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CLINICAL PHASE

ENT

DARWIN’S NOTEBOOK

TABLE OF CONTENTS

HEAD & NECK ANATOMY 1

HEAD & NECK EXAMINATION 7

HEAD & NECK CANCER 8

BENIGN HEAD & NECK DISEASE 16

OTOLOGICAL EXAMINATION 21

EXTERNAL & MIDDLE EAR DISEASE 26

INNER EAR DISEASE 32

FACIAL NERVE (CN VII) 40

NASAL ANATOMY 47

RHINOLOGICAL EXAMINATION 49

RHINOLOGY 51

UPPER AIRWAY OBSTRUCTION 60

VOICE DISORDERS 64

ENT – HEAD & NECK ANATOMY

DARWIN’S NOTEBOOK 1

Describe the basic anatomy of the neck

TRACHEA

• From C6 to T4/5 ® where it bifurcates

• Surface anatomy is from the anterior inferior margin of the cricoid cartilage to the manubriosternal angle

THRYOID GLAND

• This is located in the anterior triangle of the lower neck, on either side of the airway & digestive tract,

inferior to the position of the oblique line of the thyroid cartilage

• Find it by palpating the thyroid prominence & arch of the cricoid cartilage, and then feeling posterolateral

to the larynx

• The isthmus crosses the anterior to upper end of the trachea, and is palpable in the midline, inferior to

the arch of the cricoid cartilage

LARYNGEAL CARTILAGES

• The laryngeal cartilages include the:

o Cricoids

o Thyroid

o Epiglottis

o Arytenoids

o Corniculate

o Cuneiforms

• The most relevant of which are the cricoid & thyroid cartilages

• Thyroid cartilage:

o This is the largest laryngeal cartilage, and is located in the midline of the neck at C3/4 (upper

margin)

o The thyroid notch is palpable, and the thyroid prominence is usually visible



• Cricoid cartilage:

o This is located immediately below the thyroid cartilage at level C6, and marks the superior end

of the trachea & oesophagus

o This structure is important as it allows for the identification of the cricothyroid ligament ®

through which a surgical airway can be created

HYOID BONE

• The hyoid bone is located at C3 ® superior to the thyroid cartilage

CAROTID ARTERIES

• The right common carotid originates from posterior to the right sternoclavicular joint

• The left common carotid begins in the thorax & enters the neck near the left sternoclavicular joint

• Both ascend lateral to the trachea & oesophagus within the carotid sheath

• Near the superior edge of the thyroid cartilage, each divides into the internal & external carotid

arteries (in the carotid triangle) ® here, the carotid body & sinus are found, along with CN IX, X & XII

• The internal carotid heads to the base of the skull & enters through the carotid canal ® it gives off no

branches

• The external carotid gives off 8 different branches:

o Superior thyroid

o Ascending pharyngeal

o Lingual

o Facial

o Posterior auricular

o Superficial temporal

o Maxillary



STERNOCLEIDOMASTOID MUSCLE

• This muscle consists of two parts ® the sternal head & the clavicular head

• The sternal head originates from the upper part of the anterior surface of the manubrium of the

sternum, and inserts along the lateral half of the superior nuchal line on the occipital bone

• The clavicular head arises from the superior surface of the medial third of the clavicle, and inserts

along the lateral surface of the mastoid process ® this muscle is evident when the patient turns their

head

CERVICAL LYMPH NODES

• There are two types of cervical lymph nodes ® superficial & deep

• The superficial cervical nodes are collected along the course of the external jugular vein on the

superficial surface of the sternocleidomastoid ® these primarily receive drainage from the posterior

& posterolateral regions of the scalp (through the occipital & mastoid nodes), and send lymphatic

vessels in the direction of the deep cervical nodes

• The deep cervical nodes form a chain along the internal jugular vein, and are divided into upper &

lower groups by the omohyoid muscle (as it crosses the common carotid & internal jugular) ® the

most superior nodes in the upper group are the jugulogastric node (that receives drainage from the

tonsils & surrounding region), and the jugulo-omohyoid node (which drains the tongue)

• The deep cervical nodes eventually received lymphatic drainage from the head & neck either directly or

through regional groups of nodes ® from these nodes, the vessels form a right & left jugular trunk,

which empty into the right lymphatic duct or the thoracic duct

Describe the anatomy of the salivary glands • There are 600–1000 minor salivary glands ® they are located beneath the mucosa of the upper

aerodigestive tract, and are named according to their anatomical position (e.g. palatal, buccal, labial,

lingual, etc.)

• There are 3 pairs of major salivary glands ® each is situated outside the oral cavity, but connected to it

by a duct or system of ducts:

o Parotid glands

o Submandibular glands

o Sublingual glands

• Glands are split into lobules by fibrous septa ® the parotid glands are almost exclusively serous, the

submandibular glands are mixed, the sublingual glands are mucinous, and the minor salivary glands are

variable depending on their site

• Varying proportions of serous & mucinous cells clumped together form acini ® the acini are surrounded

by myoepithelial cells, which are drained by short intercalated ducts, which in turn drain into striated

ducts and then excretory ducts before exiting into the main ducts

• Reserve cells are found in the intercalated & excretory duct systems ® they have the capacity to

differentiate into different ductal cell types, and are thought to be the cells of origin of salivary gland

neoplasms

• There is a basal secretion of fluid from the acini, and active excretion & exchange of ions from the

striated & excretory parts of the duct system

• 1–1.5 litres of saliva are produces in 24hrs ® there is a basal secretion of saliva & regulation under

neurotransmitter control via the autonomic nervous system



• Salivary stimuli:

o Smell

o Taste ® especially acid, sugar, sweet, salt

o Psychic stimuli ® e.g. the thought & sight of food

o Chewing & mastication

o Parasympathomimetic drugs ® e.g. pilocarpine

PAROTID GLANDS

• These are wedge-shaped organs invested by fascia ® they are divided artificially by the plan of CN VII

into a superficial lobe (80%) & deep lobe (20%)

• This is the largest of the salivary glands, and is a serous gland which produces watery saliva ® it is

situated in the cheek, lying in the space between the mastoid process & the mandible

• Deep to this is the styloid process, its attached musculature, and the carotid sheath ® laterally, the

gland is flat & enclosed in parotid fascia lying close to the skin

• The secretions drain into the mouth via the parotid duct ® this opens at the level of the second upper

molar tooth

• The facial nerve emerges from the stylomastoid foramen that lies at the posterior / deep border of the

gland ® as it passes through the gland, it divides into its five branches

• Lying within the deep lobe is the external carotid artery & several parotid lymph nodes

