
radiates from. The pars flaccida is the weakest and most flaccid
area of the tympanic membrane. It plays a vital role in the
pathophysiology of cholesteatoma. The pars tensa forms the
remainder of the tympanic membrane.
Figure 25: A labelled picture of the left tympanic membrane
The middle ear structures include:

Ossicles – Malleus, incus and stapes (Figures 26, 27, 28). The
malleus is the largest ossicle. The lateral process of the malleus
is attached to the tympanic membrane. The head articulates with
the body of the incus. The long process of the incus articulates
with the head of the stapes. The stapes structure includes two
limbs (anterior crus and posterior crus), which are attached to the
oval window footplate
The tensor tympanic and stapedius muscles: these are attached
to the ossicles to regulate their movement
Chorda tympani (provides taste to anterior two-thirds of the
tongue)
Facial nerve
Pictures of the three middle ear bones:
Figure 26: Malleus (reproduced with permission from Otolaryngology

Houston, www.ghoryeb.com)
Figure 27: Incus (reproduced with permission from Otolaryngology
Figure 28: Stapes (reproduced with permission from Otolaryngology

The Inner Ear

The inner ear is located within the petrous part of the temporal bone.
It is medial to the middle ear.
Function of the inner ear:
Cochlea - Transduction of energy from sound to electrical

impulses, which are relayed and interpreted by the brain
3 Semicircular canals (superior, lateral and posterior) – Detect
angular head acceleration
Utricle and saccule – Detects linear acceleration
forwards/backwards and up/down respectively
Clinically important points:
The average human can detect sounds ranging between 20 and

20,000 Hz
The cochlear is tonotopic with high frequency sounds detected at
the basal turn of the cochlear and low frequency sounds
detected at the apex. The ability to detect high pitch sounds
decreases in older humans (presbycusis)
Dizziness and Vertigo
Description
True vertigo is most often associated with a sensation of ‘spinning’
and movement of the surrounding environment. It is important to
distinguish this from the more generalised dizziness of
disequilibrium.
Epidemiology
Male: Female ratio 1 : 3
Causes and Differential Diagnoses

Once you have established that the symptom is that of true vertigo, it
is imperative to ascertain the duration and frequency of attacks, as
this is the key to reaching the correct diagnosis and determining if
the disorder is most likely peripheral (pertaining to the ear) or central
(brain).
There are 3 common causes of vertigo originating from the labyrinth

itself:
Benign Paroxysmal Positional Vertigo (BPPV)- most common

cause of true vertigo with typical age of onset 40-60 years
Vestibular neuronitis
Meniere’s Disease
These can generally be differentiated by the duration or onset of the

vertigo and by the presence or absence of associated
audiovestibular symptoms
Another common condition that is seen is vestibular migraine.

Symptoms do not always include a headache and/or visual
symptoms and can sometimes overlap (e.g. hearing loss) making it
difficult to differentiate between conditions such as Menieres.
Signs and Symptoms

BPPV- Dix-Hallpike test positive. Rotatory vertigo on moving
head
Meniere’s – Rotatory vertigo associated with fluctuating hearing
loss often with low frequency thresholds affected. Tinnitus
usually gets worse during an attack. Patients classically get an
aural fullness before onset of vertigo.
Vestibular neuritis – Rotatory vertigo that is continuous for over
24 hours often associated with nausea and vomiting. Classically
they are confined to bed and it takes several days to weeks to
recover.
Vestibular migraine – Rotatory vertigo can last minutes to hours
to days. Classically associated with
headaches/photophobia/visual disturbance\phonophobia but
these are not always present.
Investigations
Full neurological examination
Pure tone audiometry
Dix-Hallpike test
MRI of internal auditory meatus may be appropriate with
asymmetrical sensorineural loss to exclude an acoustic
neuroma
Video head impulse testing (vHiT) – this is performed using
specialist equipment and can be used to assess the function of
the semi-circular canals by measuring visual ocular reflex (VOR)
function. It takes around 15minutes to perform and is a quick
and sensitive measure of labrythine function
Treatment
BPPV - Epley’s manoeuvre can be curative in up to 90% by
repositioning of the displaced otoconia crystals. In persistent
cases, Brandt-Daroff exercises may be advised. Surgical
management is rarely required but posterior semi-circular canal
occlusion is useful in resistant cases.
Vestibular neuronitis – Treatment is expectant with anti-emetics
during the acute phase
Meniere’s Disease – There is a hierarchy of treatments
depending on the severity of the disease and response to
previous treatments. The underlying pathophysiology is thought
to be endolymphatic hydrops. Therefore “pressure reducing”
therapies include low salt diet, medications such as betahistine
and diuretics although the evidence for these treatments is
weak. Intratympanic injection of steroid or gentamicin is used for
those that fail conservative management. Other treatment
options include saccus decompression, labyrinthectomy and
vestibular nerve section.
Vestibular migraine – Common trigger factors include
dehydration, foods (classically chocolate, cheese), anxiety and a
poor sleep pattern. A symptom diary can help identify these. In
those that do not respond to avoidance measures, there are a
variety of migraine-preventative medications available.
Hearing Loss
Description
Hearing loss may be unilateral or bilateral.
Causes of Hearing Loss

Conductive Hearing Loss
Sensorineural Hearing Loss

History
Sudden vs gradual onset. Unilateral or bilateral.
Associated otological or neuro-otological symptoms
Investigations
Pure Tone Audiogram (PTA) & Tuning fork tests (Rinnes & Weber)
are complimentary to each other – should always be used together.
Management of Hearing Loss

Audiological
Hearing aids for mild-to-profound hearing loss
Surgical
Tympanoplasty - Cartilage or temporalis fascia is used to repair

a perforation in tympanic membrane. N.B. This surgery is
normally done for recurrent ear infections or to waterproof the
ear; hearing improvement often occurs when a perforation is
closed but cannot be guaranteed.
Stapedectomy - Prosthesis used to bypass fixed
stapes/footplate in otosclerosis and allow transmission of sound
into inner ear
Bone anchored hearing aid – a transcutaneous or percutaneous
device can be surgically implanted under general or local
anaesthesia for a conductive, mixed conductive /sensorineural
hearing loss or unilateral dead ear
Cochlear implantation- There are specific NICE criteria for
cochlear implantation which includes profound sensorineural
hearing loss. However it may be of benefit in other patients –
they require a multidisciplinary team assessment.
Middle ear implant – suitable for conductive and mixed hearing
loss
Management of excessive ear wax

Tinnitus
Description
Tinnitus is a term used to describe the perception of sound when no
external sound is present. It is sometimes described, as ‘the sound
of silence’ because all people, if they are seated in a completely
quiet soundproofed room, will hear tinnitus. This noise is usually
masked by the environmental sounds. It is said to be objective when
apparent to the examiner and subjective when apparent to the
patient only (more common).
Epidemiology
No identifiable cause is found in most cases of tinnitus. It is often
associated with hearing loss.
Types of Tinnitus
Non- pulsatile tinnitus is typically referred to as a false perception
of sound that is heard by the affected individual only (subjective). It is
often described as a buzzing, high-pitched tone or a clicking or
popping.It can be associated with noise induced hearing loss,
presbycusis, Meniere’s disease, head injury, otitis media and drug
related causes (e.g. salicylates, nonsteroidal anti-inflammatory
drugs, loop diuretics)
Pulsatile Tinnitus (4%) is defined by a sound heard by an individual

that is synchronous with their heartbeat and is usually caused by
turbulent blood flow that reaches the cochlear. It may be associated
with a treatable cause. It can be classified according to the
underlying causes which is usually vascular or non vascular.
Causes of Pulsatile Tinnitus

Vascular causes
Atherosclerosis on the internal carotid artery. The eventual
stenosis of the artery may predispose the individual to pulsatile
tinnitus due to turbulent blood flow.
Vascular malformations. Arterio- venous malformations/fistulas
are abnormal communications between the arterial and venous
system. It may be congenital or acquired- the latter being
secondary to trauma or a result of venous sinus obstruction.
Glomus tumours are rare hypervascular tumours arising from
paraganglia cells. Glomus tympanicum are associated with
Jacobson’s nerve around the promontory in the middle ear.
Glomus jugulare are found along the jugular bulb and they
involve the skull base and may extend in the middle ear.
Non-vascular causes
Paget’s Disease
Otosclerosis
Myoclonus. Myoclonus of the middle ear muscles or palatal
muscles may cause objective tinnitus, which classically presents
with a clicking noise rather than a vascular thrill.
Investigations
If unilateral and associated with hearing loss, MRI should be
performed to exclude an acoustic neuroma.
Pulsatile tinnitus may be investigated using MR or CT
angiography. Carotid duplex scanning may also be helpful if
carotid artery stenosis is suspected. Arteriography is also helpful
in a limited number of cases but is associated with a small risk
of CVA.
Treatment
The vast majority of time, the patient just needs reassurance
that tinnitus is very common and that they will adapt to it. It
tends to be worse at quiet times (e.g. at night when trying to
sleep) and worrying about it generally makes the tinnitus worse.
Address any underlying cause of the tinnitus in appropriate

cases e.g. hypertension, carotid stenosis, side effect of
medications
For selected patients, behavioural therapy can be provided by
audiologist/hearing therapist who introduce coping strategies
and tinnitus retraining therapy (TRT) . A noise generator can
mask tinnitus if interfering with sleep
A hearing aid may improve tinnitus if hearing loss is present
through a masking effect
Facial Nerve Palsy
Description
Temporary or permanent paralysis of the facial nerve (CN VII)
Epidemiology
Bell’s palsy (idiopathic in origin) is most common but is a
diagnosis of exclusion (15-40 cases/100,000)
M: F, 1:1
Causes and Differential Diagnoses of

Facial Nerve Palsy
Symptoms
Dry painful eye, especially, if eye closure is impaired
Drooling from side of mouth and difficulties with eating
Psychological disturbance
Signs
Differentiate between upper and lower motor neurone (upper
motor neuron has sparing of forehead)
Test strength of each branch of the facial nerve using House-
Brackmann classification of nerve palsy - Raise eyebrows,
tightly close eyes, wriggle nose, puff out cheeks, show teeth.
Bell’s phenomenon - White sclera visible as eyeball rolls

upwards to protect cornea when eyelid does not close
Otoscopy – cholesteatoma, Acute Otitis Media
Head and neck examination - parotid tumour
Complications of Facial Nerve Palsy

Corneal scarring - Blindness if eye care advice not given
Wasting of facial muscles, synkinesis
Psychological
Investigations
Pure Tone Audiogram – Look for conductive hearing loss
(cholesteatoma) or asymmetrical sensorineural hearing loss
(cerebellopontine lesion e.g. acoustic neuroma)
MRI scan if suspecting central cause
Treatment
General: Eye care, Artificial tears/tape eyelid shut. Referral to
ophthalmology.
Medical: Bell’s palsy/Ramsay Hunt syndrome - Oral steroids and
oral antivirals although the evidence for oral antivirals in Bell’s
palsy is lacking. Treatment needs to be started within forty eight
hours to be effective.
Surgical ( rarely indicated): Depends on cause but options
include facial nerve grafting, facial re-animation if the function
does not recover.
Otalgia
Description
Otalgia is ear pain that can originate from the ear itself or can also
be referred from elsewhere in the head or neck (see referred otalgia
below)
Epidemiology
This is a very common presentation to primary care especially in
young children.
History
Referred Otolagia
Always ask about other general symptoms – There are several other
causes of otalgia, not directly related to the ear (referred pain). It is
important to enquire about dental, nasal and throat symptoms in
order to identify these. It is particularly important to identify potential
indicators of malignancy.
Pain referred to the ear is a well-documented phenomenon. Any

pathology involving the cranial nerves V, VII, IX, and X and the upper
cervical nerves C2 and C3 can cause the sensation of referred
otalgia.
Trigeminal neuralgia is the most common cranial neuralgia linked to

referred otalgia. Other causes of referred cranial neuralgia are
described below.
Otorrhoea
Description
The ear can discharge wax, pus, blood, mucus and even
cerebrospinal fluid. Remember discharging wax should be reassured
as normal.
The common bacterial pathogens in a discharging ear that can

cause an infection include:
Pseudomonas aeruginosa
Staphylococcus aureus
Proteus spp.
Streptococcus pneumonia
Haemophilus influenza
Moraxella catarrhalis
In most patients with a discharging ear, the diagnosis can be made

based on good history and examination. We will recap on a focused
history taking for otorrhoea and then revise the possible differentials
of this symptom in more detail.
History
Duration of discharge – If chronic, think chronic otitis media
including cholesteatoma especially if unilateral
Is there associated otalgia (ear pain)?
Associated fever or systemic symptoms indicates an infective
aetiology
Is there associated hearing loss or dizziness?
Do not miss a history of putting foreign bodies in the ear
especially in children
Facial nerve palsy - May occur with acute or chronic otitis media
especially if the facial nerve is dehiscent along its course in the
middle ear (10% of the population)
Check for history of trauma - CSF otorrhoea
Has there been any recent history of topical antibiotics? This
can in itself cause discharge or predispose to antifungal ear
infections if there is prolonged usage
Differential diagnosis
Otitis Externa
Description
Inflammation of the external auditory canal that can be acute or
chronic
Epidemiology
An estimated 10% of people develop otitis externa in their lifetime
and there is an increased risk after first episode. Hence, otitis
externa is an extremely common presentation when on call for ENT
or at the emergency ENT clinic.
Risk Factors
Swimming
Warm/humid climates
Underlying skin conditions e.g. eczema
Immunosuppression e.g. diabetes
Trauma e.g. excessive cleaning or scratching
Hearing aids that reduce ventilation or introduce infection into
the canal
Causes
Mostly bacterial: Pseudomonas aeruginosa, S. Epidermidis and
S. Aureus.
Otitis externa can be fungal. There is an increased risk after
prolonged antibiotic courses.
Symptoms
Otalgia (ear pain) - especially on movement of the pinna or jaw.
Can be severe.
Pruritus (itching)
Discharge
Hearing loss
Signs
Pain on moving the pinna and/ or tragus. Pinna may be very
tender indeed.
If pain is out of proportion with examination findings, there is a
history of diabetes or failure to respond to antibiotics, consider
necrotising otitis externa which is a severe, potentially fatal
progressive form of otitis externa. It is a non-neoplastic infection,
which spreads to the bone and results in osteomyelitis of the
lateral skull base. It can cause multiple lower cranial nerve
palsies. It is almost exclusively unilateral.
External auditory meatus swelling, erythema with purulent
discharge (Figure 29)
Tympanic membrane not always visible because of swelling
Complete external auditory meatus obstruction possible
If possible, examine the tympanic membrane for a perforation. It
is possible to have a secondary otitis externa associated with
otitis media
Complications
Peri-auricular cellulitis
Necrotising otitis externa
Investigations
Swab the external ear canal for MC&S
Urgent CT scan is required if necrotising otitis externa is
suspected (Unilateral, severe ear pain, elderly and/or
immunocompromised)
Treatment
Aural toilet (microsuction)
Topical antibiotic and steroid ear drops e.g. ciprofloxacin
(provides anti-pseudomonal cover)
Insertion of a Pope wick helps the antibiotic come into contact
with the canal wall and stents open a severely oedematous ear
canal. The Pope wick looks like a small thin sponge and
expands in the ear canal when wet.
Admit for diabetic control, IV antibiotics and regular aural toilet if
suspecting necrotising otitis externa
Figure 29: Otitis Externa (Courtesy of Elef-ENT)

Acute Otitis Media
Description
Acute otitis media is acute onset inflammation of the middle ear,
usually of an infective origin. Otitis Media with Effusion (OME) may
be a sequelea of acute otitis media but is regarded as a different,
non-infective condition.
Epidemiology
Occurs at all ages, but much more common in infancy
Risk Factors
Lack of breastfeeding as a baby
Attending nursery/day care
Positive family history
Age between 6-18 months
Exposure to smoking
Causes
An upper respiratory tract infection (URTI) results in
inflammation of the upper airways and swelling causes
obstruction of the Eustachian tube. Ascending infection results
in hyperaemia of the middle ear mucosa with production of a
purulent exudate. This is called acute otitis media (AOM)
Viral infections account for two thirds of cases of AOM.
Respiratory syncytial virus, rhinovirus and enterovirus are the
most common.
Bacterial organisms include Streptococcus pneumoniae,
Haemophilus influenza, and Moraxella catarrhalis.
Symptoms
Infants: fever, ear pulling, irritability, vomiting
Children and adults: otalgia (ear pain), fever, generally unwell,
hearing loss. If the tympanic membrane bursts the pain may
suddenly improve, but a purulent discharge develops from that
ear
Signs
Bulging tympanic membrane (Figure 30)
Injected tympanic membrane
If there is a perforation, there may be purulent discharge coming
through. There may also be secondary otitis externa
Figure 30: Bulging tympanic membrane in AOM (Courtesy of Elef-