• Relationships:

o Posteriorly ® zygoma, tympanic bone, cartilaginous external ear canal, stylomastoid fossa,

mastoid process, upper 1/4 of sternocleidomastoid muscle

o Anteriorly ® posterior 1/2 of masseter muscle

o Superiorly ® zygomatic arch

• Structures within the gland:

o Facial nerve trunk & 5 major branches ® temporal, zygomatic, buccal, mandibular &

cervical

o Retromandibular vein & external carotid artery (dividing into terminal superficial temporal &

maxillary arteries)

o Variable number of lymph nodes (<20) ® mostly in superficial lobe

o Parotid duct (Stenson’s duct):

§ Leaves gland anteromedially, passing through the buccinator muscle

§ Then medially to anterior border of masseter muscle

§ Exits in mouth at level of upper 2nd molar

o Secretomotor fibres ® from inferior salivary nucleus & otic ganglion

o Sympathetic fibres ® from superior cervical ganglion via neural plexuses around arteries

SUBMANDIBULAR GLANDS

• These are mixed serous & mucous glands that lie in a triangular space bounded by the mylohyoid

muscle, the mandible, and roofed by the deep cervical fascia (that is attached to the mandible & hyoid

bones)

• The gland is composed of a superficial lobe that lies on the mylohyoid muscle, and a deep lobe that

wraps around the free posterior edge of the muscle to lie in the floor of the mouth



• The submandibular duct runs from the deep lobe to open in the mouth as a papilla next to the

frenulum of the tongue

• Three important nerves are related to the gland:

o Hypoglossal & lingual nerves ® associated with the deep lobe & duct

o Marginal mandibular branch of facial nerve ® runs in the skin overlying the gland

• Relationships:

o Larger superficial & smaller lobes in continuity around posterior aspect of mylohyoid muscle ®

fills the submandibular triangle below the mandible

o Marginal mandibular branch of facial nerve is superficial to the capsule below mandible

o Lingual & hypoglossal nerves in close proximity to deep surface

o Facial artery enters the submandibular triangle under the posterior border of digastric muscle,

and creases the posterosuperior aspect of the gland before passing over the mandible

• Structures within the gland:

o Submandibular duct (Wharton’s duct):

§ Emerges from middle of deep surface, and exits in a papilla to the side of the lingual

frenulum

§ The sublingual glands & lingual nerve are in close proximity to the duct

§ Secretomotor fibres ® from superior salivary nucleus via the nervus intermedius,

chorda tympani, lingual nerve & submandibular ganglion

§ Sympathetic fibres ® from superior cervical ganglion via neural plexuses around the

facial artery

SUBLINGUAL GLANDS

• These are the smallest of the paired glands, and lie in the floor of the mouth ® along the course of the

submandibular duct:

o Floor of mouth, distal to deep lobe of submandibular gland

o Same nerve supply as submandibular gland

o Many small ducts drain into floor of mouth & Wharton’s duct

• It is oblong in shape, and is mucous secreting ® it drains its secretion by 10–15 ducts, either directly

into the mouth or into the submandibular duct

• It has similar relations to those of the submandibular gland

Outline the stages of swallowing, and how these will be affected by disease • The act of swallowing is a complex coordinated reflex action ® which is usually initiated voluntarily, but

is for the most part completed as an orderly sequence of reflexes

• The primary function of deglutition is the transfer of solid & liquid food from the buccal cavity to the

stomach

• The swallowing mechanism is described in three stages:

o The oral (or voluntary) stage

o The pharyngeal stage

o The oesophageal stage

• These three stages correspond to the three anatomical regions through which the bolus of food passes

® but it must be emphasised that swallowing is a continuous & integrated manoeuvre, and the initiation

of the first phase inevitably leads to the completion of the whole process



• There are two terms used to describe the symptoms to which patients ascribe difficulty swallowing:

o Dysphagia:

§ Difficulty with the swallowing mechanism

§ Defined as ‘difficulty with the act of swallowing, precipitated by pharyngeal movement,

which occurs within 5 seconds of having initiated that movement

§ The symptom is active & associated with swallowing

o Globus pharyngeus:

§ The sensation of pressure or tightness of or in the throat

§ Nothing present in throat ® so is a diagnosis of exclusion

§ Is not associated with the act of swallowing, and is frequently relieved by swallowing

• Touch sensation is present in the pharynx as far as the level of the cricoid cartilage (C6)

• Thermal sensation is present in the pharynx, and throughout the whole length of the oesophagus

• Pain receptors in the form of free naked nerve terminals are present in the pharynx & oesophagus, with

noxious stimuli also causing cutaneous pain ® inflammation of the pharynx lowers the pain threshold

locally, and light contact or swallowing movements will cause pain from the inflamed mucosa

• A good history is generally all that is required to make a working diagnosis of swallowing problems ®

radiology is helpful & needs to be tailored to the investigation of the symptoms

o NB: Structural abnormalities require a contrast swallow (e.g. barium swallow), and

physiological abnormalities require a cine swallow (e.g. dynamic contrast swallow or

videofluoroscopy)

ENT – HEAD & NECK EXAMINATION


Outline the relevant history for a patient presenting with head & neck symptoms • Dysphagia ® may indicate local spread of malignancy to digestive tract

• Odynophagia

• Voice changes (dysphonia) ® e.g. hoarseness

• Lumps:

o Location, central, anterior or posterior triangle

o Lymph ® primary or secondary

o Thyroid ® hyper or hypo

o Branchial cyst

o Dermoid cyst

o Haemangiomas / lymphangioma

• Ulcers ® leucoplakia

• Otalgia ® referred pain

• Duration, persistence & progression of symptoms

Describe the relevant examination for a patient presenting with head & neck symptoms • Oral cavity & oropharynx

• Salivary glands:

o Antiseptic ® IgG

o Aids in digestion

o pH ® neutral

o Aids swallowing & formation of food bolus

• Inspection ® from outside in:

o Lift lips ® look in sulcus

o Teeth ® including gingiva

o Hard & soft palate

o Tongue:

§ Frenulum

§ Submandibular & sublingual gland openings

o Cheeks:

§ Parotid gland opens next to upper 2nd molar

§ Retromolar trigone

o Arches ® palatine tonsils sit in between:

§ Anterior arch ® palatoglossal arch

§ Posterior arch ® palatopharyngeal arch

• Palpation:

o Parotid ® finger inside & outside on gland (feeling for tenderness & stones)

o Submandibular ® find on outside (feeling for smoothness & tenderness)

• Neck examination:

o Use triangles

o Important due to lymphatic drainage

ENT – HEAD & NECK CANCER


Describe the diagnostic features & presentation of head & neck malignancies • Head & neck cancer is the term given to a variety of malignant tumours that develop in the:

o Oral cavity

o Pharynx

o Paranasal sinuses

o Nasal cavity

o Larynx

o Salivary glands

§ NB: Many authorities also include thyroid carcinomas & skin tumours of the face &

neck

• Head & neck cancers are the 6th most common cancer worldwide, with an increasing incidence in the

developing world ® they are more common in men & older people

• In some cases the causes are unknown ®e.g. salivary gland cancers, sarcomas & lymphomas

• Squamous cell carcinomas are much more common in smokers & people who drink a lot of alcohol

(especially in people who do both) ® other risk factors include the following:

o Pipe smokers & people who hold cigarettes between their lips for long periods have a higher

risk of cancers in the lip area

o People who have long periods of sun exposure in their daily life have an increased risk of

cancer of the lip & skin of the head & neck ® especially the ear

o People who chew tobacco or betel nuts have a higher risk of cancers of the oral cavity

o Breathing in certain chemicals & hardwood dusts increases the risk of cancers of the nose &

sinuses

RISK FACTORS

• Factors known to contribute to the risk of developing head & neck cancers include:

o Smoking ® both tobacco & marijuana

o Chewing tobacco

o Alcohol use

o Leucoplakia ® may be considered a risk factors, as this condition becomes cancerous in ~1/3

of patients

PATHOLOGY

• Most head & neck cancers are squamous cell carcinomas ® however, other tumour types may also

be seen, including:

o Lymphoma ® most often diffuse non-Hodgkin’s lymphoma

o Salivary gland tumours ® including adenoid cystic, mucoepidermoid, acinic cell

o Thyroid ® papillary, follicular, medullary & anaplastic carcinomas

o Sarcomas

o Undifferentiated carcinomas

PRESENTATION

• The most common symptoms of cancer of the head & neck include:

o Persistent pain in the throat

o Pain on swallowing ® odynophagia



o Difficulty swallowing ® dysphagia

o Persistent hoarseness or a change in voice

o Referred pain to the ear

o Bleeding in the mouth or throat

o Enlarging neck node

o Persistent ulceration, leucoplakia, or erythroplakia

• Half of all head & neck cancers originate in the oral cavity, and sores or lesions in the mouth can be a

warning sign ® any white or red lesions that does not head or disappear in 2 weeks should be

evaluated by a specialist and considered for biopsy

• Weight loss is an unusual symptom of head & neck cancer, and is usually secondary to dysphagia or

odynophagia ® if weight loss is a predominant symptom, other diagnoses should be considered (e.g.

lung, stomach, or other systemic cancers)

• Squamous cell head & neck cancers tend to be localised unless very advanced ® however, secondary

synchronous tumours (particularly in the lungs) may be present in up to 10% of cases

• Other possible signs / symptoms include:

o Lump or thickening in oral soft tissues

o Soreness or feeling that something is stuck in the throat

o Difficulty chewing or opening mouth

o Difficulty moving the tongue

o Numbness of the tongue or other parts of the mouth

o Swelling of the jaw that causes dentures to fit poorly or become uncomfortable

• Anyone experiencing such symptoms for >2 weeks should see their GP or dentist as soon as possible

for a thorough examination ® if a diagnosis cannot be obtained, the patient should be referred to a

specialist

DIAGNOSIS

• Establishing a diagnosis for head & neck cancers typically begins with taking a detailed history and an

examination of the upper aerodigestive tract

• A fine needle aspiration for cytology (FNAC) may be performed in clinic on any neck nodes or other

lumps ® in some centres, FNA is performed under USS or CT guidance

• The initial assessment is usually followed by investigations including:

o CT / MRI of neck ® from skull base to thoracic inlet

o CXR or CT chest

o Blood tests ® U&Es, FBC, LFTs, glucose, albumin, TFTs

o ECG

o Assessment of nutritional status

• The diagnosis must be confirmed with biopsy of any identified suspected cancerous lesions or tumours

® this involved detailed examination of the upper aerodigestive tract (panendoscopy) with biopsies of

any suspicious areas, usually under general anaesthetic

• The results of the above investigations are presented to the head & neck oncology MDT ® the team will

discuss the treatment options & recommend a treatment plan to the patient



Briefly outline the different types of head & neck cancer MOUTH CANCER

• Mouth cancer is the most common type of head & neck cancers ® SCCs are common in the mouth,

and can affect the inner lip, tongue, floor of mouth, gingivae & hard palate

• Most commonly associated with tobacco use & heavy alcohol intake

• Symptoms include persistent mouth ulcers and/or a lump in the mouth ® both of which may be painful

• Cancers in the mouth are more frequently treated with surgery than any other area in the head & neck

® surgeries include:

o Maxillectomy

o Mandibulectomy

o Glossectomy

o Radical neck dissection

o Mohs procedure ® using frozen section histology

NASOPHARYNGEAL CANCER

• Nasopharynx is defined as the region in which the nasal cavities & Eustachian tube connects with the

upper part of the throat

• Some tumours have a similar histology to other cancers of the head & neck (e.g. SCC) ® however,

poorly differentiated nasopharyngeal carcinoma (known as lymphoepithelioma) is also possible

• Nasopharyngeal cancer is one of the rarest types of head & neck cancer in the UK

• Symptoms include:

o A lump in the neck ® due to the cancer spreading to lymph nodes

o Blocked nose

o Epistaxis

o Hearing loss ® usually only one ear

• Risk factors include nickel & hardwood occupations

OROPHARYNGEAL CANCER

• Oropharyngeal SCC begins in the oropharynx ® the middle part of the throat that includes the soft

palate, the base of the tongue & the tonsils

• SCCs of the tonsils are strongly associated with HPV infection ® these have a better prognosis than

those that are not

• People with oropharyngeal carcinomas are at high risk of developing other primary head & neck cancers

• Common symptoms include:

o A lump in the neck

o A persistent sore throat

o Difficulty swallowing

HYPOPHARYNGEAL CANCER

• The hypopharynx is the part of the throat connecting the oropharynx with the oesophagus & traches ®

includes the pyriform sinuses, posterior pharyngeal wall & the post cricoid area

• Tumours of the hypopharynx frequently have an advanced stage at diagnosis ® they tend to

metastasise early due to an extensive lymphatic network around the larynx, and have the worst

prognoses of any pharyngeal tumour



LARYNGEAL CANCER

• Laryngeal cancer develops in the larynx (voice box) ® cancer may also occur on the vocal cords, or on

tissues above & below the cords (i.e. supraglottic & subglottic)