ENT)
Complications
Intratemporal: tympanosclerosis (white patch on the ear drum
due scarring), hearing loss, tympanic membrane perforation,
mastoiditis, labyrinthitis, facial nerve palsy
Intracranial: meningitis, intracranial abscess, lateral sinus
thrombosis, cavernous sinus thrombosis, subdural empyema.
Investigations
Consider swab for M, C &S if ear discharging
Imaging (CT and/or MRI) if complications are suspected
Treatment
Analgesia (e.g. Ibuprofen) and anti-pyretics (e.g. Paracetamol)
If failure to improve within 24-48 hours, consider prescribing oral
antibiotics. A 10 day course of Amoxicillin is first line. If no
improvement, switch to Co-amoxiclav.
Otitis Media with Effusion
(OME)
Description
This is a middle ear effusion (fluid) without the signs of infection.
Also known as ‘glue ear’.
Epidemiology
Bimodal distribution at a peak at 2 years and 5 years of age.
Prevelance is 20% and 15% respectively.
50% of OME resolves spontaneously within 3 months
Causes
Eustachian tube dysfunction. In children, the Eusatachian tube
is smaller and more horizontal than in adults therefore middle
ear ventilation is impaired. Thus commoner in cleft palate and
other syndromic diseases affecting the face and skull base.
Beware of the adult with a unilateral middle ear effusion.
Nasopharyngeal tumours can block the drainage of the
Eustachian tube and result in a middle ear effusion
Symptoms
May be asymptomatic in an infant. Parent may notice the child has
hearing loss or behavioural problems.
Signs
Poor speech development
Otoscopy: tympanic membrane will appear dull +/- a visible fluid
level. If pneumatic otoscopy is performed the tympanic
membrane will have poor compliance (Figure 31)
Figure 31: Dull right tympanic membrane with visible fluid level
(Courtesy of Elef-ENT)
Investigations
Pure tone audiogram – this will reveal a conductive hearing loss
(i.e. air bone gap on PTA)
Tympanometry will show a flat trace due to the reduced
compliance of the tympanic membrane (i.e. ‘type b’ curve)
In an adult with a unilateral middle ear effusion ensure that
flexible nasoendoscopy (FNE) is performed to rule out a
nasopharyngeal tumour
Treatment
Antibiotics are not advised as they have no benefit in OME
Watch and wait – 50% of OME will resolve spontaneously within
3 months
Hearing aid may be useful whilst waiting for the OME to
spontaneously resolve
Myringotomy and ventilation tube insertion. This is a small
incision in the tympanic membrane with the insertion of a small
ventilation tube. Once inserted, the grommet will usually self
extrude after around 9 months. Grommet insertion can lead to
tympanosclerosis (scarring of the tympanic membrane) and
tympanic membrane perforation (if the TM fails to heal after the
grommet extrudes N.B. more common if history of multiple
grommet insertion)
Adenoidectomy may reduce the recurrence rate of OME
Chronic Otitis Media
Description
There are two types of chronic otitis media:
Mucosal: A tympanic membrane perforation in the presence of

recurrent or persistent ear infection.
Squamous: Gross retraction of the tympanic membrane with
formation of a keratin collection. (cholesteatoma)
The disease may be active (infection present) or inactive (no

infection present):
Inactive mucosal: Dry perforation

Inactive squamous: Retraction pocket, which has the potential to
become active with retained debris (keratin)
Active mucosal: Wet perforation with inflamed middle ear
mucosa and discharge
Active squamous: Cholesteatoma
Mucosal Chronic Otitis Media

Epidemiology
May occur in children and adults

Causes
Chronic infection following development of a post-infective,
traumatic or iatrogenic perforation
Pathogens: most commonly Pseudomonas aeruginosa,
Staphylococcus Aureus
Symptoms
Hearing loss
Otorrhoea
Signs
Mucosal inactive: Dry perforation (Figure 32)

Mucosal active: Wet perforation with middle ear inflammation
Otorrhoea: May be present in active disease
May develop secondary otitis externa due to the discharge
Figure 32: Right TM perforation (Courtesy of Elef-ENT)
Complications
As for acute otitis media.
Investigations

Ear swab for MC&S
Treatment
Aural toilet with microsuction ensuring that the whole tympanic

membrane is visualised
Antibiotic and steroid combination ear drops if infection is
present
Myringoplasty (also known as Type 1 tympanoplasty). This is
the surgical repair of the tympanic membrane perforation using
cartilage or fascia. It is indicated to prevent recurrent otitis
media.
Cholesteatoma
Description
Despite the name, a cholesteatoma is neither a tumour nor does it
consist of cholesterol. Instead, it is an accumulation of benign
keratinizing squamous cells which most commonly involves the
middle ear. The squamous cells are hyperproliferating and secrete
enzymes, which can be locally destructive (with potentially serious
complications). It is commonly described as ‘skin in the wrong
place’.
Epidemiology
Can occur in both children and adults but it usually has it’s origins in
childhood chronic Eustachian tube dysfunction although congenital
cholesteatoma accounts for around 5% of cases (see below). It is
more common in males.
Causes
Congenital cholesteatoma results from persistent epithelial cell rests
left within the middle ear during growth of the embryo and is
diagnosed in children who have an intact tympanic membrane and
no history of ear surgery
Acquired cholesteatoma develops after birth. Eustachian tube

dysfunction results in tympanic membrane retraction and once the
retraction is deep enough keratin migration from the tympanic
membrane to the external auditory canal can no longer occur and
the trapped keratin develops into a cholesteatoma. Keratin debris
can become infected and leads to a chronic ear discharge
Symptoms
Persistent/recurrent ear discharge despite topical antibiotics
Unilateral hearing loss
Signs
Otoscopy should be performed and micro suction should be
used to clear any wax to ensure that the whole TM is visualised
paying particular attention to the superior part of the TM (attic
area)
There is a deep retraction pocket in the TM with keratinous
debris within it. There may be granulations around the margins
of the retraction pocket and it is very common for adjacent bony
erosion to occur
If there is secondary infection there will be discharge in the ear
canal
In congenital cholesteatoma, the tympanic membrane is usually
intact but it may be bulging and a white pearly mass will be
visible through the tympanic membrane
Figure 33: Active squamous chronic otitis media in left ear: attic
retraction with retained squamous epithelial debris (cholesteatoma)
(Courtesy of Elef-ENT)
Complications
As per acute otitis media (see above)
Investigations
CT scan of the temporal bone
Treatment
Surgical management unless the patient is not fit for surgery
The aim of surgery is to remove the cholesteatoma sac and
repair the tympanic membrane and any adjacent bony defect, to
prevent recurrent discharge. The mastoid cavity is drilled to
allow access to the middle ear and all of the cholesteatoma is
removed. If there has been destruction of the ossicles, hearing
can be reconstructed (ossiculoplasty) using a variety of
techniques and the tympanic membrane is replaced with a graft
Rhinology
Nasal Function and Anatomy
Nasal Function
The primary function of the nose is ventilation.
Other functions include:
Humidification of inspired air and dehumidification of expired air

Heating or cooling of inspired and expired air
Filtering of large matter by vibrissae (small hairs) in the nasal
vestibule
Olfaction and pheromone detection
Mucus production (mucociliary escalator: mucus traps
particulate matter and carries it as far as the pharynx, where it is
swallowed and then eliminated by the digestive system)
Immune protection – lysosomes, immunoglobulin A (IgA), IgG
and nitric oxide
Ventilation of middle ear cleft via Eustachian tube
Drainage of nasolacrimal duct
Voice tract resonance
Nasal Anatomy
The anatomy of the nose can be subdivided into the external nose
and the internal nasal cavity and paranasal sinuses.
The external nose is attached to the forehead by the nasal bridge

and extends towards a free tip. The anterior openings are called the
nares or nostrils. The nares are bounded medially by the nasal
septum. The skeleton of the external nose consists of bone in the
upper third (nasal bones) and cartilages (upper and lower laterals
and septum) in the lower two thirds.
Clinically Important Point

The skin overlying the cartilaginous portion of the external nose
contains multiple pilosebaceous glands. Rhinophyma (see Figure
34) is a pathological hypertrophy of the glands, which results in an
enlarged, red bulbous nose. It begins with rosacea, which worsens
to acne rosacea. It is more common in white men between the age
of 40 and 60 years of age.
Figure 34: Rhinophyma in an elderly man (reproduced with

permission from Otolaryngology Houston, www.ghoryeb.com)
The Nasal Cavity

The nasal cavity extends from the nares anteriorly, to the choanae
posteriorly. The midline is partitioned by the nasal septum (see
Figure 35), which itself consists of structures including the maxillary
crest inferiorly and perpendicular plate of the ethmoid bone
superiorly and vomer posteriorly. The nasal septum is rarely in the
midline, but when significantly deviated, it can contribute to nasal
obstruction, particularly if the deviation is anterior.
Each half of the nasal cavity has a roof, floor, lateral and medial
wall. The roof is formed by the body of the sphenoid, cribriform plate
of the ethmoid, frontal bone, the nasal bone and the nasal cartilages.
The floor is formed by the maxilla, palatine bone and upper surface
of the hard palate. The medial wall is illustrated opposite.
Figure 35: Bony and cartilaginous septum. (reproduced with
The lateral wall of the nasal cavity consists of a series of bony

projections called turbinates (See Figure 36 below). The turbinates
are covered by pseudostratified ciliated columnar epithelium and
contain venous plexuses, which can engorge in response to external
stimuli, neural and hormonal control. They have a role in humidifying
and filtering inspired air.
Figure 36: Left Inferior turbinate as viewed with the rigid endoscope.
There are four major openings into the internal nasal cavity:
Sphenoidal air cells drain into the spheno-ethmoidal recess.

The posterior ethmoid sinuses drain into the superior meatus.
The anterior ethmoid sinuses, fontal sinus, and maxillary
sinuses drain into the middle meatus.
The nasolacrimal duct drains into the inferior meatus.
The olfactory nerve arises in the olfactory mucous membrane

adjacent to the cribriform plate. The trigeminal nerve provides
general sensation through the ophthalmic and maxillary divisions
with nerve endings distributed throughout the mucosa.
The arterial supply to the nasal cavity is derived from branches of the
internal carotid artery (anterior and posterior ethmoidal arteries) and
external carotid artery (facial artery, sphenopalatine artery).
The arteries involved in the Little’s area (which lies in the antero-
inferior part of the nasal septum) are the following:
Anterior ethmoidal artery (from the ophthalmic artery)

Sphenopalatine artery (from the maxillary artery)
Greater palatine artery (from the maxillary artery)
Superior labial artery (from the facial artery)
Epistaxis
It is not a trivial condition and can potentially be life threatening. If
the patient is actively bleeding, see them in A&E Resus, not in an
isolated treatment room without resuscitation facilities/help.
History
You may have to take a focused history whilst simultaneously
resuscitating and stabilising the patient (establishing intravenous
access, sending off the pertinent bloods and setting up IV fluids).
Important points to remember are:
Unilateral Predominance- which side did it start or more

commonly comes from, which can then focus your assessment
for the likely source.
Anterior/Posterior – often patients can tell initially if it runs out
the front first or down the back of the throat, which may guide
further management
Frequency – how often is it troubling them?
How much blood loss has occurred – estimating blood loss can
be notoriously difficult and bleeding from the nose can be very
distressing. By focusing on common measures such as a
teaspoon, a cupful, or a kidney dish full of blood can help
prioritise your patient’s resuscitation requirements.
Co-morbidities such as hypertension, cardiac history, anti-
coagulant use and previous nasal surgical history can all have
an effect on patient management.
Antecedents – traumatic bleeding can have a different
anatomical source to other forms of bleeding
Management techniques, risk factors, smoker, occupation,
allergy to nuts
Examination
Most epistaxis occur in Little’s Area (otherwise known as
Kisselbach’s plexus), located in the anterior part of the septum
where an anastomosis occurs between the branches of the internal
and external carotid arteries.
Initial management options for epistaxis include leaning forwards

and pinching the soft part of the nose to apply pressure to the
septum (not the bony part of the nasal bridge - Figure 37 and Figure
38). Sucking on ice cubes or applied to the forehead may help slow
bleeding by causing vasoconstriction of the feeding vessels. The
next step should ideally be identification of the bleeding point for
cautery (see Cautery in Practical Procedures Chapter)
Figure 37: Incorrect method of pinching the nose.

Figure 38: Correct method of pinching the nose
Surgical Management of Epistaxis

If these measures fail to control the bleeding (or bleeding from more
posteriorly in the nasal cavity is responsible), an endoscopic
sphenopalatine artery ligation under general anaesthesia is
undertaken (see Figure 39).
Traumatic epistaxis (for example from a sports injury) is usually
anterior and related to the anterior ethmoidal artery. Ligation of this is
often performed through an external incision at the medial aspect of
the orbit.
When dealing with acute traumatic injuries of the nose, it is important

to rule out a septal haematoma (Figure 40), which can starve the
underlying septal cartilage of oxygen and cause ischaemic necrosis
and cartilage loss, resulting in a saddle nose. It is therefore important
to drain these at an early opportunity.
Trauma to the front of the nose may cause one or both nasal bones
to be displaced. Assessment of any nasal vault deformity should be
made after 5 days once the swelling has subsided. There is a
window of opportunity in the weeks after the injury for the nasal
fracture to be reduced under local or general anaesthetic.
When the cartilaginous septum is fractured, deformed or displaced it

may be corrected with a septoplasty (cartilage remodelling)
procedure.
Figure 39: An endoscopic clinical photograph of the right

Sphenopalatine artery being clipped in the back of the nose under
general anaesthetic for epistaxis. 2 clips have been applied to the
main branch.
Nasal obstruction
Causes of Nasal Obstruction
There are a number of causes for nasal obstruction, many of which
are beyond the scope of this chapter. More common, acquired
causes of nasal obstruction can be classified as seen below. A
thorough history, good clinical examination and tailored
investigations will often reveal the underlying aetiology:
Infectious – viral; bacterial or fungal infections causing

rhinitis/rhinosinusitis
Allergy – inflammation with or without nasal polyps
Developmental - resulting in septal deviation, bony deviation or both;
cleft lip
Traumatic – same as above (+/- septal haematomas, perforations,
etc)
Iatrogenic – previous surgery (eg septoplasty) causing scar tissue
(adhesions); residual septal deformities; mucocoeles
Drugs – chronic use of decongestants (rhinitis medicamentosa); side
effects of medication (eg. Beta-Blockers, oral contraceptive pill);
cocaine abuse resulting in vasculitis or septal perforation
Neoplastic – benign or malignant masses
Inflammatory/Systemic Diseases – eg. Granulomatosis with
Polyangiitis (GPA); Eosinophilic Polyangiitis (EPA/Churg-Strauss);
Sarcoidosis; Cystic Fibrosis; Kartaganer’s Disease
Fractured Nose
Nasal fractures do not need to be X-rayed.
If the patient is well and there is no epistaxis and no septal

haematoma (a boggy swelling of the septum which is usually seen
bilaterally and insensate when probed with a jobson-horn- see
Figure 40) they can be sent home.
If there has been no change in shape and no new nasal obstruction

since the injury the patient does not need to be seen by ENT and
can be discharged with advice.
However, if the swelling and bruising are such that any deformity is
obscured, then they should be reviewed in 5-7 days (once the
swelling has subsided) in the ENT emergency clinic for assessment
of the injury and discussion as to whether the patient wants to
proceed to manipulation under anaesthetic.
The patients will need to be consented and listed for an MUA

(manipulation under anaesthesia- Figure 41) after seeing them in the
SHO emergency clinic. The common risks for the procedure include
pain, bleeding, the need to pack the nose, the need to wear a splint,
bruising and failure to get the nose back to its original shape.
If the clinician is confident, however, and the patient will tolerate it, a
manipulation under local anaesthetic can be undertaken. Using a
dental syringe infiltrate over the nasion down to bone and then either
side of the nasal bones. Then firm pressure over the deformity will
usually result in the bones being realigned into the midline. Patient
selection is key to a successful procedure. They will need to wear a
splint for 1 week which can be removed by the patient themselves or
their GP practice nurse.
If a septal haematoma is present, the patient must have this drained