• Symptoms of laryngeal cancer include:

o A change in voice ® such as persistent hoarseness

o Difficulty or pain when swallowing

o Noisy breathing

o Shortness of breath

o Persistent cough

o Lump or swelling in the neck

• It is strongly associated with tobacco smoking

• Surgery can include:

o Laser excision of small vocal cord lesion

o Partial laryngectomy

o Total laryngectomy ® permanent tracheostomy

SALIVARY GLAND CANCER

• There are three main pairs of salivary glands:

o Parotid glands ® located between cheeks & ears

o Sublingual glands ® located under tongue

o Submandibular glands ® located under each side of the mandible

• Salivary gland cancer most commonly affects the parotid glands

• The main symptom is a lump / swelling on or near the jaw, or in the mouth or neck ® although the vast

majority of these lumps are benign

• Other symptoms include unilateral numbness or facial drooping

NOSE & SINUS CANCER

• The symptoms of nose & sinus cancer are similar to viral or bacterial infections:

o A unilateral persistent blocked nose

o Epistaxis

o Decreased sense of smell

o Mucous running from the nose or down the throat

Outline the treatment and staging of head & neck cancers • Head & neck cancer is a complex subject, with many different sites & staging systems ® however,

current therapy offers several alternative, including:

o Surgery

o Radiation

o Chemotherapy

§ NB: Treatment can be either curative or palliative

• Combined modality therapy is becoming the principal method of treating patients with locally advanced

head & neck cancers ® the most suitable plan is discussed at an MDT meeting after reviewing the

results of investigations & the general performance status of the patient



STAGING

• The stage of a cancer is determined by its size, the location of the primary tumour, and whether it has

spread to other areas

• Staging involves using the TNM system:

o T ® the size of the primary tumour

o N ® the degree to which regional lymph nodes are involved

o M ® the presence or absence of distant metastases

• Once the T, N & M are determined ® a ‘stage’ of I, II, III or IV is assigned:

o Stage I cancers are small, localised & usually curable

o Stage II–IV cancers typically are locally advanced and/or have spread to local lymph nodes

and/or have distant metastases

• The staging system for head & neck cancers is a bit complicated ® though the nodal & metastasis

staging categories are the same, the tumour staging systems are different for different anatomical

regions

o NB: The presence of distant metastases automatically indicates Stage IVc

Describe benign & malignant salivary gland tumours

• Neoplastic disease of the salivary glands is uncommon 80–90% of salivary neoplasms arise in the

parotid gland, and a similar proportion of these are benign in nature

• Tumours arising in the submandibular or minor glands are uncommon ® but are much more likely to be

malignant

• Investigations include:

o Fine needle aspiration (FNA) of the mass

o CT scanning

o MRI

• Although FNA may be helpful ® when the exact diagnosis is still in doubt, excision biopsy of the gland

may be needed

o NB: Incision biopsies should not be undertaken, as there is a risk of seeding the tumour &

increasing tumour recurrence

BENIGN TUMOURS

• Benign neoplastic tumours classically present as slow-growing, painless masses ® the patient may

have noticed a small mass for some time, and facial or other nerve palsies do not tend to occur

• Locations:

o 80% of salivary gland tumours occur in the parotid

o 80% of these are benign

o 80% are pleomorphic adenomas

o 60% of submandibular gland tumours are benign

o 30% of minor salivary gland tumours are benign ® away from the mouth & oropharynx, all

minor salivary gland tumours are malignant

• Affect 1 in 100,000, with a slight female preponderance ® mainly affects adults, but children rarely have

salivary tumours, and they tend to be malignant

• Cause is mostly unknown ® but previous radiation is a factor in some



• Pathologically, most tumours are classified according to the resemblance of the tumour cell to normal

non-neoplastic cells ® reserve (stem) cells are present in the intercalated & excretory ducts

• Examination usually reveals a smooth subcutaneous swelling with no attachment to skin

• There are two main types of benign salivary gland tumours:

o Pleomorphic adenomas ® 80%

o Warthin’s tumour (or adenolymphoma) ® 2–6%

• Pleomorphic adenomas:

o Are the most common salivary gland tumours

o Usually arise in the parotid ® but originate from intercalated duct reserve cells

o They are benign ® but if they are present for many years then malignant change may occur

o They are investigated using FNA cytology ® sometimes USS or CT is required

o Treatment is by surgical excision (partial or total parotidectomy) with care being taken to

remove it completely & to include a cuff of normal parotid tissue around the palpable lump

• Warthin’s tumour (or adenolymphoma):

o Also tend to arise in the parotid ® particularly parotid lymph nodes

o Most commonly found in the tail of the parotid

o Usually occurs in older men (8:1)

o Presents as soft, cystic masses in the tail of the parotid ® is occasionally bilateral

o Treatment is by surgical excision

• There are 7 other types of adenoma that can be found in the salivary glands, all of which are rare & can

be divided into further subtypes ® some can be considered to be low grade malignancies, and they are

mostly treated by surgical excision

MIXED BENIGN & MALIGNANT TUMOURS

• Mucoepidermoid carcinoma:

o Originates from epithelial cells of interlobar & intralobular ducts ® 90% are found in the

parotid

o Prevalence is highest in the 5th decade ® it is more common in females (2–4:1)

§ NB: It is the commonest salivary gland carcinoma in children

o Well differentiated (low grade) tumours grow slowly & painlessly ® while poorly differentiated

(high grade) tumours grow rapidly, painfully, invade local structures & metastasise to local

lymph nodes (30%), lungs, bones & brain ® many are intermediate in differentiation

o They are composed of 3 cell types:

§ Mucin-secreting

§ Epidermoid

§ Intermediate

o Low grade tumours should be managed by local resection & prolonged follow-up ® high

grade tumours require more radical resection & adjuvant radiotherapy

o There is up to 30% recurrence rate ® cure rate at 15yrs is ~50% for low grade and ~25% for

intermediate & high grade tumours

• Acinic cell carcinoma:

o Accounts for 2–4% of all parotid tumours

o Originates from reserve epithelial cells of terminal or intercalated ducts ® 99% found in parotid

gland



o Prevalence is highest in the middle-aged & elderly ® but can occur in children

o More common in females

o Can occur bilaterally

o Grow slowly

o Management is local resection (with a CN VII preservation) & prolonged follow-up

o Behave as low grade tumours, with a tendency to recur locally (35%) ® can occasionally

metastasise to lymph nodes (10%)

o Cure rate is 55% at 15yrs

MALIGNANT TUMOURS

• Malignant salivary gland neoplasms are relatively uncommon

• Symptoms include a rapidly growing swelling, often with pain & the involvement of other structures ®

facial nerve palsy with a parotid tumour is almost diagnostic of malignancy

• Local lymph node metastases may occur ® so the neck must be included in the examination

• Malignant tumours are more common in the sublingual & minor salivary glands than in the parotid ®

therefore, swellings in these areas must be treated with a higher index of suspicion

• Minor salivary glands are dispersed through the oral & nasal cavities ® as a result, minor salivary gland

tumours may occur anywhere within these areas

• Adenoid cystic carcinoma:

o Accounts for 14% of parotid gland cancers ® it is the commonest malignant tumour

o Originates from reserve epithelial cells in the intercalated ducts

o Tumours are found in:

§ Parotid (2%)

§ Submandibular (16%)

§ Sublingual (28%)

§ Minor salivary glands (13%)

o Majority of patients are between 40–60yrs ® tumours in submandibular glands are generally

seen in women, but minor salivary gland tumours are equal in both sexes

o Grows slowly & insidiously, but local spread may be extensive ® propensity for perineual

infiltration (skip lesions), so presents with palsies & pain

o Management is using a wide local resection (± sacrifice of CN VII) & prolonged follow-up

® radiotherapy is controversial

o 15yr survival is 10–26% ® local recurrence is 50%, and can also spread to bone, liver & lung

• Carcinoma ex pleomorphic adenoma:

o 3–12% of all cancers of the salivary glands

o Can develop within a pleomorphic adenoma ® but presents 10–15yrs later

o Pain or a palsy usually heralds onset

• Adenocarcinoma:

o 2.5–4% of all parotid neoplasms

o Highly malignant ® there are several histological types

o Poor prognosis, with a 10% 5yr survival

• Lymphoma:

o Comprise 40% of non-epithelial tumours of the salivary glands

o Non-Hodgkin’s lymphoma is the commonest



o Usually arise between 5th & 7th decades

o Some are associated with benign lymphoepithelial lesions

o Present as firm, rapidly enlarging masses, and occasionally lymph node metastasis

o Diagnosis is made by open biopsy

o Treatment depends on clinical stage & histological type

o Metastases:

§ Local skin ® melanoma, squamous cell carcinoma

§ Distant ® lung, breast, kidney or upper GI tract

Outline leucoplakia & erythroplakia LEUCOPLAKIA

• Leucoplakia are white patches adhering to the oral mucosa that cannot be removed by rubbing ® they

are usually asymptomatic, and represent a hyperkeratosis of the oral mucosa

• This is usually associated with local irritation ® e.g. smoking, alcohol, dentures, strong spices, etc.

• 3% of these lesions will undergo malignant change over 5yrs

• The problem is found in less than 1% of people, most commonly between 50–70yrs ® it is more

common in men than women (2:1)

• The patches are most commonly found on the tongue, and are bright white with sharply defined edges

• The patches are slightly raised above the normal mucosa ® erosions or ulcerations can occur, and are

a sign of malignant change

• Management is first by general measures (such as stopping smoking & drinking) ® retinoids have

been shown to be effective in some cases, and surgical excision is also an option

• Another form of this condition is hair leucoplakia:

o This is associated with HIV & EBV

o It is often asymptomatic ® but some symptoms may include mild pain, dysaesthesia, alteration

of taste & cosmetic impacts

o Treatment is which antiviral therapy, topical retinoids & surgery

o Vigorous brushing of the tongue can also help remove these

ERYTHROPLAKIA

• These are red patches in the mouth that cannot be attributed to any other pathology

• It is often associated with dysplasia ® hence, is a precancerous lesion

• Most are found in the floor of the mouth, the tongue & the soft palate

• It is red & macular / papular, with well-defined borders, and has a soft / velvety texture ® an adjacent

area of leucoplakia may be noticed

• Treatment involves biopsy & surgical excision

ENT – BENIGN HEAD & NECK DISEASE


Outline the various salivary gland inflammatory diseases • Non-cancerous disease of the salivary glands can be divided into:

o Viral infection

o Sialadenitis

o Sialolithiasis

o Granulomatous disease

o Sjögren’s syndrome

• It is also important to remember that the two main symptoms of salivary gland disease are pain &

swelling ® there may also be lacrimal gland involvement, which needs to be assessed with systemic

disease

SYSTEMIC VIRAL INFECTIONS

• Mumps is caused by paramyxovirus ® the most common cause of bilateral parotid gland enlargement

• The submandibular gland can also be affected ® but this is rare

• It occurs mainly in children ® presents with a systemic upset, swelling & pain (which are due to the

stretched parotid capsule)

• Infection with HIV can also be associated with infection of the major salivary glands

PAROTITIS

• Parotitis is an inflammation of one or both parotid glands ® it is the salivary gland most commonly

affected by inflammation

• Viral causes:

o Aetiology ® mumps, echovirus, coxsackie B virus (HIV causes diffuse enlargement & multiple

cysts)

o Investigation ® do mumps titres

o Management ® analgesia & hydration

• Bacterial causes:

o Aetiology ® often staphylococcal infection (or TB)

o Presentation ® debilitated, may be on anticholinergics, dehydrated

o Management ® sialagogues, massage, or drain pus if present

• Fungal causes (rare):

o Aetiology ® candidiasis

o Presentation ® immunosuppressed

• Other causes ® include sarcoid or drugs (e.g. dextropropoxyphene)

SIALADENITIS

• Sialadenitis is an acute infection of the parotid or submandibular gland ® presents with pain & swelling

of the gland

• Acute parotitis commonly occurs in older debilitated patients ® who may be dehydrated & have poor

oral hygiene

• Treatment is with high dose antibiotics, rehydration & oral hygiene (citrus mouthwashes will also

improve saliva flow) ® if untreated, a parotid abscess may occur & needs surgical drainage



• A chronic form of this can also occur, with recurring inflammation & pain that may follow an acute

infection, or be more insidious in onset ® pain & swelling are common symptoms that occur episodically

or after meals

• With repeat infections, there is scarring of the architecture of the gland, and surgical excision may be

necessary

SIALOLITHIASIS

• Sialolithiasis describes the formation of stones (calculi) within the salivary glands ® often occurs

alongside chronic sialadenitis

• Most stones occur in the submandibular gland, as the secretions are thicker ® but may also occur in

the parotids

• These calculi usually present with postprandial swelling & pain in the affected gland, or in association

with repeated infection

• On examination, the gland may be tender & swollen ® if the calculus has migrated into the

submandibular duct, then it may be palpated in the floor of the mouth

• The calculi can be seen on X-ray, or when injecting radio-opaque dye into the duct

• Initial treatment is with oral fluids & sialagogues (e.g. lemon drops to stimulate secretions), as the

stones sometimes pass by themselves ® if the situation worsens, the stone or the gland can be

surgically removed

SIALECTASIS

• Sialectasis is dilation, stenosis & necrosis of acini forming cysts ® the cause is unknown

• It is the initial event in sialolithiasis ® 85% of which affect the submandibular gland duct

• Investigation is with plain X-ray & sialogram

• Management is by removal of calculus & marsupialisation of the duct ® occasionally, gland excision is

necessary

GRANULOMATOUS DISEASE

• Both tuberculosis & non-tuberculous disease (e.g. sarcoidosis) can affect the submandibular &

parotid glands

• This will be seen as a cold abscess of the lymph nodes adjacent to the gland

SJÖGREN’S SYNDROME

• Sjögren’s syndrome affects many organ systems ® thought to be autoimmune in cause

• Classified as either:

o Primary Sjögren’s syndrome ® sicca complex:

§ Dry eyes ® xerophthalmia

§ Dry mouth ® xerostomia

o Secondary Sjögren’s syndrome:

§ Xerophthalmia

§ Xerostomia

§ Connective tissue disease ® RA in ~50%, but also SLE, scleroderma & polymyositis