(in theatre) as soon as possible to prevent infection and subsequent
destruction of the septal cartilage. This will lead to saddle deformity
of the nose. They will need to be started on antibiotics to prevent
secondary infection of the haematoma causing a septal abscess.
Figure 40: Septal Haematoma after nasal trauma. This requires

urgent drainage to avoid complications such as abscess and septal
cartilage necrosis.
Figure 41: Pre-operative image of trauma resulting in significant
nasal deformity.
Septoplasty/Septorhinoplasty
When the underlying midline cartilaginous or bony septum is
deviated, a septoplasty can be undertaken to remodel and improve
the functional nasal airway. It is often performed under general
anaesthesia, as a day-case procedure. It can also be performed to
gain better access to the nose for other endoscopic procedures e.g.
limited access for epistaxis surgery or for septal cartilage harvest for
graft harvesting.
A septorhinoplasty may be indicated if the septum and bony vault

are deviated. This operation can be carried out via an external
approach (via an incision in the columella) or endonasally. It can be
performed for functional and cosmetic indications, and has important
implications for both, so patients require appropriate pre-operative
counselling.
Both of these procedures, if indicated, are not done acutely after the
nasal injury and would be done on an elective list often 6 -12 months
after the initial injury.
Rhinitis and Rhinosinusitis
Description
The term ‘rhinitis’ describes inflammation of the lining (mucous
membranes) of the nose, characterized by nasal congestion, a runny
nose, sneezing, itching and post-nasal drip. It can be usually divided
into allergic and non-allergic causes.
The term ‘rhinosinusitis’ describes inflammation of the lining of the

nose and paranasal sinuses. It has a number of manifestations, the
commonest symptoms being anterior or posterior rhinorrhea (runny
nose or post-nasal drip), nasal blockage/congestion or obstruction,
and facial headache or reduction in sense of smell.
Allergic Rhinitis
Description
IgE-mediated Type 1- hypersensitivity reaction of the nasal mucosa.
This condition can significantly affect quality of life with negative
impacts on activities of daily living, school and work attendance.
Epidemiology
Allergic rhinitis (AR) is common and increasing in western
populations. It can be associated with atopic disease such as
eczema and asthma (1 in 3 patients with AR have asthma). There
can be a family history noted.
Causes
Intermittent (previously known as seasonal)- e.g. grass/tree
pollen (hay fever) – late Spring/Summer.
Persistent (previously known as perennial)- e.g. house dust
mite, moulds, dogs, cats
Food allergens causing rhinitis – this is a controversial area and
not fully proven but may be a contributory factor
Symptoms
Rhinorrhoea (seasonal)
Nasal irritation /itching (seasonal)
Sneezing (seasonal)
Nasal obstruction (seasonal and perennial)
Ocular symptoms e.g. itchy/watery eyes
Signs
Inflamed nasal turbinates and mucosa- bluish and pale hue to
turbinate mucosa, watery nasal discharge and gross turbinate
hypertrophy
Investigations
Clinical diagnosis can be made with a combination of history &
examination
The mainstay of investigation is the skin-prick allergy test (SPT),
which can be done cheaply and quickly in clinic. Positive
(histamine) and negative (saline) controls are inserted into the
skin (dermis), along with solutions of the various common
inhaled aero-allergens (Figure 42), eg grass and tree pollen,
dog and cat dander. A positive result is a wheal response after
20 minutes (Figure 43). Resuscitation equipment should be
ready in case of anaphylaxis. Contra-indications include severe
eczema/dermatographism or anaphylaxis. Patients should avoid
taking anti-histamine tablets for 72 hours prior to the test in case
they mask a response.
Serum RAST (Radio-allergosorbent test) is a blood test to find
specific IgE to an allergen. There is no risk of anaphylaxis, but
this is more expensive and takes time for the results. This may
be also useful in children who may not tolerate SPT.
Figure 42: Skin Prick Allergy Testing (SPT) Droplets of various
allergen solutions are placed onto the forearm and the skin is
punctured
Figure 43: After 15-20 minutes the results can be shown by the
positive wheal reaction
Treatment
General advice- avoiding allergen exposure. E.g. washing bed
linen at high temperature to reduce house dust mite allergen
burden
Nasal douching and barrier ointments/creams
Oral non-sedating antihistamine, eg. Loratidine, Cetirizine,
Fexofenadine
Intra-nasal steroids e.g. Fluticasone (Flixonase or Avamys nasal
spray), Beclomethasone (Beconase Nasal spray), or
Mometasone (Nasonex Nasal spray) - 1 – 2 sprays, once or
twice a day titrated to the patient’s symptoms for a minimum of
4-6 weeks. Check formulary for appropriate prescribing ages.
Intra-nasal steroid sprays are suitable for long-term use if
tolerated. Escalation to steroid drops or oral steroids can be
considered on rare occasions for severe symptoms, but caution
must be taken over longer courses due to the numerous
systemic side-effects.
Combination steroid and anti-histamine nasal sprays (eg.
Dymista manufactured and distributed by Mylan®) – prescribed
by specialists as 2nd line topical management for more effective
relief in allergic rhinitis due to the synergistic combination of
medications.
Leukotriene antagonists e.g. montelukast, (orally) useful if
patients also have asthma
Immunotherapy- Desensitisation therapy works by gradually
increasing the exposure to an antigen. It can be given sublingual
or via subcutaneous injection. Immunotherapy to grass pollens
and house dust mite is available in a few specialist centres.
Non-Allergic Rhinitis
Description
Inflammation of the nasal mucosa.
Epidemiology
Very common. Up to 50% of all cases of rhinitis in adults
Causes
Irritants: tobacco, pollution, cleaning products (occupational)
Vasomotor: temperature changes- especially cold, dry air
Gustatory: Spicy food
Pharmacological: rhinitis medicamentosa (rebound nasal
congestion following prolonged use of topical decongestants),
substance abuse- cocaine
Infection
Systemic- Granulomatosis with polyangitis (GPA), sarcoidosis.
Physiological- exercise, positional, hormonal
Atrophic rhinitis
Symptoms
Nasal congestion, rhinorrhea, post-nasal drip, hyposmia
Signs
Nasal congestion and hypertrophic turbinates
Investigations
Allergy testing to exclude allergic cause
Treatment
Non-surgical treatment. Non-surgical treatment should always be
tried and is the mainstay of treatment.
General advice- avoidance of trigger, eg smoking cessation.

Nasal douches and intranasal steroids
Other: Ipratropium. Decongestants (short-term only)
Surgical treatment
Surgery is not a permanent, curative procedure as the

underlying pathology is to do with the lining of the nose.
However, surgery may help improve the nasal airway and allow
better delivery of topical nasal steroids, which the patient will
need to continue postoperatively.
Turbinate reduction surgery for obstructing inferior turbinates.
Vidian Neurectomy – cutting the parasympathetic nerve supply
to the nose (rarely indicated).
Acute Rhinosinusitis (ARS)
Description
Acute rhinosinusitis (ARS) is caused by symptomatic inflammation of
the mucosal lining of the nasal cavity and paranasal sinuses.
There is sudden onset of two or more symptoms, one of which should

be either nasal blockage/obstruction/congestion or nasal discharge
(anterior/posterior nasal drip):
± facial pain/pressure
± reduction or loss of smell; for <12 weeks
Epidemiology
An average child is likely to have 6-8 colds (ie, upper respiratory tract
infections) per year, but only approximately 0.5-2% of upper
respiratory tract infections in adults and 6-13% of viral upper
respiratory tract infections in children are complicated by the
development of acute bacterial sinusitis. Therefore, antibiotics should
be prescribed sparingly (see below for indications).
Causes
Most commonly ARS is viral i.e. a common cold caused by
Rhinovirus, Coronavirus, Parainfluenza virus or Respiratory
Syncytial Virus (RSV).
Streptococcus pneumonia, Haemophilus influenzae and
Moraxella Catarrhalis account for the majority of bacterial
causes.
Symptoms
Main symptoms are nasal obstruction and coloured discharge
Facial pain occurs more commonly in the acute presentation of
rhinosinusistis
Hyposmia/ anosmia (reduced/absent smell)
Ask about pain elsewhere. e.g. dental infections can spread into
the sinus
Systemic features of fever and malaise
Double sickening (deterioration after an initial milder phase of
illness), which may indicate acute post-viral rhinosinusitis or
bacterial rhinosinusitis.
Signs
Facial tenderness can occur but is uncommon
Anterior rhinoscopy- inflammation, discharge
Nasendoscopy - pus discharging from sinus openings e.g.
middle meatus (Figure 44)
Figure 44: Mucopurulent discharge from the Right Middle Meatus
(Sinus Drainage pathway) may be indicative of bacterial infection.
(NS) Nasal septum, (MT)Middle Turbinate, (IT) Inferior Turbinate.
Complications
Intracranial: meningitis, cavernous sinus thrombosis, intracranial
abscess (rare)
Associated with severe, sudden onset headache, vomiting &
photophobia
Extracranial: Osteomyelitis, orbital or pre-septal cellulitis, orbital
abscess
Investigations
Bloods: FBC for WBC, CRP,blood culture only if very ill or other
comorbidity
If complicated/not responding…
Swab for microscopy, culture and sensitivity
High definition CT scan with contrast, of sinuses and brain if
above complications occur. Intra orbital complications are a
surgical emergency as vision can be threatened in the presence
of intra orbital sepsis (see Figure 45)
Figure 45: Evidence of a sub-periosteal abscess secondary to
sinusitis causing right eye proptosis, peri-orbital swelling, chemosis
and loss of the pupillary reflexes. Urgent surgery is required to reduce
pressure on the optic nerve.
Treatment
If symptoms less than 5 days and mild:
Analgesia and nasal saline irrigation

Fluid rehydration
Nasal decongestant e.g. xylometazoline or Pseudo-ephidrine for
period of 1 week only.
If symptoms are persistent after 10 days or worsening after 5 days;
As above
Topical intranasal steroids
If severe (at least 3 of: discoloured discharge, severe local pain,

fever, elevated ESR/CRP, double sickening)
Broad-spectrum antibiotics for 7days. e.g. amoxicillin

Topical intranasal steroids
If recurrent or chronic symptoms, refer to an ENT specialist for further

management, and possible endoscopic sinus surgery.
Chronic Rhinosinusitis (CRS)
Description
Inflammation of the nasal mucosa and paranasal sinuses for
>12 weeks.
Can be divided into CRS with polyps or CRS without polyps.
Epidemiology
Common. CRS accounts for 85% of outpatient visits for
rhinosinusitis in adults.
Can follow ARS.
Causes
Multifactorial and still not fully understood:
Allergic: Intermittent or Persistent.
Other non-allergic causes – Occupational, Hormonal,
Granulomatous/ Inflammatory, Infective (Viral, Bacterial,
Fungal), Anatomical, Iatrogenic, secondary to medication (eg.
Rhinitis Medicamentosa/Cocaine abuse)
Symptoms and Signs

The European Position Paper on Rhinosinusitis and Nasal Polyps
(EPOS 2012) defines the diagnostic criteria for CRS below:
Inflammation of the nose & sinuses causing 2 or more

symptoms
Nasal blockage/obstruction/congestion
Nasal discharge (ant/post nasal drip)
+/- facial pain/pressure

+/- reduction/loss smell
And either:
Endoscopic signs of polyps, middle meatal oedema or

mucopurulent discharge
CT mucosal changes of the ostiomeatal complex/sinuses
Investigations
CT Sinuses. Can assess the extent of disease and provide
anatomical detail for pre-operative planning (see Figure 46).
Figure 46: CT Scan in coronal section showing bilateral maxillary
sinusitis. R = Right side. Disease is worse on the left hand side
mostly in the maxillary sinus and there is hypertrophy of the left
inferior turbinate (reproduced with permission from Otolaryngology
Treatment
Non-operative. Appropriate medical management should be
attempted primarily, including:
Saline Nasal Irrigation

Nasal decongestants (short course only)
Anti-histamines (if there is an underlying allergic component)
Oral steroids with CRS with polyps – (caution with side effects),
followed by topical therapy
Topical Steroids with CRS without polyps-
Drops include: betamethasone or fluticasone (A typical
regime might be for a period of 4-6 weeks)
Then switch onto maintenance intra-nasal cortico-steroid
spray (INCS) such as fluticasone or mometasone for 3
months until review.
Antibiotics – Certain antibiotics may help by their anti-bacterial
and anti-inflammatory mechanisms. The true benefit of
antibiotics in CRS is undergoing evaluation by ongoing trials.
The EPOS guidance suggests macrolides are useful in non-
polyp CRS when the IgE levels are not raised and the
cardiac history has been taken into account due to possible
effects on prolongation of the QT interval (e.g.
Clarithromycin 500mg OD PO for 3 weeks).
In polyp patients, the antibiotic of choice is Doxycycline (50-
100mg OD PO for 3 weeks) if tolerated.
Local formulary guidance should be sought if patients are
allergic to first line options.
Operative: Functional endoscopic sinus surgery (FESS).
The principles of FESS are to remove diseased tissue, relieve

obstructions and to restore the normal function and anatomy of
the paranasal sinuses. Often it can involve removing the bony
septae obstructing the sinus outflows whilst preserving mucosa,
to widen the sinus drainage pathways and increase access for
subsequent topical medical therapies.
Sinus surgery should be seen as an adjunct in the management
of CRS where medical treatment alone has failed, rather than
stand alone definitive treatment.
Patient selection is key, and quality of life screening tools such
as the SNOT-22 (Sino-Nasal Outcome Test of 22 questions) can
help identify appropriately symptomatic patients who may gain
benefit from surgery.
Nasal Polyps
Description
Nasal polyps are very common and are typically bilateral. They
typically present with symptoms of nasal blockage with or without a
change in smell perception. They are benign. They include:
Inflammatory/Allergic Polyps – sino-nasal polyposis, often

multiple grey, oedematous polyps associated with CRS (see
Figure 47)
Antro-choanal polyp – single polyp arising from maxillary sinus
extending out towards nasopharynx causing unilateral nasal
obstruction.
Figure 47: Clinical photograph of left nasal cavity showing

inflammatory nasal polyps arising from the sinus drainage pathway
(Middle Meatus) blocking nasal airway
Treatment
Medical
Medical treatment involves some form of steroid-based treatment
combined with nasal saline rinses. If there are no contra-indications,
a typical regime might consist of a short course of oral steroids
(Prednisolone 0.5mg per kg PO for 7 days with PPI cover), followed
by intra-nasal steroid drops for 4-6 weeks, and subsequently a
maintenance intra-nasal corticosteroid spray (INCS) such as
Mometasone until further review.
There is some evidence from the EPOS guidance that certain

antibiotics are of added benefit if the levels of IgE in the serum are
not raised (eg. Doxycycline).
Surgical
The principles of surgery for CRS with polyps are to establish good
access for further medical treatment, when medical therapy alone
has failed. Simple endoscopic nasal polypectomy or Functional
Endoscopic Sinus Surgery (FESS) is usually performed under
general anaesthesia and aims to remove the polyps and re-establish
the natural drainage pathways of the paranasal sinuses. The extent
of surgery will be governed by disease factors, patient factors and
the experience of the operating surgeon.
When consenting patients for surgery, certain risks should be

included such as pain, infection, bleeding, the need to pack the
nose, intra-cranial complications (CSF leak and meningitis), intra-
orbital complications (double vision/blindness) and possible
recurrence of polyps/sinus disease.
Other Sinonasal Lesions
Benign lesions
Papilloma/Wart – verrucous lesion, commonly in nasal vestibule,
often multiple and painless, presents with bleeding. Local
excision is mainstay of treatment
Pyogenic Granuloma – friable lesion that bleeds, usually from
trauma often arising on septum. Commoner in pregnancy
Other rarer pathology can have the appearance of a “unilateral
nasal polyp” during nasal examination. Examples include
Inverted Papilloma – benign but locally aggressive polyp that
has a predisposition for recurrence if not completely cleared
including its site of origin. Can rarely transform into malignancy
over time (see Figure 48)
Juvenile Nasopharyngeal Angiofibroma (JNA) – vascular benign
tumour exclusively present in adolescent males (may have
hormonal element). These are extremely rare but classically
present with nose-bleeds and nasal obstruction in teenage boys.
Embolisation and subsequent surgical removal (endoscopic or
open depending on extent) is the mainstay of treatment.
Meningoencephalocoele/glioma – herniation of intracranial
contents through a weakness in skull-base containing
meninges, brain (rarely functioning) or support tissue. Imaging
with MRI needed before biopsy.
Figure 48: Inverted papilloma right nasal cavity arising from lateral
wall of nose
Malignant
Sino-nasal malignancies are rare but present late, resulting in a poor
prognosis. Presenting symptoms include unilateral nasal obstruction,
unilateral glue ear, bleeding, pain, neck lumps, unexplained weight
loss, eye symptoms, headaches or cranial nerve deficits. The
commonest are squamous cell carcinomas (see Figure 49 and
Figure 50), adenocarcinomas (associated with wood-working) and
nasopharyngeal carcinomas (arising from the nasopharynx)
Imaging and histology are essential and the results are discussed in
a multi-disciplinary team meeting, where recommendations for which
treatment is best suited for the patient can be made.
Treatment can be curative or palliative and may include surgery,

chemotherapy (drugs), radiotherapy (ionizing radiation) or a
combination of these. Nasopharyngeal cancers are commonly
treated with radiotherapy or chemoradiotherapy.
Figure 49: SCC of the Left Maxillary Sinus
Figure 50: Endoscopic image of SCC Left Maxillary Sinus

Cleft Lip and Palate
Description
A cleft is a gap or split in the upper lip and/or roof of the mouth
(palate) resulting in an abnormal connection between the oral and
nasal cavity. A cleft lip and palate is the most common facial birth
defect in the UK, affecting around one in every 700 babies.
It can range in severity from a submucous cleft (the muscles of the

soft palate not fully joining) which may be relatively asymptomatic to
a bilateral cleft lip and palate with immediate concerns at birth
regarding airway and feeding.
It can be an isolated occurrence or associated with other genetic and

developmental abnormalities.
Important Considerations
Feeding – poor suction, lengthy feeds, nasal regurgitation,
excessive air intake, poor airway protection and expending too
much energy can cause failure to thrive. Bottles with special
nipples can help improve this.
Otologic – high incidence of glue ear and delayed resolution
(poor Eustachian tube function secondary to abnormally
developed palate muscles predisposes to middle ear effusions)
means hearing assessment early on is a priority with onward
referral for grommets or hearing aids.
Speech/Swallow – speech and language therapy to combat
problems with palate dysfunction and reflux
Cosmetic – lip and nasal deformities will require addressing
within 1st year of life and revision often required later as patient
grows
Dental – restoration / prosthesis may be required for normal
function and cosmesis
Psychology, Social Work & MDT – parental counselling and
assistance is important starting pre-natally and ongoing
throughout childhood. Paediatricians are often well placed to
help co-ordinate global development.
Figure 51: Unilateral left cleft lip and palate (Courtesy of Elf-ENT)
Head and Neck
Head and Neck Anatomy
As medical students and junior doctors, being able to apply anatomy
in a clinical context is important. You do not need to have an in depth
knowledge of complex head and neck anatomy. Instead, being able
to grasp the basic anatomy to inform your examination skills and
interpretation of findings is more advisable.
Facial Muscles
Muscles develop from the second arch mesoderm and are attached
to the dermis and arranged into sphincters, dilators and muscles of
facial expression. The groups can be subdivided into muscles of
mastication (nervous supply: trigeminal nerve) and muscles of
expression (nervous supply: facial nerve).
Orbicularis Oris
A complex muscle which encircles the mouth