• Xerostomia & keratoconjunctivitis sicca are characteristic ® other symptoms include:

o Glossitis



o Secondary candidiasis

o Stomatitis

o Dental caries

o Dry vagina

• 40% feel parotid gland enlargement (but only 20% show it) ® those with enlargement have a higher

chance of developing lymphoma

• Many of these patients will also have diffuse parotid gland enlargement ® minor & major salivary glands

can be affected, leading to a reduced saliva flow

• Other associated conditions include:

o Primary biliary cirrhosis

o Chronic hepatitis

o Vasculitis

o Cryoglobulinaemia

o Hypergammaglobulinaemic purpura

o Polyarteritis

• 15% will have thyroiditis, and many of these will develop pancreatitis ® also achlorhydria, disorders of

oesophageal motility, and nasal crusting

• Immunological defect is the loss of suppressor T-cell activity & an alteration in T-suppressor-helper cell

relationship

• Investigations include:

o HLA A1, B8, DR3 ® especially in primary Sjögren’s

o Specific antigens ® SSA & SSB

o Schirmer’s test ® for lacrimation

o Carlsson-Crittendon test ® for salivary flow

o Labial biopsy ® diagnostic test for Sjögren’s

• 1 in 6 with Sjögren’s syndrome will develop Non-Hodgkin’s B-cell lymphoma ® there is also a higher

risk of Waldenström’s macroglobulinaemia

• Treatment includes:

o Steroids for bouts of parotid swelling

o Artificial tears, artificial saliva & lubricants

o Diagnostic parotidectomy if rapid growth

Describe the clinical presentation of branchial & thyroglossal duct cysts BRANCHIAL CYSTS

• Branchial cysts are congenital & tend to present before the age of 30

• They present as a lump in the neck situated in the middle third of the sternocleidomastoid muscle,

and can be painful if infected

• It is thought they result from epithelial inclusions within a lymph node, which later undergo a process of

cystic degeneration

• FNAC will result in a pus-like aspirate, which is rich in cholesterol crystals

• Treatment is by surgical excision

THYROGLOSSAL DUCT CYSTS

• Thyroglossal duct cysts are congenital ® but tend to present in childhood or adulthood



• They result from a defect in the development of the thyroid gland

• The thyroid develops at the tongue base, and descends downwards around or through the hyoid bone,

and through the tissues of the neck, to eventually overlie the trachea & thyroid cartilage

• As a result of this, a tract is left which runs from the foramen caecum of the tongue to the thyroid gland

® the tract usually resorbs, but it can remain & hence cyst or fistula formation of the tract can result

• The lesions are almost exclusively present in the midline, and will move upwards when the patient

sticks out their tongue (due to the attachment with the hyoid & the tongue base)

• The patient may notice a swelling at the front of the neck ® or a discharge if a fistula

• Treatment consists of surgical excision of the whole tract, including the body of the hyoid bone ®

excision of small parts is usually ineffective, as the condition can recur

Describe the clinical presentation of thyroid masses • Thyroid masses can develop over the thyroid, anywhere between the base of the tongue & thyroid

gland, or in surrounding lymph nodes

• There are two broad categories of thyroid enlargement ® benign & malignant

• Goitre:

o Can be separated into diffuse or nodular enlargement

o Diffuse enlargement can occur as a result of Grave’s disease, iodine deficiency or in

pregnancy ® it is due to excess stimulation by TSH

o Nodular enlargement (with single or multiple nodes) must raise the question of malignancy,

although multiple nodes can result from alternative episodes of iodine deficiency or TSH

hypersecretion

• Malignant conditions:

o Tumours of the thyroid may arise from follicular cells (papillary, follicular & anaplastic

carcinoma) or parafollicular cells (medullary carcinoma)

o 50% are papillary, 25% are follicular, 20% are anaplastic, and 5% are medullary

o Papillary carcinoma:

§ Most common between 40–50yrs, and tend to be multifocal ® 60% of patients have

neck nodes involved at presentation

§ There is a 90% survival if the tumour is confined to the gland ® 60% if not

§ Since it is multifocal, a total thyroidectomy (± neck dissection) is the treatment of

choice ® radioactive iodine is given after to ablate any viable thyroid left

o Follicular carcinoma:

§ Most common between 50–60yrs, and tend to have a well-defined capsule

§ These tumours tend to spread haematologically rather than by invasion

§ Treatment is similar to papillary carcinomas

o Anaplastic carcinoma:

§ This is a deadly tumour, of which 92% of patients will die within 1yr despite treatment

§ It tends to affect elderly women who have long-term thyroid enlargement

§ Patients present with a rapidly enlarging mass, pain, referred otalgia, and symptoms

due to invasion of the larynx, trachea or oesophagus

§ Radical radiotherapy offers the only cure ® but early recurrence is common



o Medullary carcinoma:

§ This tumour arises from the parafollicular cells which secrete calcitonin ® as a result,

the plasma level of these hormones is raised, but the level of calcium remains

constant

§ Regional lymph nodes are affected in 30% of cases

§ Total thyroidectomy plus radiotherapy is recommended

• Benign adenoma ® this is a benign tumour which may or may not secrete thyroxine

o An actively secreting tumour will take up radioiodine or technetium, and is known as a ‘hot’

nodule ® symptoms of thyrotoxicosis may develop, and surgery or radioiodine may be

required if suppressant treatment fails

§ NB: Hot nodules are rarely malignant

o Non-functioning adenomas also occur, which do not take up iodine ® these are referred to as

‘cold’ nodules, and 10–20% will represent malignant rather than benign tumours

ENT – OTOLOGICAL EXAMINATION


Briefly outline the anatomy of the ear



Outline the history & examination of an otology patient OTOLOGY HISTORY

• History of presenting complaint:

o Changes in hearing:

§ Bilateral or unilateral

§ Acute or chronic

§ Progression

o Otalgia:

§ SOCRATES

§ Onset

§ Referred ® specifically from the throat (e.g. tonsillectomy or malignancy)

§ Associated symptoms

o Otorrhoea:

§ Otitis media ® pain until discharge

§ Otitis externa ® constant pain & discharge

§ Bilateral or unilateral

o Tinnitus:

§ Noise induced hearing loss

§ Wax impaction ® not common

§ Infection

§ Trauma

§ Ototoxic drugs ® e.g. gentamicin & vancomycin

§ Ménière’s disease ® hearing loss, tinnitus & vertigo

§ Vascular ® pulsatile / whooshing in tandem with heartbeat (e.g. carotid stenosis or

aneurysm)

o Vertigo:

§ Duration

§ Associated symptoms

• Family history ® e.g. Ménière’s or otosclerosis

• Drug history ® e.g. gentamicin, vancomycin, furosemide

• Social history ® noise exposure, work, hobbies

• Past surgical history ® previous ENT surgery

• ICE ® e.g. vertigo, pain, tinnitus

• Systems review:

o Neurological ® vision, migraine, speech

o Respiratory ® infection

EAR EXAMINATION

• Always ask about pain ® start on normal ear

• Inspection ® outer ear:

o Pinna

o Pre-pinna

o Behind pinna ® including mastoid



• Palpation:

o Tragus for tenderness ® otitis externa

o Mastoid ® for mastoiditis

o Lymph nodes

• Otoscopy:

o Turn on & check light

o Hold otoscope like a pen

o Little finger rests on cheek

o Pull the ear back & up (adults) or back & down (children)

o Go in far enough so the speculum is past hair cells

o Look at acoustic meatus

o Move up, down, left & right to view entire tympanic membrane:

§ Handle of malleus

§ Pars flaccida (attic) & pars tensa

§ NB: Handle of malleus always points anteriorly

• Tuning fork ® 256Hz or 512Hz:

o Rinne’s test ® bone conduction < air conduction:

§ Checks for conductive hearing loss (if BC>AC)

§ Normal is a positive test

§ Abnormal is negative ® but false abnormal can occur with a dead ear

o Weber’s test ® centre of the head:

§ Conductive ® localises to injured ear

§ Sensorineural ® localises to opposite ear

• Facial nerve ® check using muscles of facial expression

Describe Rinne’s & Weber’s tuning fork tests, the common audiometric patterns on pure tone audiometry, and tympanometry RINNE’S & WEBER’S TESTS

• When using tuning forks, it is important to use the correct frequency for hearing (512Hz)

• Rinne’s & Weber’s tests help to determine whether a hearing loss is unilateral or bilateral, and whether it

is conductive, sensorineural, or mixed

• Weber’s test:

o Here the tuning fork is placed on the patient’s forehead, and the patient is asked where sound

is heard best

o Unilateral or asymmetrical hearing loss:

§ Conductive ® localises to the affected ear

§ Sensorineural ® localises to the non-affected ear

o Bilateral or symmetrical loss of either type causes the sound to be heard equally in both ears

• Rinne’s test:

o This is to determine if sound is heard best through air conduction or bone conduction

o The tuning fork is held against the mastoid process for a few seconds, and then placed in front

of the ear

o The patient is then asked which they can hear better

§ Rinne’s positive (AC>BC) ® normal response, or sensorineural hearing loss



§ Rinne’s negative (BC>AC) ® conductive hearing loss

§ Rinne’s false negative ® if the test ear has profound sensorineural hearing loss, then

the opposite ear may pick up some of the sound & give a false picture of conductive

loss (so masking should be used)

PURE TONE AUDIOGRAMS

• Pure tone audiograms are the most commonly performed hearing test, and help determine a patient’s

hearing threshold

• Tones are played through a set of headphones at varying volumes, and the patient is asked to respond

when they hear a noise ® one ear is done at a time, and sometimes masking can be used on the other

ear

• Sound can also be delivered by a bone vibrating device to assess bone conduction

• In the left ear, air conduction is labelled X & bone conduction is ] ® in the right ear, air conduction is O

& bone conduction is [

• A normal picture is all frequencies between 0 and 20 dB in both air & bone conduction



TYMPANOMETRY

• Tympanometry measures the compliance / stiffness of the eardrum, as well as ear canal volume * the

pressure within the middle ear

• The probe is inserted into the ear & has three channels:

o A speaker

o A microphone

o A device to vary pressure

• Maximal sound energy passes through the ear drum when the pressure in the ear canal is the same as

the middle ear ® hence a peak should be seen on the graph at 0, but normal ranged between -100 and

+100

• A negative middle ear pressure forces the graph to the left, and fluid in the middle ear gives a flat trace

® an excessively tall peak can indicate a hypermobile drum (such as in perforation)

• Overview:

o Canal volume ® >2ml suggests perforation

o Height ® compliance of ear drum / resistance behind eardrum

o Location ® amount of pressure in the middle ear

ENT – EXTERNAL & MIDDLE EAR DISEASE


Describe the basic pathophysiology, diagnosis & management of presbyacusis • Presbyacusis is a term applied to hearing loss due to ageing ® it is the most common cause of

sensorineural deafness

• It is a degenerative disorder caused by atrophy of the labyrinth & cochlear nerve fibres

• It is usually bilateral & symmetrical ® characterised by a gradual hearing loss in both ears (± tinnitus)

• The age of onset is variable, but 50yrs is considered the lower limit of onset

• Audiometry often reveals a high frequency loss ® which are typically consonants, and are crucial for

speech intelligibility

• Many patients complain that while they know people are speaking, they cannot understand what is

being said ® they often say that words merge into one another, or that speech is ‘muffled’ ® they

function well on a one-to-one basis, but have great difficulty with group conversation and when there is

background noise

• Many patients are concerned that they may lose their hearing completely, and reassurance on this front

is important ® emphasising their good low & mid frequency hearing

• There is no cure ® but a hearing aid can help by amplifying sound & masking the tinnitus

Describe the basic pathophysiology, complications, diagnosis & management of cholesteatoma

• A cholesteatoma is a cyst or sac of keratinising squamous epithelium ® most commonly occurs in the

attic or epitympanic part of the middle ear

• This will frequently cause chronic foul-smelling discharge ® as a result, it is classified as a subtype of

chronic suppurative otitis media

• Signs & symptoms include:

o Foul-smelling discharge ® due to anaerobic bacteria

o Conductive hearing loss

o Attic retraction filled with squamous debris

o Discharging attic perforation

o Attic aural polyps

• Patients may also present solely with a complication of cholesteatoma ® such as facial palsy, vertigo,

or intracranial sepsis

• Aetiology is unknown, but it is not thought to be congenital ® the most common theory is that a

negative pressure in the middle ear has its maximal effect on the pars flaccida, causing it to balloon

backwards and forming a retraction pocket, trapping the outer layer of epithelium ® this ball of

squamous debris slowly enlarges & invariably becomes infected with Pseudomonas

• It tends to grow upwards into the attic region & backwards into the mastoid ® it is able to erode bone,

so all important structures in or around the middle ear & mastoid are at risk, including

o Ossicles ® causing a conductive deafness of 50 dB or more

o Lateral semicircular canal ® causing vertigo

o Facial nerve ® causing facial palsy

o Labyrinth / cochlear ® causing sensorineural hearing loss (total or partial)

o Roof of the middle ear ® causing intracranial sepsis

o Sigmoid sinus ® causing it to thrombose

• Treatment is surgical removal ® but the operation required depends upon the extent of the disease



Outline the basic pathophysiology, diagnosis & management of otitis media • Otitis media is an inflammation of the middle ear characterised by the formation of an effusion ® this

may be sterile (as in otitis media with effusion) or suppurative (as in acute otitis media)

• Repeated attacks can lead to weakening of the ear drum & eventually a perforation which is non-healing

® this is now chronic suppurative otitis media (CSOM)

ACUTE OTITIS MEDIA

• Acute otitis media is common in children ® it is usually associated with an infection of the upper

respiratory tract which spreads to the middle ear via the Eustachian tube

• An accumulation of pus in the middle ear leads to pressure on the tympanic membrane, and hence pain