Contraction of this muscle narrows the mouth and closes the
lips
It is most evident when performing the act of whistling
Buccinator
This quadrilateral muscle forms the muscular component of the

cheek. It lies between the mandible and the maxilla
It is the deepest muscle of the face
It acts to prevent accumulation of food between the teeth and
cheek
Clinically important points:
The temporalis muscle is covered by tough fascia. This fascia

can be used to repair a perforated tympanic membrane
(myringoplasty)
The masseter is the most powerful muscle of mastication owing
to the multipennate arrangement of its fibres
The lateral pterygoid muscle is the only muscle of mastication
which is attached to the temporomandibular joint
The facial nerve has a long course from the brainstem to
innervate the muscles of facial expression. Damage of this
nerve results in facial weakness. Supranuclear lesions (e.g.
stroke) spare the forehead, usually due to bilateral innervation.
Infranuclear lesions produce a lower motor neuron paralysis
with both upper and lower facial muscles- there is typically
unilateral weakness.
Paralysis to the orbital muscles occurs when there is damage to
the facial nerve. Ptosis results with secondary consequences of
exposure keratitis and corneal surface ulceration
Inability to form facial expression on one side of the face can be
the first sign of facial nerve damage
Blood Supply to the Face and
Neck
External Carotid is a branch of the common carotid artery, which
gives off several branches in the neck
Mnemonic: “Some Anatomists Like Freaking Out Poor Medical

Students!” describes the branches of the external carotid from most
inferior to superior aspect:
Superior thyroid artery (Anterior branch)

Ascending pharyngeal artery (Ascending branch)
Lingual artery (Anterior branch)
Facial artery (Anterior branch)
Occipital artery (Posterior branch)
Posterior auricular artery (Posterior branch)
Maxillary artery (Terminal branches)
Superficial temporal artery (Terminal branches)
Clinically Important Points
The common carotid bifurcates at the level of the superior

border of the thyroid cartilage
The carotid sinus (baroreceptor) and carotid body
(chemoreceptor) are located at the bifurcation
The internal carotid artery has no branches. In surgery, at least
2 or more branches from the external carotid artery should be
identified to distinguish it from the internal carotid artery when
considering ligating the external carotid artery
The Major Salivary Glands
Parotid Gland
Large serous salivary gland anterior and inferior to the ear. Saliva is
drained via the Stenson duct which lies superficial to the masseter.
After piercing through the buccinators, it enters the oral cavity
opposite the 2nd upper molar tooth
Submandibular Gland
Mixed serous and mucous salivary gland. Closely related to and
indenting the mandible
Forms majority of saliva when not eating. The gland drains into the
floor of oral cavity via Wharton’s duct, one to either side of the
frenulum
Sublingual Gland
Mucous gland. It drains via multiple openings into the submandibular
duct and sublingual fold in the floor of the oral cavity.
Oral Cavity
The main function of the oral cavity is to provide the ability for
satisfactory mastication, including formation of a food bolus, drinking
and breathing. Speech is also an important function.
Dentition
Adults have 32 teeth and children 20 (milk teeth). Teeth are
important for mastication. They require saliva to ensure they remain
healthy. Dental health can be affected by a variety of problems, not
least a poor diet, smoking and alcohol. Poor oral health can have
adverse consequences on general health. Complications of dental
disease include submandibular abscesses, deep neck space
abscesses and are part of the differential diagnosis of acute tonsillitis
and peritonsillar abscesses.
The oral cavity is bounded by (Figure 52):
Anteriorly by the lips

Posteriorly by the palatoglossal arches (anterior pillars of the
fauces)
Laterally by the teeth and cheeks.
Inferiorly by the floor of mouth and mylohyoid
Superiorly by the hard palate
Figure 52: Oral cavity (reproduced with permission from
Nerve Supply of the Tongue
Clinically Important Points
The surface of the tongue is covered with 3 types of coarse

papillae called filiform, fungiform (which contain taste buds) and
circumvallate papillae (which are aligned in V shaped formation
dividing the anterior 2/3rds of the tongue from the posterior 1/3
of the tongue)
The apex of the circumvallate papillae (foramen caecum)
represents the embryological site of the thyroid gland. A lingual
thyroid may present as a mass in this area if there is failure of
migration
Unilateral hypoglossal nerve palsy will result in deviation of the
tongue towards the affected side with associated muscle
atrophy.
Ludwig’s angina is a necrotising cellulitis+/- abscess formation
of the floor of mouth, which can extend into the neck and can be
caused by dental root abscesses. It's most dangerous
complication is a potentially life threatening airway obstruction
due to the swelling within the mouth/neck.
Topography of the Neck
The regions are described as levels and assigned a roman numeral.
It is particularly useful when describing the location of a neck lump.
These levels can be divided into subdivisions but for the purposes of
this handbook we have not discussed this.
Figure 53: Levels of the neck (courtesy of Elf-ENT)
The neck can also be divided into anterior and posterior triangles.
The anterior triangle is bounded superiorly by the mandible, laterally
by the sternocleidomastoid muscle and medially by the midline. The
posterior triangle is bounded anteromedially by the
sternocleidomastoid, inferiorly by the clavicle and posteriorly by
trapezius muscle
Fascial Layers of the Neck
Superficial layer- This layer forms a thin sheet of fascia that encircles
the platysma muscle.
Deep Layer consists of 3 separate layers:
Investing layer (external) (Figure 54)- It splits to invest the

trapezius, sternomastoid and parotid, and its deeper layer
invests the great vessels to form the carotid sheath.
Pretracheal layer (visceral) (Figure 55)- covers the salivary
glands, muscles, thyroid gland and other structures located in
front of the trachea
Prevertebral layer (internal) (Figure 56)- covers the prevertebral
muscles. The interval between the pharynx and the prevertebral
fascia is called the retropharyngeal space
Figure 54: Investing layer of fascia (Image courtesy of Elef-ENT)

Figure 55: Visceral layer of fascia (Image courtesy of Elef-ENT)
Figure 56: Prevertebral layer of fascia (Image courtesy of Elef-ENT)

Nervous Supply of the Head
and Neck
Physiology of Swallowing
1. Oral Stage (voluntary)
Oral preparatory - Food bolus is formed and held in the anterior part
of the oropharyngeal cavity. The oral cavity is closed posteriorly by
the soft palate and tongue to prevent leakage into the pharynx
Oral Propulsive - The dorsum of the tongue gradually propels the

food bolus to the back of the oral cavity
2. Pharyngeal Stage (involuntary-

CNIX)
The soft palate elevates and closes the nasopharynx at the same
time as the bolus comes into the pharynx- this prevents bolus
regurgitation into the nasal cavity
The larynx is closed, elevated and tucked under the base of the
tongue to prevent aspiration.
The pharyngeal constrictor muscles contracts from top to the bottom,
squeezing the bolus inferiorly
3. Oesophageal Stage
The food bolus enters the upper oesophageal sphincter, which
includes the cricopharyngeus muscle. This muscle relaxes at the
arrival of the food bolus
Peristalsis propels the food bolus at a rate of 4cm/s towards the
lower oesophageal sphincter which also relaxes
Gravity aids peristalsis in the upright position
Figure 57: Swallowing Physiology
Taking History of a Neck Lump
Opening
How old are you?
What do you do for a living?
Why have you come to see me today?
History of Presenting Complaint

What made you notice the lump?
How many lumps have you noticed?
Where do you notice the lump?
Has the lump changed in size?
Is the lump always there or does the lump come and go?
How long have you had the lump?
Associated symptoms
Has the lump been painful at all?
Any sore throat?
Have you had any difficulties swallowing?
Have you had painful swallowing?
Have you had any problems with breathing?
Any coughs or colds?
Have you noticed any blood?
Have you noticed any weight change?
Have you had any ear pain?
Have you noticed any sweating at night/ temperatures?
Has your voice changed?
Past Medical and Surgical History - to
include:
Have you had any previous investigations for this neck lump
Have you received any treatments for this lump
Medication and Allergies

Do you take any regular medications?
Are you allergic to anything?
Social History
Ask about smoking & quantify
Ask about drinking alcohol and quantify
Red Flag Symptoms for urgent

referrals (with or without a neck lump)
Unexplained neck lump that has changed over a period of 3- 6
weeks
Hoarse voice > 3weeks
New onset dysphagia
Unexplained persistent swelling in the salivary glands
Otalgia > 4 weeks and normal otoscopy
Unexplained persistent sore or painful throat
Non healing ulcers
White or red lesion in the mouth or oropharynx
Causes of Neck Lump
Commonest aetiology of
lymphadenopathy relative to age
Child / young adult: inflammatory > congenital > neoplastic
Adult: inflammatory > neoplastic > congenital
Older adult: neoplastic > inflammatory
Branchial Cysts
Description
These present as upper neck masses in young adults, often in the
third decade of life. They represent epithelial inclusions within lymph
nodes.. They sometimes become infected. In middle aged and older
adults consider cystic masses to be oropharyngeal or thyroid cancer
metastasis until proved otherwise
Investigations
Neck ultrasound and fine needle aspiration cytology (FNAC). Cross
sectional imaging is usually performed as well.
Treatment
Surgical excision.
Dysphagia
Description
Dysphagia is difficulty in swallowing
History
Establish the level of dysphagia (pharynx, upper, mid or lower
oesophagus
Is it dysphagia mainly to solids, liquids, saliva?
Ask about associated symptoms such as
Hoarseness
Odynophagia (painful swallowing)
Otalgia
Regurgitation
Gastrointestinal bleeding
Weight loss
Are the symptoms progressing?
Ask about risk factors for cancer of oesophagus & pharynx e.g.
smoking and alcohol excess
Refer to General Skills in ENT for notes on neck and thyroid
examinations and oral examination.
Causes of dysphagia
Extraluminal (external pressure on the pharynx and oesophagus)
Neck mass (e.g. retrosternal goitre)

Vascular abnormalities (e.g thoracic aortic aneuryism, double
aortic arch)
Any type of mediastinal mass eg secondary cancer
Lung cancer
Intramural Causes (pharyngeal/ oesophageal)

Motility problems
Motor neuron disease/ Multiple sclerosis
CVA
Achalasia
Oesophageal spasm
Pharyngeal pouch
Benign/malignant stricture
Candidiasis
Intraluminal Obstruction (oesophageal)
Foreign body
Oesophageal or pharyngeal cancer
Candidiasis
Oesophageal web/Plummer-Vinson syndrome
Investigations
FBC- may show iron deficiency anaemia
Chest radiograph
CT or MRI Scan of the neck (mainly if suspecting malignancy)
Barium swallow
Panendoscopy which includes laryngoscopy and upper
oesophagosopy
Dynamic investigations (e.g. video fluoroscopy if investigating
motility disorders)
Dysphonia
Description
Dysphonia means hoarseness. It is disorder characterised by altered
vocal quality, pitch, loudness or vocal effort that impairs
communication.
Causes
Malignant e.g. squamous cell carcinoma
Benign e.g. vocal cord nodules, papillomas, or cysts
Neuromuscular e.g. Vocal cord palsy
Trauma e.g. surgery, intubation, excess use
Endocrine e.g hypothyroidism
Infective e.g. laryngitis, candida (inhaled corticosteroids may
predispose to this)
Iatrogenic e.g. recurrent laryngeal nerve palsy secondary to thyroid
surgery
Functional e.g. muscle tension dysphonia
Investigations
Flexible nasendoscopic examination of the larynx is an essential
investigation that can be done in clinic
Blood tests as appropriate e.g. thyroid function tests
Treatment
Treatment depends on the underlying cause.
Patients with dysphonia and red flag symptoms should be
considered for urgent referral to ENT.
Red flags in patients with dysphonia
History of smoking and alcohol use
Concomitant neck mass
Unexplained weight loss
Accompanying neurological symptoms
Accompanying haemoptysis, dysphagia, odynophagia, otalgia.
Hoarseness that is persistent and worsening (rather than
intermittent)
Hoarseness in an immunocompromised patient

Tonsillitis
Description
Tonsillitis is an infection of the palatine tonsils. It may be bacterial or
viral.
Epidemiology
Acute tonsillitis is most common in children and young adults.
The causative agents are mostly viral (70%) and to a lesser
extent bacterial (30%). As a result, antibiotics are typically not
efficacious in the majority of cases.
Group A beta hemolytic streptococci is the most common cause
of bacterial tonsillitis. Other bacterial examples include
Haemophilus influenza, Streptococcus pneumonia and
Staphylococci- the latter being more associated with
dehydration and previous antibiotic use.
Symptoms
Sore throat
Odynophagia (painful swallowing) and dysphagia
Earache
Systemic upset: Malaise and headache
Viral tonsillitis may present with milder symptoms
Signs
Pyrexia
Swollen tonsils +/- exudate
Thick or ‘hot potato’ voice with enlarged tonsils
Presence of trismus indicates a peritonsillar abscess (quinsy)
Bilateral cervical lymphadenopathy
Figure 58: Acute Tonsillitis illustrating white follicles on the tonsils

(reproduced with permission from Otolaryngology Houston,
www.ghoryeb.com)
Figure 59: Left Sided Peritonsillar Abscess (Quinsy) (reproduced
with permission from Otolaryngology Houston, www.ghoryeb.com).
Natural history
Resolves after 5-7 days, may recur after symptom free interval
Complications
Peritonsillar abscess (quinsy)- severe, usually unilateral pain,
“hot potato” voice, trismus, and uvula pushed to opposite side
by peritonsillar swelling (see figure 53)
Parapharyngeal and retropharyngeal abscesses- potentially life
threatening complications of tonsillitis. They may present with
non-resolving sore throat, systemic upset, neck stiffness and
neck tenderness
Investigations
FBC, U&Es, glandular fever screen, CRP, Blood cultures (if
pyrexial)
Treatment of acute tonsillitis

Regular IV/PO analgesia e.g. paracetamol and ibuprofen
Topical Analgesia e.g. Benzdyamine (Difflam)
Fluid resuscitation (important, these patients are often
dehydrated from not drinking adequate fluid)
Antibiotics
Use the Centor Criteria to guide this decision. There is a 50%
chance of the tonsillitis being bacterial if:
Pus on tonsils (tonsillar exudate)

Pyrexia
No cough
Tender cervical lymph nodes
Antibiotics should be given to those who meet 3 or 4 criteria.
Penicillin V (phenoxymethypenicllin), 500mg QDS for 10 days.

Erythromycin is an alternative in penicillin allergic patients. Avoid
amoxicillin- this causes a rash if the patient has glandular fever due
to type IV hypersensitivity.
Tonsillectomy
The following are recommended as an indication for tonsillectomy for
recurrent acute sore throat (SIGN 2010):
Sore throats are due to acute tonsillitis

Episodes of sore throat are disabling and prevent normal
functioning
7 or more well documented episodes of significant sore throats
in the preceding year or
5 or more such episodes in each of the preceding 2 years or
3 or more such episodes in each of the preceding 3 years
Postoperative care and complications of a tonsillectomy are

discussed in further detail in the “ENT Operation” chapter of this
handbook.
Pharyngeal Pouch
Description
Also known as Zenker’s diverticulum, this is an out-pouching of the
mucosa and submucosa in the pharynx. It occurs between 2
muscles (cricopharyngeus and thyropharyngeus) of the upper
oesophageal sphincter on the posterior pharyngeal wall in an area of
weakness termed Killian’s dehiscence.
Epidemiology
More common in elderly men.
Uncommon- incidence is approximately 2/100,000 per year in
the UK.
Cause
Aetiology is unknown
However, one theory of pathogenesis describes incoordination
between opening of cricopharygneus and peristaltic contractions
propagating the bolus through the hypopharynx
Symptoms
May be asymptomatic if small
Progressive dysphagia
Sensation of lump in throat
Regurgitation of undigested food
Halitosis (bad breath due to stasis of undigested food in pouch)
Recurrent chest infections due to aspiration
Signs
Gurgling
Halitosis
Usually no signs, with normal ENT examination
Investigations
Barium swallow is the definitive investigation.
Rigid oesophagoscopy may be useful to exclude carcinoma of
the pouch wall.
Management
If asymptomatic- conservative management.
If symptomatic, particularly if risk of aspiration and recurrent
pneumonia- endoscopic stapling is the first line. If not
appropriate for endoscopic management, open approaches may
be used. Division of the cricopharyngeus is important in
resolving the pathological abnormality causing the pouch.
Figure 60: Zenker's Diverticulum(reproduced with permission from
Globus Pharyngeus
Description
This is the sensation of a lump, discomfort or foreign body in the
throat without an obvious cause. It is a diagnosis of exclusion, linked
to stress or anxiety and a form of somatization. It is associated with
laryngopharyngeal reflux (30%), cricopharngeal spasm and
oesophagitis. It is a very common presenting symptom to an ENT
clinic.
Investigations
Thorough ENT examination including flexible
nasopharyngolaryngoscopy to rule out other causes. If there is a
history of smoking or excess alcohol consumption, consider a barium
swallow, CT scan or upper GI endoscopy to exclude oesophageal
pathology (as the post-cricoid region can be difficult to examine on
clinical examination)
Treatment
Reassurance, lifestyle advice, and optimal anti-reflux therapy
Thyroid Masses
The commonest presentation of thyroid disease is the presence of a
thyroid mass. These can also cause compressive symptoms such as
dyspnoea or dysphagia.
Investigations of thyroid masses

First line imaging is ultrasound of the neck to risk stratify thyroid
lesions and look for malignant cervical lymphadenopathy.
This can distinguish whether a patient has a solitary thyroid
nodule or a suspicious nodule within a multinodular goitre.
Suspicious features on ultrasound include solid hypoechogenic
nodules with microcalcifications, irregular margins, taller than
wider, and lymphadenopathy. Ultrasound scans are graded U2
(benign) to U5 (malignant); U3 and U4 are equivocal and need
further investigation (see below)
Suspicious nodules should undergo ultrasound guided FNAC
(fine needle aspiration cytology). This can diagnose papillary
carcinoma but cannot distinguish follicular adenoma (benign)
from follicular carcinoma therefore the entire nodule must be
assessed (by performing a diagnostic hemithyroidectomy).
Follicular carcinoma has perivascular or pericapsular invasion
which can only be detected by histology rather than cytology
(which is what FNAC is).
Thyroid function tests
Thyroglossal cyst or sinus
Description
Cyst of epithelial remnants of the thyroglossal tract
Epidemiology
Most commonly in children. But 1/3 present in over-20s.
Most common congenital cyst in neck.
Associated with ectopic thyroid. May also contain ectopic (and
very rarely the only) thyroid tissue
Cause
Embryological remnant of thyroglossal tract during descent of
the thyroid from the foramen caecum at the tongue base
Thyroid descends with intimate contact to central portion of
hyoid bone to end as a bilobed structure connected by an
isthmus at the level of the second and third tracheal cartilages.
The tract is normally resorbed in utero
Symptoms
Often asymptomatic.
May enlarge/become tender in upper respiratory tract infections
May become infected, form an abscess or discharging sinus
Signs
Palpable neck lump, small, midline. Can occur anywhere
between base of tongue and trachea
Usually in proximity to the hyoid bone
Moves up on tongue protrusion and swallowing
Complications
If infected and ruptures, there is a risk of discharging sinus formation
Investigations
USS +/- Fine needle aspiration cytology. Delineates anatomy and
demonstrates normal thyroid gland. Must ensure that thyroid gland is
present. Removal of the only thyroid tissue in thyroglossal cysts
renders patient hypothyroid.
Treatment
Most require no treatment unless there are complications e.g
recurrent infections. Surgical treatment (Sistrunk’s procedure) entails
excision of cyst, thyroglossal tract and central portion of hyoid bone.
Multinodular goitre
Epidemiology
Commonest cause of goitre in the western world
Cause
Unknown aetiology. Occurs as a result of continuous change in
thyroid activity as part of its role in homeostasis. Patients are almost
always euthyroid. Pathologically can be hyperactive or atrophic
Symptoms
Neck lump which can be asymptomatic
Cosmetic deformity
If very large- pressure symptoms. e.g. breathlessness,
orthopnoea, dysphagia
If cyst ruptures/haemorrhage into cyst- pain and acute swelling
Signs
Palpable/visible neck lump- neck lump moves on swallowing
Multiple nodules, irregular. May be one dominant nodule
Dullness on percussion of manubrium in retrosternal goitre
Complications
Mass effect/compression, cosmetic appearance
Nodule haemorrhage. Presents with acute pain and neck
swelling
Thyrotoxicosis-related complications
Investigations
Blood tests- TSH. Consider free T4 and FBC
Thyroid US +/- Fine needle aspiration cytology
CT scan neck and chest if concerns of retrosternal extension.
Pulmonary function tests can show obstructive pattern.
Treatment
Depends on the cause.
Non-operative
Watch and wait
Anti-thyroid drugs +/- beta-blockers if hyperthyroid (usually
under the care of the endocrinologist)
Operative
If mass effect or suspicion of cancer. Replacement thyroxine
required afterwards if total thyroidectomy performed plus/minus
calcium (parathyroid gland function may be impaired temporarily
or permanently)
Thyroid cancer
The incidence of thyroid cancer in the UK has increased with time
(approximately 3.4 cases per 100,000) but the mortality has
remained consistently low (0.4 per 100,000). It is more common in
women and risk factors include radiation exposure and family history.
The order of prevalence is papillary, follicular, medullary, anaplastic
thyroid cancer, as well lymphoma of the thyroid gland.
Thyroid cancers are staged using ultrasound of the neck to look at

the size, lymph nodes, and the presence of metastasis. Non-
contrast CT/MRI may be used in selected cases.
Thy Classification of Thyroid Nodules

Thyroid nodules undergo further cytological classification, which is
called THY, which is related to risk of malignancy. All patients should
be discussed at a thyroid multi-disciplinary meeting which includes
an ENT surgeon, oncologist, radiologist and histopathologist.
THY1: non diagnostic due to lack of cellularity.

THY2: non-neoplastic.
THY3: follicular lesion. Patient should undergo surgical resection of
the nodule (lobectomy) to distinguish between a follicular adenoma
and carcinoma (as cytology insufficient to assess perivascular or
pericapsular invasion). If histology confirms carcinoma, patient
should undergo completion thyroidectomy.
THY4: Suspicious but non-diagnostic of malignancy. Surgery is
indicated as there is a 60-75% risk of malignancy. If the results are
non-diagnostic and medullary carcinoma or lymphoma are
suspected, then the FNAC should be repeated.
THY5: Diagnostic of malignancy
MDT will recommend appropriate combination of surgery +/-
radiotherapy +/- chemotherapy if indicated
Papillary and Follicular Thyroid
Cancer
Summary of Papillary & follicular thyroid cancers management
Thyroid MDT to recommend treatment in the form of a thyroid

lobectomy (<1cm diameter papillary or low-risk follicular) or total
thyroidectomy (>1cm papillary or high risk follicular carcinoma)
A neck dissection is considered if pre-operative imaging has
established metastatic cervical lymphadenopathy. Papillary
thyroid cancer is known to metastasise to the cervical lymph
nodes early, so if neck nodes are negative on preoperative
imaging, a selective level 6 / 7 neck dissection may be
therapeutic in around 20% of patients, and may reduce the need
for postoperative radio-iodine therapy
The MDT recommendation for postoperative radioiodine (iodine-
131) ablation is individualized, but generally it has proven
survival benefit in patients with differentiated thyroid cancer >
1.5cm. Ablation eradicates all thyroid cells including residual
microscopic disease. Its risks include a small risk of second
malignancy as well as dry mouth or sialadenitis.
Levothyroxine (T4) will both replace thyroid function, and
suppress TSH which reduces the chance of recurrence
Follow up required with measurement of thyroglobulin (acts a
tumour marker) at least 6 weeks postoperatively and
ultrasound/FNAC if indicated
Medullary thyroid carcinoma

Medullary thyroid cancers originate from the parafollicular cells (C
cells) of the thyroid. Middle-aged patients are most commonly
affected. It is the 3rd most common thyroid cancer and it represents
5% of all thyroid cancers. 80% are sporadic. Hence, 20% are
inherited- there are 3 inherited syndromes:
FMTC: familial medullary thyroid cancer

MEN 2A: MTC, phaechromocytoma, hyperparathyroidism
MEN 2B: MTC, phaechromocytoma, Marfanoid habitus,
mucosal neuromas
Investigations
USS neck & FNA

Tumour markers (calcitonin and carcinoembyronic antigen) as
well as genetic screening (RET proto-oncogene in both MEN 2A
and 2B). A urine sample (24 hours urine metanephrine) study
can be used to assess for phaeochromocytoma (which is
important to assess prior to potential surgical intervention)
Treatment
Treatment is surgical (total thyroidectomy and neck dissection) in
confirmed cases of medullary thyroid cancer. Prophylactic surgery
can be considered in children with MEN syndromes.. Radioiodine
cannot be used as there is no iodine uptake (since the cancer is of
neuroendocrine cells and not follicular cells).
Anaplastic thyroid cancer

Anaplastic thyroid carcinoma is a rare and aggressive
undifferentiated thyroid cancer. It represents 1% thyroid cancer and
has a tendency to affect the elderly.
It presents as a rapidly enlarging bulky, hard, neck mass. Appears

over 2-3 months. Diagnosis often requires an ultrasound guided core
biopsy or open biopsy rather than FNA. Prognosis is extremely poor
and treatment is mostly palliative.
Thyroid lymphoma
This is a rare cancer and mostly consists of diffuse large B cell
lymphomas (DLBCL). The only known risk factor is Hashimoto’s
thyroiditis. It presents as a rapidly enlarging goitre with compressive
symptoms. Diagnosis is confirmed on core biopsy or open biopsy
(FNA unreliable). Treatment is chemotherapy +/- radiotherapy as per
lymphoma regimens guided by oncology team.
Benign and Malignant
Neoplasms of the Salivary
Glands
Description
Neoplasms of salivary glands represent 3-6 % of all head and
neck neoplasms.
The parotid gland accounts for about 80% of salivary gland
tumors and the majority (80%) are benign.
The submandibular and sublingual glands account for about
20% of salivary gland tumors and the incidence of malignancy is
higher.
The commonest ‘benign’ tumours are pleomorphic adenomas.
Malignant transformation is seen in 2-5 % of cases.
The commonest malignant tumours are mucoepidermoid
carcinoma or metastases from skin primaries in some
populations e.g. in Australia.
Epidemiology
Pleomorphic adenomas are more common in women. Malignant
neoplasms have an equal sex distribution.
Symptoms
Slowly growing painless mass
Facial palsies suggest malignancy.
Red Flags
Hardness
Rapid growth
Tenderness
Infiltration of surrounding structures
Overlying skin ulceration
Facial weakness
Figure 61: Pleomorphic adenoma of the parotid gland (reproduced

with permission from Otolaryngology Houston, www.ghoryeb.com)
Summary of the Commonest Benign

Salivary Tumours
Summary of Malignant Salivary
Tumours
Carcinoma of the Oral Cavity
Description
Carcinomas of the oral cavity can affect the lips, tongue, floor of the
mouth, alveolar ridge, hard palate or buccal lining
90% of these carcinomas are squamous carcinomas (SCC).
Epidemiology
Typically seen in the middle age or older male patient
Increasingly seen in women (due to increased smoking in this
demographic group)
Risk Factors
Multifactorial
Smoking
Alcohol
Betel Nut (particularly in the Indian subcontinent population)
Chronic dental infection
Immunosuppression
Symptoms
Painless ulcer or lump. Pain is a late symptom
Increasing size of the tumour can affect speech and swallowing.
Signs
Painless swelling.
Discoloration
Red, erythematous, velvety mucous membrane (erythroplakia)
which is strongly associated with malignancy
White (leukoplakia) or mixed red/white lesions (speckled
leukoplakia)
Lichen planus
Non healing ulcer
Neck swelling if metastases are present
Carcinoma of Lip
Remains one of the most curable carcinomas in the head and

neck
Sun exposure is a well-established link
Lower lip is hence most affected – 89%
Risk factors: male, fairer skinned patient and older patient
Treatment
Smaller tumours- excision and primary closure

Larger tumours- local skin flaps for reconstruction
Carcinoma of the Oral Tongue
Incidence rate is increasing in younger adults

Lateral border of tongue is most commonly affected, and most
commonly in anterior 2/3 tongue.
Often presents with a persisting ulcer
Treatment
Smaller tumours. Surgical excision.
Advanced cancer- resection of primary lesions, neck dissection
and post-operative radiotherapy. Sometimes reconstruction with
flaps is needed with larger tongue resections Chemotherapy
(for e.g. cisplatin) may be used in conjunction with surgery and
radiotherapy
Treatment goals in carcinoma of the

oral cavity
Multidisciplinary team management approach
Long term control of the cancer with preservation of cosmesis
and function of the oral cavity
Factors affecting choice of treatment

Staging of tumour (TNM classification most commonly used)
Extent of resection necessary
Method of reconstruction
Carcinoma of the Pharynx
Carcinoma of the pharynx can be subdivided into the following
regions:
Nasopharynx
Oropharynx
Hypopharynx
Figure 62: Divisions of the pharynx
Risk factors
Multifactorial
Smoking
Alcohol
Virus- Human Papilloma Virus (oropharynx), Ebstein Barr Virus
(EBV, Nasopharynx)
Radiation
Carcinoma of the Nasopharynx
Description
This is a rare tumour of the postnasal space. Highest incidence in
the South Asian and North Asian population. EBV is believed to
have a major causative role in this carcinoma.
Symptoms/Signs
Cervical lymphadenopathy.
Ear pain, secretory otitis media, hearing loss and cranial nerve
palsies.
The nasal involvement can present with epistaxis*, discharge,
changes in smell and nasal obstruction
Persistent unilateral otitis media with effusion and no preceding
URTI
Epistaxis in a young adult may be secondary to “juvenile

nasopharyngeal” angiofibroma. The majority arises in the lateral wall
of the nose of young males. This is a benign but locally invasive and
highly vascular rare tumour. If suspected a biopsy should not be
carried out. Diagnosis is by imaging. Management of choice is
surgical resection – if the lesion is unresectable then radiotherapy
may be used.
Investigation
Detailed Head and Neck exam
Nasendoscopy
Formal biopsy
FNA of any neck nodes
Imaging
MRI (better to assess soft tissue involvement)
CT (better to assess bony involvement)
Management
Combined chemotherapy and radiotherapy.
Carcinoma of the Oropharynx
Tumours of the tongue base (posterior third of the tongue) and the
tonsils (or tonsillar fossae if the tonsils have been previously
removed). 70% of tonsillar carcinomas are SCC and minority are
lymphomas.
Risk factors
Smoking
Alcohol
Strong association with HPV 16 and HPV 18
Incidence rate is increasing in younger adults , particularly in
non smokers due to the increasing incidence of HPV related
carcinomas
Symptoms
Painless tonsillar swelling (unilateral)
History of throat discomfort with worsening dysphagia
Referred otalgia (involvement of Arnold’s nerve- branch of
vagus)
A ‘lump in the throat sensation’ or evidence of metastatic
cervical lymphadenopathy; jugulodigastric lymphadenopathy is
often present
Trismus is a red flag for surrounding structure infiltration
Investigation
A detailed Head and Neck Exam.
Panendoscopy + Biopsy
FNA of any neck nodes
Imaging: MRI to delineate the margins of tumour. Staging CT
neck and chest/ abdomen.
Treatment
Surgery +/- radiotherapy or chemotherapy
Chemoradiotherapy
Carcinoma of the Hypopharynx
Hypopharyngeal cancers are named for their location. Most cancers
arise in the pyriform sinus. Virtually all malignant tumours are of SCC
origin. Metastases are very common from the primary site. Patients
are typically men aged 55-70 years old with a history of tobacco use
and/or alcohol use.
Symptoms
Cervical lymphadenopathy, pain that radiates from the throat to
ear, sore throat, progressive difficulty with or painful swallowing,
voice changes
Paterson- Brown- Kelly syndrome: dysphagia , hypochromic
microcytic anaemia, oesophageal webs and potential
development of postcricoid carcinoma
Investigation
Endoscopy
Biopsy
Pharyngo- oesophagoscopy
Imaging
Barium swallow
MRI
Staging CT neck and chest/abdomen
Management
Early cancers (rare)- surgery + radiotherapy.
Advanced cancers- surgery + radiotherapy +/- neoadjuvant
chemotherapy
Many hypopharyngeal cancers are incurable at presentation and
best supportive care may be the most appropriate option for
management
Carcinoma of the Larynx
The larynx is subdivided into 3 components.
Supraglottis: from tip of epiglottis to laryngeal ventricle
Glottis: true vocal folds and 1cm inferiorly
Subglottis: down to lower border of cricoid cartilage
Laryngeal carcinoma can be subdivided into supraglottic (27%),

glottic (69%) and subglottic (4%). Glottic cancer is the most
common. Histology is squamous cell origin in 90% .
Figure 63. Left glottic squamous cell carcinoma- encroaching on the

anterior commissure (reproduced with permission from
Epidemiology
More common in males and elderly
In younger population male: female ratio closer to 1:1.
Risk factors
Smoking (most important)
Alcohol consumption (cumulative risk increases with smoking)
Symptoms
Hoarseness is the most common presentation overall, and
commonest in glottic cancer. Progressively worsening over 6- 12
weeks
Noisy breathing/stridor. Late presentation in supraglottic cancer
Cough. Haemoptysis.
Odynophagia
Dysphagia (commonest in supraglottic carcinoma)
Neck lymphadenopathy (commonest in supraglottic carcinoma)
Investigations
Oral cavity, ENT and neck examination
Flexible nasoendoscopy
Microlaryngoscopy for biopsy
CT neck and chest for staging
MRI neck and PET CT occasionally indicated
TNM classification to stage disease
Treatment
Depends of the TNM staging of the tumour. Decisions made in
multidisciplinary (MDT) team meeting
For smaller tumours (T1 and T2) treatment is single modality
with options being radiotherapy or endoscopic laser excision.
Larger tumours (T3 and T4);
Multimodality which may be either larynx sparing
(Chemoradiotherapy) or larynegectomy with postoperative
radiotherapy
Laryngopharygeal reflux (LPR)
Description
LPR describes a group of upper respiratory tract symptoms
secondary to irritation from gastric contents.
Symptoms
The commonest symptoms are hoarseness, throat clearing, chronic
cough, globus pharygeus and dysphagia. Symptoms of indigestion
and heartburn are poorly correlated with LPR.
Diagnosis
The Reflux Symptom Index (RSI) is a commonly used self-report
patient questionnaire. A score of >13 signifies LPR.
Visualisation of the larynx using a fibreoptic laryngoscopy or video

laryngostroboscopy may demonstrate laryngeal (or specifically vocal
cord) oedema or erythema, posterior commissure hypertrophy or
thick endolaryngeal mucus. Laryngeal granulomas or pseudosulci
are commonly linked to LPR but the evidence to support this is
weak.
The Reflux Finding Score (RFS) is an objective measure that takes

into account the above physical findings, with good sensitivity but
low specificity. A score of >7 indicates LPR
The gold standard for diagnosing LPR is 24 hour dual probe pH

manometry combined with intraluminal impedance studies.
Transnasal oesophagoscopy (TNO is an investigation increasingly

used to exclude other causes for these symptoms by inspecting the
entire oesophagus. This can be performed readily in the outpatient
setting.
Treatment
Conservative measures include lifestyle modification. This
includes
Avoiding eating three hours prior to going to sleep
Stopping smoking and reducing alcohol intake
Addressing obesity
Avoid fizzy drinks
Avoiding throat clearing
Speech therapy can help as well as acid suppression using alginates

or proton pump inhibitors. Alginates are seaweed compounds that
has been proven to reduce reflux. Proton pump inhibitors are widely
prescribed although there is little high quality or statistically
significant evidence to support their use. Failure of medical therapy
warrants referral to a gastroenterologist or upper GI surgeon for
further investigations and management.
Snoring and Obstructive Sleep
Apnoea (OSA)
Snoring implies upper airway resistance that causes an undesirable
sound during sleep that affects up to 50% of the population.
However, OSA is associated with apnoea (breath-holding for >10
sec leading to arousal from sleep) or hypopnea (reduced airflow with
oxygen desaturation). Not all snorers have OSA but most patients
with OSA snore.
It affects 1-4% of adults, more commonly men, and is classified

using the apnoea-hypopnea index (AHI) as mild (5-15), moderate
(16-30) or severe (>30)
The consequences of untreated OSA include neurocognitive

impairment, type 2 diabetes, cardiovascular disease (hypertension,
coronary artery disease / infarction, heart failure, stroke, pulmonary
hypertension) and increased mortality.
Cause
In children, the most common cause are large tonsils and adenoids.
However other causes affecting airway anatomy/physiology should
be looked for (e.g. large tongue, muscle hypotonia in Downs
syndrome)
In adults it is predominately multifactorial. A raised body mass index

is not uncommon but consider each potential anatomical level that
may obstruct airflow
Nasal obstruction – e.g. obstructive nasal polyps

Oropharynx – large tonsils
Pharyngeal airway collapse: obesity
Symptoms
OSA can manifest with different symptoms but the diagnosis should
be considered with witnessed breath-holding / gasping / choking,
restlessness, daytime sleepiness and irritability. Take a history from
the patient and their partner if applicable. It is not uncommon
nowadays for parents/partners to use a mobile phone to film the
patient’s pattern of sleep.
Diagnosis
A detailed history is required.
ENT examination including:
Measuring BMI
Neck circumference
Maxillofacial structures (including pro/retrognathia and
oropharyngeal crowding from a large tongue / uvula / tonsils or
elongated palate)
Flexible nasopharyngolaryngoscopy to assess anything that
may obstruct the passage of airflow from the nasal cavity to the
level of the vocal cords.
The Epworth Sleepiness Score (a self-reported patient

questionnaire) is often used to screen for excessive daytime
sleepiness (abnormal score is >10)
The gold standard for diagnosis of OSA is nocturnal

polysomnography which can record upper airway airflow oxygen
saturation monitoring, ECG, EMG, EEG, and body position.
Treatment
Conservative measures include lifestyle modification. This includes
Weight loss
Avoiding excessive alcohol
Adapt sleeping position for adults (supine causes the tongue to
fall back)
Nasal Dilators or Oral appliances such as a mandibular
advancement device that pushes the mandible and tongue
forwards
Noninvasive ventilation such as CPAP that prevents airway
collapse by splinting
Medications for nasal obstruction due to rhinitis or sinus disease

include intranasal corticosteroids, decongestants (short term use)
and saline douches.
Surgical measures address the underlying anatomical level of

obstruction, which may be multi-level and thus require a thorough
work-up and planning.
In children this commonly includes adenotonsillectomy, which is

highly effective.
In adults, surgery may be considered if the patient fails conservative

measures or as an adjunct to conservative measures in the setting of
moderate to severe OSA. Patient selection for surgical intervention is
crucial and obese patients tend to be poor candidates for surgery.
Operations for adult OSA include palatal surgery, tonsillectomy,

septoplasty or endoscopic sinus surgery. However none have a good
evidence base for effectiveness and surgical intervention, particularly
nasal surgery should be undertaken with caution and careful
preoperative counselling.
ENT Emergencies
Acute Airway Obstruction
Description
Acute airway obstruction is an emergency.
Causes
In adults, this can be classified into Infectious and Neoplastic.
The common infectious causes include supraglotitis and deep
neck space infections. Neoplastic conditions are most
commonly head and neck cancers e.g. tongue base,
orophaygenal or laryngeal tumours
In children, infection (e.g. croup, epiglottitis) or foreign bodies
are more common. Congential causes should also be
considered e.g. laryngomalacia, subglottic stenosis etc.
Symptoms
Shortness of breath/noisy breathing particularly on inspiration
(stridor)
Stridor can be classified into inspiratory, expiratory or biphasic.
Inspiratory suggests obstruction is between glottis and
supraglottis, expiratory suggests the obstruction is below the
carina and biphasic suggests the obstruction is between the
glottis/subglottic. This is only a guide, not diagnostic!
Change in voice
Cough
Signs
Tachypnoea
Agitation/cyanosis
Respiratory distress. There will be use of accessory muscles
Facial/airway trauma
Listen for type of breathing sounds
Snuffle- nasal obstruction; important in children
Stertor- “sounds like snoring” which suggests pharyngeal
obstruction
Stridor (as described above)
Wheeze- level of obstruction is intra-thoracic trachea or small
airways. May occur in anaphylaxis
Decreased breath sounds- indicates acute
decompensation/fatigue
Complications
Respiratory arrest
Airway compromise must be recognised early. Children may
decompensate rapidly
Investigations
Investigations are secondary to immediate management.
Imaging should not be performed in unstable patients.
Nasendoscopy, if safe to perform, can help identify the cause
Investigations which agitate patients may risk precipitating total
loss of airway e.g. epiglottitis in children
Treatment
Initial airway management is similar for all patients. Specific
management depends on the aetiology.
Senior help early- ENT, anaesthetics, paediatrics (if child).
Oxygen, or Heliox if available (79% helium and 21% oxygen).
Lower density of heliox improves airflow
Nebulised adrenaline. 1mL of 1:1000 adrenaline in 4 mL saline.
Steroids. Nebulised and IV. 0.1mg-0.2mg/kg dexamethasone.
Effect is usually delayed.
If condition fails to improve/worsens- consider further
management (this will be orchestrated by seniors):
Intubation. Secures airway. Awake fibreoptic intubation can be
useful.
Nasopharyngeal airway may bypass obstruction if obstruction is
high (e.g. swollen tongue secondary to angio-oedema)
Tracheostomy. Front of Neck Access to the airway to bypass the
obstruction may be necessary either by cricothyroidotomy or
tracheostomy.
Summary of the Important Airway

Pathologies
Epistaxis (Nose Bleed)
Figure 64: Little areas on the left nasal cavity (reproduced with
History
Epistaxis is a common ENT emergency. Unless urgent
management is required, a good history is essential.
When did it begin? Was trauma a trigger?
How much blood? Try to quantify.
Where?
Which nostril? Does it change, or always that side?
Blood coming out of nose only (Anterior epistaxis likely), or also
trickling back and being swallowed (likely posterior bleeding)?
Risk factors/causes
Local
Trauma/foreign body/nasal sprays
Infection
Previous nasal surgery
Systemic
Drugs- warfarin, aspirin, NOAC (novel oral anticoagulants e.g.
apixaban), Substance abuse e.g. cocaine.
Coagulopathies. Bleeding elsewhere? Heavy periods?
excessive bruising ?
Pregnancy
Hypertension.
Liver/renal/EtOH
Hereditary Haemorrhagic Telangiectasia (HHT)
Management
Management depends on the urgency of the situation. If active
bleeding- is the patient haemodynamically stable or unstable?
Stable patients and those without active bleeding:
Examine for bleeding source. Use headlight and Thudicum’s

speculum. Aid visualisation with: suction & adrenaline-soaked
cotton wool
Apply simple pressure for 10 minutes. Head should be tilted
forward. Fingers pinching septum over Little’s area bilaterally
(not bony part of nasal bridge!)
Next, try chemical cautery to bleeding point (usually Little’s
area) with silver nitrate sticks. Do not apply this bilaterally as this
risks septal perforation from septal ischaemia
Unstable patients, or stable patients for whom above measures fail:
Get senior help early and manage according to the ALS

algorithm
Give oxygen and suction of any obstructing clots as appropriate
Obtain iv access, take bloods and fluid resuscitate. Patient
needs to be admitted
A high BP will require treating
Perform anterior nasal packing (unilateral or bilateral - see
Practical Procedures Chapter)
Perform posterior nasal packing if bleeding persists. Examples
include a Foley catheter being passed intranasally & then the
balloon being inflated so it the inflated balloon lies against the
back of the septum in the postnasal space. The patient will also
require an anterior pack at the same time.
If bleeding continues, the patient will most likely need surgery.
Examples include: Ligation of (in order of increasing severity):
sphenopalatine artery, anterior ethmoid artery, maxillary artery,
external carotid artery.
In certain cases, it may be appropriate to consider interventional
radiology embolization.

Foreign body in the nose
A foreign body in the nose is more common in children. Foreign body
examples include beads, peas, nuts and sweets. This presentation
can be dangerous if the foreign body is inhaled into the airway
causing airway obstruction. In particular, if the foreign body is a
battery (button battery) this can quickly erode nasal mucosa and
cartilage leading to septal perforation.
Figure 65: Foreign body (screw) in the nose of a child.
Symptoms
Unilateral nasal discharge (often offensive if present for a while)
Nasal obstruction
Irritability in infants
Management
Try positive pressure through mouth (can be done by the
parents)
Examine with the Thudichum’s speculum. Earwax hook or
alligator forceps may be used to extract the foreign body. Avoid
pushing the FB further back
Removal under GA
Nasal septum haematoma
Figure 66: Right sided septal haematoma
Description
A septal haematoma is blood which collects between the
perichondrium and septal cartilage. There is an increased risk of
devascularisation of the septal cartilage and this can lead to
necrosis, perforation and deformity.
Presentation
Usually due to nasal trauma. Associated with nasal bone
fracture.
Can be unilateral or bilateral (usually bilateral).
Complications
Abscess formation
Septal perforation leading to saddle-nose deformity
Management
Ensure the patient is stable and any head injury is managed
appropriately.
The patient needs an urgent incision and drainage under
general anaesthetic . A delay in surgery risks permanent
deformity
Antibiotic cover
Foreign body in the ear
Figure 67: Foreign body in the ear (reproduced with permission from
A foreign body in the ear is more common in children. However,

broken ends of cotton bud ends or pieces of tissue can be found in
the embarrassed adult! It is particularly dangerous if the foreign body
is a button battery as rapid erosion may occur.
Presentation
Hearing loss
Discharge- may be foul smelling or blood if FB is left long term.
Management
The foreign body needs to be removed using appropriate equipment
– the method used depends upon what the object is and its shape.
Examples include using a wax hook (e.g. small hard, round objects),
alligator forceps (paper) or microsuction.
Perforated Tympanic Membrane
Figure 68: Central perforation of left tympanic membrane(reproduced

with permission from Otolaryngology Houston, www.ghoryeb.com)
Causes
Previous surgery e.g. grommets
Infection (Acute otitis media with perforation)
Trauma (blow to the ear or barotrauma)
Presentation
Ear pain when perforation occurs. Blood may discharge at this
time
Hearing loss
Recurrent discharge
Management
Most cases can be managed conservatively by advising the
patient to keep the ear free of water (e.g. use cotton wool
smeared with Vaseline in the bath/shower, swimming cap/ear
plugs for swimming). The perforation often heals within 6-8
weeks if traumatic in origin or secondary to an episode of otitis
media with perforation.
Infected perforations ears may require antibiotic ear drops.
Reconstruction of eardrum (myringoplasty/tympanoplasty) may
be required in appropriate cases e.g. recurrent ear infections,
patients wanting to waterproof their ear
FB in the pharynx or
oesophagus
Causes
In children, this tends to be an inanimate object such as a coin .
There should always be a high suspicion of battery as these can
look very similar to a coin on a plain X-ray. A battery causes a
chemical burn that can perforate the oesophagus within hours.
In adults, it tends to be a food bolus. The most important
question is whether there is any bone as this requires immediate
removal because the oesophagus is at a higher risk of
perforation.
Presentation
Dysphagia, odynophagia, drooling
In children, the presentation can be very non-specific. e.g. off
their food, lethargic
Management
Depends upon the nature of the foreign body, duration of the
symptoms and the clinical status of the patient.
Batteries – removal as soon as possible. This is a surgical
emergency and should be treated with the same urgency as a
significant bleed or an airway problem.
Food bolus with bone – needs to be removed as soon as
possible to minimize the possibility of perforation
Food bolus without bone – this may spontaneously pass
overnight (the oesophageal muscles & sphincters relax when a
patient sleeps) or muscle relaxants such as hyoscine
butylbromide (Buscopan) can be given. If it does not pass,
patient may need an upper rigid oesphagoscopy or an OGD (for
a lower food bolus). Asking the patient to swallow a sip of water
can be useful (immediate regurgitation implies a high
obstruction whereas delayed regurgitation implies a low
obstruction).
Deep neck space infections
Causes
The causative agent is normally bacterial & it often originates from
poor dental hygiene particularly in the case of Ludwig’s angina
(Figure 69)
Figure 69: Ludwig’s Angina (courtesy of E-lfENT)
Presentation
This depends upon which deep neck space is affected. Symptoms to
watch out for include pain, trismus (unable to open mouth fully),
dysphagia, dysphonia, stridor and drooling. Patients typically look
very unwell with pyrexia and malaise.
Management
The “ABC” approach should initially be used as these patients
are often very ill. The airway is at risk so should be secured if
compromised (this may require intubation or tracheostomy).
Fluid administration and broad-spectrum antibiotics need to be
administered (e.g. Co-amoxiclav).
Imaging (CT scan with contrast) is normally performed to
confirm the diagnosis and delineate which deep neck space
compartments are affected.
Definite treatment involves surgical drainage of the abscess
(surgery may be per-oral/external or both). Small collections (<
1cm) may respond to intravenous antibitocs.
Microbiology results from pus/blood cultures are very important
to target the specific pathogen.
In children, retropharyngeal infections tend to be more common than

in adults. They present with difficulty swallowing and trismus and
when examined have limited neck movement or torticollis (hold their
neck in a twisted position)
In adults, parapharyngeal infections are more common.

Nasendoscopy may show a parapharyngeal bulge.
Quinsy (Figure 70)– this is a peri-tonsillar abscess. Patients present

with pain, odynophagia and a “hot-potato” voice. Trismus is common.
Treatment is per-oral aspiration and/or incision & drainage which can
be done under local anaesthetic.
Figure 70: Right quinsy (courtesy of Elf-ENT)

Ludwig’s angina – this infection typically arises from poor dentition
and spreads rapidly involving the floor of the mouth, submandibular
space and into adjacent deep neck spaces. Treatment involves
draining the collection and removing the source of infection (e.g. a
rotten tooth)
Penetrating neck trauma
Causes
There are a large number of potential causes of penetrating neck
injuries but most commonly these are due to a knife, broken glass
(e.g. a bottle being used as a weapon) or gunshot wound.
Figure 71: Knife laceration to neck (courtesy of Elf-ENT)
Presentation
It is important to obtain as much history as possible e.g. when and
how it occurred, length of knife etc. Examination of the neck should
include specific reference to the site of injury. This can help with
identifying the most likely structure involved. The neck is divided into
three zones
Figure 72: Zones of the Neck (courtesy of Elf-ENT)
Figure 73: Important landmarks in the neck (courtesy of Elf-ENT)
Zone I extends from the clavicle to the cricoid. It contains a number

of important vessels – the common carotid artery, internal jugular
vein, the trachea and oesophagus.
Zone II extends from the cricoid to the angle of the mandible and is
the most commonly affected zone of injury. This area contains the
laryngeal structures and pharynx. It also contains the vascular
structures including the common carotid artery, bifurcation into the
internal and external carotid, the internal jugular vein, the cranial
nerves including the spinal accessory (XI), the vagus (X) and the
hypoglossal nerves.
Zone III extends from the angle of the mandible to the skull base. It
is associated with trauma to the internal carotid artery, trauma to the
skull base and injury to the cranial nerves passing through.
Management
Patients are treated using the ATLS protocol (A-airway, B-breathing,
C- circulation, D – disability & neurological status, E – exposure).
Airway may need securing by intubation or a a surgical airway
(criocthyroidotomy, tracheostomy). In a haemodynically stable
patient, imaging may be performed (e.g.CT angiogram, CT head &
neck) to look for vascular injury and/or intrancranial/C-
spine/tracheal/oesophageal injury. Surgical exploration is normally
performed if the platysma muscle has been breached. It is
increasingly being recognised that surgical exploration is not
mandatory in stable patients.
Medications in ENT
Antibiotics
Antibiotics can be administered topically (e.g. ear drops), orally or
intravenously.
Common antibiotics used in ENT include:
Phenoxymethylpenicillin
Used to treat a sore throat caused by a bacteria e.g. tonsillitis.
Duration is typically a 10-day course.
Amoxicillin
Can also be used for sinusitis, otitis media, where bacteria are the
likely cause, but NOT for sore throats due to possibility of Glandular
Fever. It should be avoided if there is possible glandular fever due to
inevitability of a systemic skin reaction and Stevens-Johnson
syndrome.
Flucloxacillin
Used for staphylococcal infections including cellulitis
Macrolides e.g. erythromycin or clarithromycin
Used for the treatment of bacterial infections where the patient is
allergic to penicillin
Often used for chronic rhinosinusitis without polyposis
Aminoglycosides e.g.
Gentamicin/steroid eardrops
Used for otitis externa, (Pseudomonas is a commensal and an
opportunistic pathogen)
Used with caution in a perforated ear drum and ears with grommets
(due to risk of ototoxicity)
Quinolones
Ciprofloxacin drops are unlicenced for use in the ear in the UK but
are frequently used in its eye drop form as it is not ototoxic. It is
increasingly used in preference to aminoglyside antibiotics.
Used for pseudomonal otitis externa, chronic suppurative otitis
media with perforated tympanic membrane
Antifungals
Clotrimazole is often used for fungal otitis externa (Candida
infections)
Steroids
Topical nasal steroids
Topical nasal steroids are commonly used for the treatment of
allergic rhinitis and chronic rhinosinusitis (with and without
polyposis). They usually require a 2-3 week lead in period before the
patient notices any effect. Alternative therapies should be considered
if there is no improvement after 8 weeks of consistent use.
Common examples include:
Fluticasone spray. They can also be given as nasal drops

(nasules).
Mometasone spray
Beclomethasone spray or nasules
Practical points:
These are steroids but there is minimal systemic absorption

Common side-effects include dryness/crusting which can cause
bleeding (which can be prevented by applying vaseline to the
nose) and irritation within the nose
Oral steroids
These are typically used in adults (dose 1mg/kg for one week) in the
following conditions.
Significant nasal polyposis – oral steroids are used in conjunction

with topical nasal steroids. They are also sometimes prescribed in
conjunction with antibiotics for the treatment of acute sinusitis.
Bell’s palsy - steroids should be prescribed (ideally within 24-48
hours of the onset of facial palsy). There is a good evidence base
that this improves facial nerve recovery when prescribed
early(versus low evidence for anti-virals which has been traditionally
prescribed together with oral steroids)
Sudden onset sensorineural hearing loss - traditionally oral steroids

were given although there is limited evidence for it. There is
increasing evidence that intratympanic injections of steroids such as
dexamethasone may be beneficial. They can be given under local
anaesthetic in the ENT clinic.
Antihistamines
They are useful in rhinitis when the main symptoms include
sneezing, rhinorrhoea and/or eye itching. (Note that intra-nasal
steroids are aimed more specifically at the nasal obstruction)
although topical nasal antihistamine preparations are available.
Antihistamines are used in a complementary fashion with or without

topical corticosteroids.
Side effects if taken systemically include sedation, dry mouth, blurry

vision, urinary retention and acute angle glaucoma

Vestibular sedatives and
Meniere’s disease
Prochlorperazine
This is a dopamine antagonist that is commonly prescribed for
nausea and vertigo due to labrynthitis. It is not uncommon to find
patients have been using this medication for a long period of time; it
should not be given for over 2 weeks as this will prevent the brains
“central compensation” which naturally occurs after an episode of
labrinythitis.
Cinnarizine
It is an antihistamine and calcium antagonist used for nausea and
vertigo.
Betahistine
Traditionally this is used in the treatment of Menieres disease
although there is increasing evidence that it lacks efficacy. It is
thought to improve blood flow to the inner ear which in turn reduces
the endolymphatic pressure (a raised endolymphatic pressure is
thought to be the cause of Menieres Disease)
Intratympanic dexamethasone or
gentamicin
Intratympanic injections of dexamethasone and gentamicin are used
to treat Menieres Disease. The medication is absorbed through the
oval/round window membrane and “reduces” vestibular nerve
function. Dexamethasone is preferred if the patient has good hearing
(gentamicin is ototoxic whereas dexamethasone is not)
Practical Procedures in ENT
Nasal Cautery
Silver nitrate cautery of the anterior septum is a core skill for any
ENT junior doctor. Universal precautions, a good headlight and
suction (Zollner or Fraser) are useful.
First decongest and numb the nose with a combined lignocaine and
phenylephrine spray either sprayed directly into the nose or applied
on cotton wool pledgets. Close examination of the anterior septum
can often reveal the likely point of bleeding e.g. right Littles area
(Figure 74) The vasoconstrictive element helps reduce any active
septal bleeding to a slow ooze which may be amenable to cautery.
Figure 74: Prominent vessels over Little’s area on the right.
Silver nitrate cautery (Figure 75) should be applied in a ‘rose-petal’

pattern (see Figure 76). Often Naseptin cream (a combination
Chlorhexidine and Neomycin cream - caution with Nut allergy as it
contains Arachis oil from peanuts) is applied topically post-cautery
for 2 weeks which can aid healing. Caution should be taken not to
cauterize both sides of the septum directly opposite each other for
fear of creating a septal perforation. In some units bipolar cautery
may be available, but the underlying principles of cautery remain the
same.
Figure 75: Silver nitrate sticks.
Figure 76. Cautery Applied in a ‘Rose Petal’ Pattern to

to fully deal with the efferent and afferent tributary vessels.
Anterior Nasal Packing
If a bleeding point has not been found, or cannot be controlled with
cautery, then nasal packing may be the next option. Nasal packs can
be classified as anterior or posterior.
Anterior packs commonly encountered include Merocel nasal
tampons (which form a scaffold for clot stabilization) or Rapid Rhino
nasal packs (which help clot formation but also contain an internal
balloon to provide some pressure on bleeding vessels).
Again, as with cautery, a headlight, suction and universal

precautions are useful when packing a nose. An assistant is also
helpful. Anaesthetise the nose appropriately as described in previous
sections.
Consent and counsel the patient of what you are going to do. Advise
them that they may experience some discomfort on pack insertion.
Lift the tip of the nasal cavity and firmly insert the nasal pack along
the floor of the nose (not up towards the skull-base), see Figure 77.
Try and slide the pack between the septum and inferior turbinate.
Deviations of the septum or other anatomical variations can make
this difficult.
Try to only pack the side of active or recent bleeding. However, if a

side cannot be identified from history or examination, or unilateral
packing does not control the epistaxis, occasionally bilateral packing
may be required. Be aware that this can exacerbate
cardiopulmonary problems.
Ensure adequate analgesia has been prescribed for the patient to

tolerate the nasal pack. Appropriate resuscitation should continue
and the patient admitted to the ward as appropriate. Any clotting
abnormalities should also be addressed with advice from the
appropriate specialists (e.g. Haematology, Cardiology).
Return to examine the patient after 15 minutes to ensure the
bleeding is controlled. Examination of the posterior pharyngeal wall
can reveal if bleeding is continuing posteriorly despite an anterior
pack being in place.
If anterior packing does not control the bleeding, or a posterior bleed

is identified, a posterior nasal pack may be required. It is a good idea
to get your seniors involved, and posterior packs should ideally be
placed with senior supervision. A Foley urinary catheter using the
balloon to occlude the post nasal space with anterior ribbon gauze is
the convention, but there are a number of modern options for
posterior packing now available (Antero-Posterior Rapid Rhino’s,
Brighton Epistaxis Balloons, etc).
Figure 77. Nasal Packing with Rapid Rhino nasal pack. It should be
inserted along the floor of the hard-palate (direction of arrow) and
NOT upwards.
Nasendoscopy
Description
This uses a flexible fibreoptic endoscope or a rigid straight or angled
scope to examine the nose, postnasal space, pharynx and larynx. It
can be performed in the outpatients department and is commonly
done without the need of any anaesthetic spray.
Figure 78: Flexible nasendoscopy

Figure 79: Flexible nasendoscopy schematic.
Indications
To examine the nose, the sinuses, pharynx and larynx for pathology
To assess the voice
To evaluate swallowing
To evaluate the airway and assist in intubation
Technique of flexible fibreoptic

nasendoscopy
The endoscope should be accompanied with a high quality light
source with a cable, and the image may be viewed through the
eyepiece or on a screen which has the added benefits that it assists
in teaching, allows the patient to appreciate the view and allows
photographs and videos to be recorded. Some endoscopes can be
battery operated which means they are portable and can be easily
taken to wards and various departments.
Some patients require to be sprayed with local anaesthetic/

decongestant spray such as lidocaine/phenylephrine however most
can tolerate this quick procedure without it.
The patient should be seated upright with their head in slight flexion
position. The clinician should have the screen ideally situated and
the endoscope should be focused to give a sharp image and a white
balance should be performed if required. The endoscope should be
lubricated, however the tip should be clean, if necessary using an
alcohol wipe, to provide a clear image.
The patient should be given clear instructions and reassured

throughout.
The examination requires inspection of the following structures:
The nasal turbinates and their corresponding meati.

Septum and Nasal mucosa.
Presence of mucus, pus or polyps in the nasal cavity
Nasopharynx including the Eustachian tube orifices and the
fossa of Rosenmuller.
Posterior pharyngeal wall
Soft palate, uvula and tonsillar region
Tongue base and vallecula
Epiglottis
Both pyriform fossae
Vocal folds and their mobility by asking the patient to say

‘eeeeeeeee’
Do not force the endoscope into the nose, simply use the weight of
the scope to gently pass the tip into the nasal cavity.
The patient may start to produce tears when the endoscope is

passed. This is a normal reflex and does not necessarily indicate the
patient is in discomfort. However, you should regularly check the
patient’s face or ask if they are in any pain throughout the entire
procedure.
The whole procedure takes less than 2 minutes and it is important to
warn the patient to avoid any food and drink for 30 minutes if their
nose and throat has been sprayed with local anaesthetic
Oto-Microscopy and Foreign
Body Removal
Description
Examination of the ear under the microscope is a skill that can be
acquired with the help of some basic principles and handy tips.
Normally done by ENT team due to the need for specific equipment.
Indications
To examine an ear
Removal of impacted ear wax
Treatment of ear infections
Removal of a foreign body
Technique
The patient should be lying on their back on a couch; the head
end can be elevated for patients who may become dyspnoeic
when lying flat. The clinician should sit on a chair and adjust the
height of the chair to a comfortable level and ensure their back
is straight.
Familiarise yourself with the controls of the microscope before
seeing a patient.
Firstly adjust the inter-pupillary distance so that one image is
seen and note this for future reference. Secondly set the focus
of the lens by adjusting each lens to the zero position, then
using some printing/writing on a piece of paper adjust the height
of the microscope until the image can be seen clearly through
the dominant eye (usually the right one). Then close that eye
and check if the image is still clear. If not adjust eyepiece until
the image is sharp. Again make a note of these settings.
The focus should remain sharp even when the magnification is
changed.
Other equipment that may be required is suction, a wax hook,
Jobson-Horne probe, crocodile forceps and an aural speculum.
For foreign body retrieval, you need a cooperative patient and
usually the first attempt is the best chance to remove it
particularly in children. Otherwise a general anaesthetic may be
required.
Soft foreign bodies such as cotton wool can be grasped with
crocodile forceps. Hard objects like a bead are best removed
using a wax hook or Jobson-Horne probe.
Insects (if alive) should be drowned in olive oil first.
ENT Investigations
Description
Pure tone audiometry is a subjective test that aims to evaluate the
quietest sound that can be heard with each ear at various frequencies
i.e. the hearing threshold. Hearing is usually reported on the decibel
scale, which is a logarithmic scale. In general, a whisper from 1m has
an intensity of 30dB, normal conversational voice is 60dB, shouting
equates to about 90dB and discomfort can be felt at around 120dB.
Technique
The audiometer is a machine which provides pure tone sounds at
varying frequencies
The test must be conducted in a soundproof room and the subject
should not be able to see the machine or the tester adjusting the
controls as this may influence the results.
Before conducting the test, the ears must be examined to exclude an
active infection, foreign body or occluding wax. The patient then
wears headphones to test air conduction followed by a bone vibrator
placed on the mastoid process to test bone conduction
Air conduction is tested at 250, 500, 1000, 2000, 4000 and 8000 Hz
while bone conduction is tested at 500-4000 Hz.
Masking helps to deal with cross hearing, which occurs from bone
conduction to the contra-lateral cochlea. It involves presenting a
sound to the non-test ear (masking noise) to prevent it from detecting
the sound being presented to the test ear
Interpretation
Hearing Disability is defined as:
Normal hearing is defined to be 20dB or better.
Mild hearing loss is between 21-40dB.
Moderate hearing loss is between 41-70dB.
Severe hearing loss is considered to be 71-90dB.
Profound hearing loss is worse than 90dB.
Figure 80: An audiogram
Figure 81: An audiogram showing normal hearing in the right ear

A 5 years old child is brought to see the GP by his mother who is
concerned about his hearing. She feels he often mishears and can
even ignore her at times. There have been similar concerns raised at
his school including a slight speech delay and 2 failed hearing tests.
The boy demands to have the television on loud and can often be
loud and boisterous himself. In the past 6 months he has complained
of earache several times which responds to paracetamol. He is
referred to the community audiologist for a hearing test.
Figure 82: This audiogram shows left conductive hearing loss.

The most common cause in a child would be otitis media with
effusion commonly referred to as “glue ear”. This condition has a
bimodal distribution peaking at 2years of age and then again at 5
years of age
A 72 years old lady presents to her GP rather upset that her family
keep complaining about her hearing. She has no earache, no
dizziness, no previous ear complaints and has never worked in a
noisy environment. She has noticed some mild ringing in both ears
for the past 6 months and does admit to lip reading at times. She is
quite anxious that she will be given a bulky hearing aid and but
agrees to have a hearing test.
Figure 83: This audiogram shows right sensorineural hearing loss.

Bilateral, progressive symmetrical sensorineural hearing loss with no
history of noise exposure in a patient over 60 is typically due to
presbyacusis, otherwise known as age-related hearing loss.
Tympanometry
Description
Impedance is the resistance to the passage of sound. Tympanometry
indirectly measures the “compliance” or freedom of movement of the
middle ear structures. Sound transmission from the outer to the
middle ear is optimal when the pressure in the ear canal matches the
middle ear pressure.
Technique
A test probe consisting of a sound producer, sound receiver and a
component to alter the air pressure in the external auditory meatus is
used. An air tight seal is required in the ear canal.
A test tone is transmitted to the middle ear system, some of which will
be absorbed and some of which will be reflected. The air pressure in
the ear canal is varied from 200mmH2O to -200mmH2O. This allows
compliance to be measured.
Compliance should be maximum when there is no pressure
difference across the ear drum.
Interpretation
Type A describes a Normal tympanogram. The peak occurs around 0
decaPascals or mmH2O. The peak may be shallow indicating
stiffness of the drum (e.g ossicular fixation or tympanosclerosis) or
may be high indicating a flaccid ear drum (e.g ossicular
disarticulation)
Type B describes a flat or very low peak. This is typical of a middle

ear effusion. It can also be seen if there is an ear drum perforation
but the ear canal volume will be higher. Normal ear canal volume is
less than 2 cubic centimetres.
Type C shows low pressure in the middle ear and is seen in
Eustachian tube dysfunction.
Figure 84 Tympanogram describes Type A (green), Type B (red),
Type C (orange) patterns (Courtesy of Elf-ENT)
Hearing Tests In Children
Otoacoustic Emissions
Outer hair cell vibrations can be detected in the external
auditory meatus as otoacoustic emissions and can be used as
an objective measure of cochlear function.
Transient evoked otoacoustic emissions occur in response to
short stimulatory acoustic signals in the form of clicks or tone
bursts.
Their presence usually indicates that the hearing threshold is
better than 40dB and they are used in the NHS Newborn
Hearing Screening Programme. This screens for congenital
hearing loss; if the test is failed then the baby is referred for a
more detailed hearing assessment.
Behavioural Techniques
Used in 0-6 months age
Based on presenting a sound stimulus and observing the baby’s
response. A significant change in activity represents a positive
response.
Distraction Techniques
Used in 6-18 months
In this test the parents are given the instructions and advised
that they must not react to the sounds. An assistant distracts the
baby with a toy, which is then phased out. The tester in the
mean time presents a sound from behind the baby and from the
right or left side. A positive response is if the baby turns in
response to the sound
Visual Reinforcement Audiometry
Appropriate for 9-36 months
This test involves the child sitting and playing with toys. Sound
stimuli are produced by one of two loud speakers positioned at
either side of the child. On turning to the sound the child is
rewarded by a visual stimulus such as a flashing light or toy
bobbing above the speaker
Performance Testing
Appropriate for 24-60 months
The child is conditioned to participate in a certain task such as
placing a toy in a box in response to a sound. The child is then
rewarded. Once it is clear that the child understands, the
hearing can be tested by using sounds of different frequencies
at different intensities.
Pure tone audiograms

Generally used in children above the age of 5 years.
ENT Operations
Grommet Insertion
Description
A grommet is a ventilation tube which helps to ventilate the middle
ear. The procedure can be performed under local or general
anaesthetic.
Indications
Otitis media with effusion persisting for more than 3months
Recurrent acute otitis media
Tympanic membrane retraction secondary to impaired
Eustachian tube function
Technique
The patient is positioned supine on an operating bed with their
head resting on a head ring and turned to the side.
The largest aural speculum that can be accommodated is used
to visualize the tympanic membrane via an operating
microscope.
After de-waxing the ear if necessary, the tympanic membrane
should be examined fully to assess for other pathologies (e.g. a
cholesteatoma).
A long enough radial incision (called a myringotomy) is made in
the safe antero-inferior quadrant of the tympanic membrane and
any glue is suctioned from the middle ear.
The ventilation tube is grasped using a crocodile forceps in line
with the forceps either from the top or the bottom flange
(depending on the surgeon’s preference).
The ventilation tube free flange is then inserted through the
myringotomy and inserted into position using a Cawthrone hook
or a straight needle.
Peri-Operative Care
This is usually performed as a day case procedure. Ears should
be kept dry for 2 weeks. An audiogram is usually performed in
6-12 weeks time.
The grommet tends to self extrude after 6-12 months and the
majority of eardrums will heal up.
Complications and consent

Infection which most commonly manifests as otorrhoea.
Tympanosclerosis (scarring of the eardrum)
Tympanic membrane perforation (2-5%)
Figure 85: Grommet in situ

Middle ear and Mastoid surgery
Myringoplasty
A procedure to repair a perforation of the tympanic membrane. It
can also be called a ‘Type I Tympanoplasty’
The following procedures aim to reconstruct the hearing mechanism

and can be combined with a myringoplasty and /or mastoid surgery if
there is co-existing middle ear disease.
Tympanoplasty
Type II Tympanoplasty is when the malleus handle is absent

and the tympanic membrane is reconstructed over the malleus
remnant and long process of incus.
Type III Tympanoplasty is when the malleus and incus are
absent and the TM is reconstructed on the head of the stapes.
Type IV Tympanoplasty is when only the stapes footplate
remains.
Type V Tympanoplasty occurs when the stapes footplate is fixed
and a fenestration of the lateral semicircular canal is made.
Type VI Tympanoplasty is when the TM reconstruction lies on
the promontory.
Ossiculoplasty
This involves reconstruction of the middle ear ossicles –the method
used depends upon which ossicles are missing/present.
Common examples are TORPs (total ossicular replacement

prosthesis) and PORPs (partial ossicular replacement prosthesis).
The latter is used if the stapes head is present and the former is
used if the stapes is absent.
Common prosthetic materials used are hydroxyapatite or titanium.

Bone cement can also be used for small defects e.g. absent long
process of incus.
Mastoidectomy
This can be classified as “Canal wall up or “Canal wall down” – this
refers to the preservation/removal of the posterior external auditory
canal wall respectively
Canal wall up
This is also known as Combined Approach Tympanoplasty (CAT) –

this technique uses a cortical mastoidectomy and permeatal
approach to eradicate disease (e.g. cholesteatoma) leaving the
posterior canal wall intact.
A cortical mastoidectomy is a procedure to expose the mastoid air

cells usually in acute mastoiditis. It is also performed as part of
procedures for cochlear implantation and combined approach
tympanoplasty,
Canal wall down
Also known as modified radical mastoidectomy - the posterior canal

wall is removed as part of the procedure. Most commonly done for
cholesteatoma.
Peri-operative care
A recent pure tone audiogram (ideally within last 3 months)

The ear should be dry ideally with no active underlying
infection(in practice, this is not always possible)
The risks attached are bleeding, infection, hearing loss, dizziness,
tinnitus, disturbance of taste (secondary to injury/removalof the
chorda tympani), facial nerve weakness and CSF leak and
recurrence.

Tonsillectomy
Indications
Recurrent tonsillitis
Quinsy
Obstructive sleep apnoea
Suspected malignancy
Contraindications/Cautions
Coagulopathy (haematological input may allow this)
Acute infection (However, a tonsillectomy may be done in an
acute setting for a quinsy that does not respond to aspiration)
Cleft palate (risk of velopalatal insufficiency which can cause
nasal regurgitation with eating/drinking)
Surgical Technique
There are a number of surgical techniques. A common
technique is described below
The procedure is performed under general anaesthesia
The surgeon wears a head light
The patient is positioned with their neck extended using a
shoulder bag. A metal gag (Boyle Davis) is used to hold the
mouth open and allow access to the tonsils. Draffin rods are
used to secure the Boyle Davis gag in position.
The surgeon makes a mucosal incision with scissors and starts
by freeing the superior pole of the tonsil
The use of gentle retraction medially helps to identify the correct
plan and dissection can be blunt using a Gwynne-Evans tonsil
dissector or using bipolar diathermy to allow simultaneous
haemostasis too
The lower pole can then either be clamped and ligated with an
appropriate tie (e.g. linen or silk) and the tonsil removed
Haemostasis is achieved using ties +/- bipolar diathermy
The gag is then released to check for tension related
haemostasis and any bleeding points are controlled.
The post nasal space and pyriform fossae are suctioned with a
flexible nasal catheter to remove any “coroner’s clot”. This is a
clot that if missed can suddenly obstruct the airway once the
patient is extubated.
The teeth and TMJ should be checked for any damage and
documented in the operation notes.
Peri-operative Care
The surgery can be performed as a daycase.
Regular analgesia
Encourage an early return to a normal diet
2 weeks recovery period.
Consent and complications

Need to warn patients about the risk of primary (within first 24 hours)
and secondary haemorrhage (usually day 4-7), infection, dental
injury, taste disturbance and 2 weeks off work/school.
Adenoidectomy
Indications
Nasal obstruction +/- obstructive sleep apnoea
Recurrent otitis media
Contraindications/Cautions
Cleft palate/submucousal cleft
Bleeding disorder or coagulopathy
Velopharyngeal insufficiency (hypernasal speech and nasal
regurgitation)
Surgical technique
Performed under GA often in combination with a tonsillectomy
and/or grommet insertion depending on the indications. A mouth
gag is used to open the mouth and the postnasal space and
adenoid tissue is palpated.
Monopolar suction diathermy is used to remove the adenoid
tissue to clear the choanaes without damaging the laterally
positioned Eustachian tubes. This is done under direct vision
using a postnasal space mirror/angled endoscope. An
alternative technique is to use an appropriately sized curette to
remove the adenoids followed by haemostasis with
packs/bipolar.
The post nasal space is suctioned with a flexible nasal catheter
to remove any “coroner’s clot”
Consent- Risk of postoperative haemorrhage, dental trauma,
velopalatal insufficiency, transient hypernasal speech.
Peri-operative care
A period of observation is required to ensure no bleeding, but can be
done as a daycase.
Functional Endoscopic Sinus
Surgery (FESS)
Indications
Acute or Chronic Sinusitis not relived by medical management
Nasal Polyposis
Orbital complication of Sinusitis
Drainage of mucocoele/pyocoele or pneumatocele
Endonasal tumour
Access to skull base
Surgical Technique
Pre-operative planning includes nasal endoscopy and imaging,
usually CT +/- MRI paranasal sinuses.
Performed under GA with the patient’s head resting on a head
ring for stability and with the head up and the eye exposed.
Most surgeons will use a preoperative preparation to help
decongest the nose and aid in haemostasis. This usually
consists of a mixture of lignocaine, epinephrine, and cocaine
(Moffat’s solution).
Most of the procedure is performed with a 0 degree endoscope;
other viewing angles are also available for specific steps. The
sequence of steps commonly performed are uncinectomy
(removal of the uncinate bone), followed by enlargement of the
maxillary ostium, anterior and posterior ethmoids air cells are
then cleared, followed by clearance of the sphenoid and frontal
recess if required. During this process microbiology swabs may
be taken if pus is encountered or biopsies taken of polyps or
abnormal tissue. Cysts may be drained and washouts of the
sinuses performed. Overall the aim of this procedure is to
remove disease in the osteomeatal complex in order to allow the
natural drainage pathways of the sinuses to function.

The consent process needs to involve warning the patient about
bleeding which may require the insertion of nasal packs, infection,
injury to the nasolacrimal duct, numbness in the region of the canine
and incisor teeth, orbital injury that rarely includes diplopia and
blindness, CSF leak and anosmia. The patient needs to be aware
that he or she is likely to require nasal sprays long term postop.
Peri-operative Care
This procedure can be performed as a day case however some
centres prefer an overnight stay depending on the extent of disease
and the comorbidities of the patient. Blood stained nasal secretions
are common and tend to settle over the next few days. Regular
analgesia is required and usually a period of 2 weeks recovery is
advised. Patients may be instructed to use saline nasal douching +/-
steroid nasal drops post operatively. If infection was found antibiotics
may be prescribed.
Parotidectomy
Indications
Neoplasms (benign & malignant)
Rarely performed by may be part of a first-arch branchial abnormality
excision
Types of parotidectomy
Superficial conservative parotidectomy (excision of lesions
affecting the superficial lobe of the parotid)
Total conservative parotidectomy (excision of lesions affecting
the superficial and deep lobe with preservation of the facial
nerve)
Total radical parotidectomy (involves sacrifice of the facial nerve
and may be combined with a nerve graft)
Surgical Technique
Performed under GA without muscle relaxant. A facial nerve monitor
is used and when draping the patient the ipsilateral eye and corner
of the mouth should be exposed.
A cervico-mastoid-facial incision is created and skin flaps are

elevated to allow adequate exposure. Greater auricular nerve may
be sacrificed to allow adequate exposure. The facial nerve is located
most commonly using the tympanomastoid suture as the nerve
bisects the apex of this grove 5mm below the bony meatal edge. The
nerve is also known to lie just superior to the posterior belly of
digastric and 1cm deep and inferior to the tragal pointer. In
particularly difficult cases, retrograde dissection of the peripheral
branches is an option. The nerve stimulator can be used to verify the
presence of the nerve and great care must be taken to avoid thermal
damage when using diathermy. Great care is taken to avoid tumour
spillage as this increases the chance of tumour recurrence.

During the consent process, patients must be warned about bleeding
and the potential of a haematoma and the need of postoperative
drains. There is a 10% risk of temporary facial weakness or 1% risk
of permanent weakness. The lower half of the pinna may be numb
postoperatively due to great auricular nerve sacrifice. Also there is a
risk of a salivary fistula and Frey’s syndrome, which is characterised
by gustatory sweating due to cross over innervation between local
parasympathetic secretomotor fibres with sympathetic sweat fibres
after severing the parasympathetic fibres of the auriculotemporal
nerve.
Peri-operative Care
Most patients will have a postoperative drain in place to avoid a
wound haematoma and reduce the dead space. This means they are
admitted into hospital until the drain is removed which is usually 24-
48 hours later.
Thyroidectomy
Indications
Suspicion of Malignancy
Compression symptoms e.g dysphagia/difficulty in breathing in a
large retrosternal goitre
Cosmesis
Types of thyroidectomy
Hemithyroidectomy
Total thyroidectomy
Surgical Technique
Performed under GA with the patient positioned with a head ring
and shoulder bag to extend the neck.
A collar incision is made 2 fingers’ breadth above the
suprasternal notch in a skin crease. Subplatysmal flaps are
elevated superiorly and inferiorly.
The strap muscles are then divided in the midline and retracted
to expose the thyroid.
The superior thyroid artery and vein are ligated and divided
close to the gland to avoid injury to the external branch of the
superior laryngeal nerve. The middle thyroid vein and inferior
thyroid vessels are also ligated and divided close to the thyroid
gland to avoid disrupting the blood supply to the parathyroids.
The thyroid gland is mobilised and the recurrent laryngeal nerve
is identified and preserved.
The nerve is closely related to the inferior thyroid artery and
after ascending from the mediastinum in the tracheoesophageal
grooves, enters the larynx behind the cricothyroid joint.
Parathyroid glands must also be looked for and preserved.
The thyroid is then freed from the ligament of Berry and
removed followed by haemostasis and wound closure.

Patients should be warned of bleeding and the need for surgical
drains. Bleeding can rarely result in a haematoma and airway
obstruction.
There is a risk of infection.
The external laryngeal nerve may be affected causing difficulty
with changing the pitch of the voice and voice fatigability.
Unilateral recurrent laryngeal nerve palsy could give rise to
hoarseness and dyspnoea on exertion. Bilateral vocal cord
palsy can cause airway obstruction with the need for a
tracheostomy.
There is a risk of hypocalcaemia due to inadvertent direct injury
to the parathyroid glands or their vascular supply.
In patients with thyrotoxicosis, surgical manipulation of the gland
can cause a ‘thyroid storm’ with sudden release of thyroid
hormones into the circulation; therefore patients should ideally
be euthyroid.
Postoperative Care
Most patients will be kept in hospital overnight for a period of
observation to ensure no wound haematoma. Patients who have had
a total thyroidectomy need postoperative calcium checks and
appropriate management of any subsequent hypocalcaemia. A total
thyroidectomy would require patients to take lifelong thyroxine.
Neck Dissection
Indications
Almost always for metastatic carcinoma
Types of Neck Dissection

Selective neck dissection describes removal of one or more
lymph node groups (but not all 5) and preservation of all 3 non-
lymphatic structures (sternocleidomastoid (SCM), accessory
nerve (AN) and internal jugular vein (IJV)
Modified radical neck dissection is removal of levels 1-5 but with
preservation of one or more of the non-lymphatic structures i.e.
SCM, AN or IJV.
Radical neck dissection involves removal of the lymph nodes
from level 1-5 plus removal of the SCM, AN & IJV
Extended radical neck dissection is a radical neck dissection but
with removal of further lymph node groups and/or additional
non-lymphatic structures such as the external carotid artery or
posterior belly of digastric.

Complications include bleeding and haematoma, infection, risk of
chyle leak, nerve damage, facial lymphedema and disease
recurrence.
Surgical Tracheostomy
Description
A tracheostomy is a surgically created opening in the front of the
neck into the trachea. It can be performed electively or as an
emergency depending on the indication and can be permanent or
temporary.
Indications
Airway obstruction (See Chapter on ENT Emergencies)
Weaning. Tracheostomy reduces physiological dead space
therefore helps with weaning patients from mechanical
ventilation and allows trachea-bronchial suctioning.
Surgical Technique
Ideally performed under general anaesthetic, however, if
endotracheal intubation cannot be achieved, tracheostomy can
be performed under local anaesthesia.
The patient is positioned supine with a shoulder roll and a head
ring to achieve neck extension.
A horizontal neck incision is made midway between the cricoid
and sternal notch.
The strap muscles are divided in the midline and retracted.
The thyroid isthmus is divided in the midline using diathermy or
can be hemitransfixed.
At this point the trachea should be visible and the anaesthetist
should be alerted that you are close to making an incision into
the trachea. Ensure the tracheostomy tube is ready along with a
size smaller tube. Ensure the cuff of the tube has been tested
and that your assistant has suction to hand.
A window is created into tracheal rings 3 and 4 or alternatively a
linear incision can be created.
The anaesthetist at this point withdraws the endotracheal tube
slowly to allow insertion of the tracheostomy tube. The cuff is
inflated and connections are made to the anaesthetic circuit.
The position is verified by looking for a CO2 trace, the
anaesthetist checks for bilateral air entry into the lungs and then
the tube is secured around the back of the neck with tape
plus/minus sutures through the flange of the tracheostomy tube

Intraoperative or postoperative bleeding
Dislodged tube or false passage
Blocked tube
Infection
Subcutaneous emphysema, pneumothorax or
pneumomediastinum
Peri-operative Care
Humidification and regular suctioning is essential
Care of the inner tube is required to avoid blockage
Stoma wound care including dressing changes and skin
protection if necessary.
Decannulation (removal of the tracheostomy tube) if appropriate
should be considered as soon as possible to avoid long-term
complications. This should be preceded by down sizing of the
tube plus/minus capping the tube off to ensure it is tolerated.
Tracheostomy tubes
Several types of tracheostomy tube are available
Most tracheostomy tubes have an inner and outer tube. The
inner tube can be “unlocked” from the outer tube by twisting it
and allows the inner tube to be cleaned/unblocked whilst
keeping the airway patent with the outer tube in-situ.
Inner and outer tubes can be fenestrated or non fenestrated.
Fenestrated tubes allow for speech although speech can still be
obtained with a non-fenestrated tube if there is a sufficient air
leak around it.
Tracheostomy tubes may be cuffed or uncuffed. A cuffed tube
provides a closed circuit, which is required for mechanical
ventilation through a tracheostomy. An inflated cuff also
prevents aspiration of saliva.

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Students and Foundation Trainees in Otolaryngology (SFO UK)

Ear, Nose and Throat: The Official Handbook for Medical

By the Students and Foundation Doctors in Otolaryngology (SFO

Generic Skills in ENT

Head and Neck

Practical Procedures in ENT

This “E-book” has been written to provide a practical guide to the

Congratulations to the authors and to my colleagues on the SFO UK

Whether you become a GP or an A&E doctor, you will encounter

This book complements the national ENT curriculum written by

Topics are presented systematically in an easy-to-read format

ENT is a very hands-on specialty and ENT doctors are generally

Professor Anthony Narula

Typical working week

Structure of history taking

At the end of the history

Figure 1: Correct positioning of a child for ear exam

Inspect each ear individually - Start with the normal ear

Figure 3: Normal right tympanic membrane

External auditory canal: Wax or discharge, erythema, swelling

Tympanic membrane (See Figure 3): Is there a normal light

(i) Free field speech testing

Free field testing is a good screening tool for hearing loss

If he/she can repeat:

Figure 4: Weber’s test

Vibrating 512Hz tuning fork applied firmly to the midline of the

Place vibrating tuning fork with base on mastoid process

Interpretation of Weber’s and Rinne’s test

Facial Nerve Examination

Figure 6: Separation of the nose into bony pyramid, cartilaginous

Figure 7: Upper, middle and lower thirds of the nose.

How to hold a Thudicum’s speculum

Figure 8: How to perform anterior rhinoscopy with a Thudicum’s

Look especially for these common pathological findings:

Septal deviations (see Figure 9)

Figure 9: Septal deviation to the right

Figure 13: Left-sided inflammatory nasal polyp

Other nasal tests

Cottles & Modified Cottles Test

Modified Cottle’s Test which involves placing a Jobson Horne probe

Examine the oropharynx

Perform Flexible Nasendoscopy (FNE)

There main areas of examination are as follows:

Figure 17: Endoscopic view of the right middle metal region

Tender (infection, inflammation i.e. thyroiditis) /non-tender

Thyroid status examination

Hands and arms

Examine for tremor (hyperthyroidism) by asking patient to put

“Peaches and cream” complexion of hypothyroidism.

Inspect for pre-tibial myxedema which is present in

CN II, III, IV, VI: Optic nerve,

CNV: Trigeminal nerve

Both motor and sensory

Corneal reflex. The afferent limb of this reflex is mediated by

CNVII: Facial nerve

CNIX, and CNX: Glossopharyngeal

CNXI: Accessory nerve

CNXII: Hypoglossal nerve

Figure 22: External auditory canal and middle ear (Elf-ENT)