• Rupture of the membrane leads to otorrhoea * a rapid reduction in otalgia

• Other symptoms include:

o Conductive hearing loss

o Otalgia

o Otorrhoea

o Pyrexia

o Systemic upset

• Treatment is with simple analgesia ® or antibiotics if lasting longer than 4 days or there is discharge

• If a perforation occurs, then the ear must be kept dry until it has healed

OTITIS MEDIA WITH EFFUSION (GLUE EAR)

• The underlying basis is poor ventilation of the middle ear cavity ® which leads to sterile (non-purulent)

and often thick & sticky effusion

• Possible causes include:

o A sequelae of acute otitis media

o Infection or allergy of the middle ear mucosa

o Eustachian tube dysfunction

• Glue ear affects 70–80% of children at some point in their lives, and most resolve spontaneously ® in a

small but significant number, it may last months or years

• Most common in children who have large adenoids, previous acute suppurative otitis media, or a cleft

palate

• It usually leads to a mild hearing loss of between 10–40 dB ® in the long term, this can disrupt the

child’s behaviour, development & schooling

• A chronic effusion also predisposes to repeat attacks of acute otitis media as a result of infection

spreading from the Eustachian tube

• There is a high spontaneous resolution rate ® if glue ear is confirmed at first attendance, the child is re-

evaluated at 3 months

• If it does not resolve over 3 months and if it is symptomatic, then treatment may be required ®

consisting of insertion of grommets (although hearing aids are an alternative)

• The function of the grommet is to aerate the middle ear (not to drain it) ® there is no evidence that

swimming in treated water is harmful to children with grommets in situ

• Grommets will extrude spontaneously, on average in 9 months ® but retention for 2 years is not

unusual



• Persistent OME may result in thinning of the tympanic membrane, give rise to retraction pockets, and

cause collapse of the tympanic membrane ® 20% of children will need a second grommet insertion for

recurrent OME

• In adults it may be unilateral ® here, carcinoma of the postnasal space obstructing the Eustachian tube

orifice must be excluded

• Decongestants & antihistamines have no beneficial effect

• Decision to treat is primarily based on the adverse effects of the hearing loss, social, educational or

speech deficits, repeated attacks of acute otitis media, or development of eardrum sequelae

• Adenoidectomy appears to reduce the risk of recurrence, but is not usually performed at the first

grommet insertion

CHRONIC SUPPURATIVE OTITIS MEDIA (CSOM)

• Prolonged & repeated bouts of otitis media in childhood can cause damage to the tympanic membrane,

and a non-healing perforation may occur

• Symptoms can include hearing loss & otorrhoea ® the hearing loss is usually 10–20 dB if the tympanic

membrane is involved, but can be up to 50–70 dB if the ossicles are disrupted

• Treatment is regular aural toileting, and a combination of antibiotic & steroid ear drops ® surgical

repair of the ear drum may also be necessary

ACUTE MASTOIDITIS

• Acute mastoiditis is a fairly uncommon complication of AOM ® however, it is a serious condition

which can cause significant morbidity & mortality

• Infection spreads from the middle ear cavity, and pus forms in the mastoid air cells causing bony

erosion ® the pus may spread out through the bone, either subperiosteally or into the subcuticular

region in the postauricular region

• A typical history is of an AOM that fails to settle associated with persistent otalgia, otorrhoea & hearing

loss ® a unilateral headache should ring alarm bells, as it may be a sign of the development of an

intracranial complication

• The patient is frequently systemically unwell ® the canal may be full of pus, and a polyp may be seen

through a perforated tympanic membrane

• Other classical signs include:

o Sagging of the posterosuperior canal wall

o Tenderness over the bone immediately above the ear canal (McEwen’s triangle)

• If the pus breaks through posteriorly ® the skin becomes oedematous & erythematous, and the pinna

may become pushed forward

• In the early stages, the patient may be treated with high dose IV antibiotics in hospital ® but if it does

not settle within 48hrs or complications arise (e.g. subperiosteal abscess, facial nerve palsy,

labyrinthitis, petrositis, or spread outside the temporal bone), the patient should have a cortical

mastoidectomy

Describe the basic pathophysiology, diagnosis & management of otosclerosis • Otosclerosis is a disease of the otic capsule or bony labyrinth ® causes conductive hearing loss

• The hard, compact bone of the labyrinth is replaced by patches of spongy bone ® this bony overgrowth

affects the footplate of the stapes, resulting in its fixation & a conductive hearing loss



• Aetiology is unknown, but it is thought to be a familial condition which is Mendelian dominant with

incomplete penetration ® it is thought that up to 1 in 100 people have this condition, but only a minor

proportion are symptomatic

• The hearing loss is bilateral & begins at around the age of 30 ® with symptoms being worse during

pregnancy for women

• An usual symptom called paracusis willisii (hearing better with background noise) can occur in these

patients ® tinnitus & positional vertigo can be additional problems

• This diagnosis should be considered in patients who present with a conductive hearing loss & a normal

ear drum ® the only way to conclusively diagnose this is by surgical examination of the stapes footplate

• Treatment can be observation if mild or a hearing aid if symptomatic ® a large conductive loss can be

treated by replacing the stapes with a Teflon piston (stapedectomy), and this can give dramatic results

® but there is a small risk of developing sensorineural hearing loss after surgery

Describe the basic pathophysiology, diagnosis & management of otitis externa, furuncle & blunt trauma

• There are three types of otitis externa:

o Diffuse otitis externa

o Malignant otitis externa

o Furuncle otitis externa

DIFFUSE OTITIS EXTERNA

• This can be either acute or chronic, and is a common generalised inflammation of the external

acoustic meatus (EAM)

• The causes are often multifactorial, and general skin conditions such as eczema can predispose to

infection, as well as local factors such as trauma ® the end result is a swollen & narrowed EAM, which

is itchy & often acutely tender

• Typical symptoms include:

o Ache or pain

o Otorrhoea:

§ Bacterial ® pus & debris in EAM

§ Fungal ® dry or wet debris, or yellow / black spores (Aspergillus flavum / niger)

§ Viral ® vesicles around introitus of EAM (Herpes zoster) or soft palate, or

haemorrhagic vesicles on tympanic membrane (bullous myringitis) associated with

thin, watery, blood-stained discharge

o Hearing loss ® due to narrowing of the EAM

• The inflammation can spread to the auricle or surrounding facial tissue ® causing facial oedema

• On examination, the tragus is tender on movement, and there may be some tenderness behind the ear

® the skin may crack & crust, which increases the likelihood of a fungal infection occurring ®

chronically, the skin may become thickened or fissured & permanently moist

• Treatment consists of an aural toilet & topical antibiotics or steroid ear drops ® antifungal agents

& glycerine (to withdraw moisture) can be used ® systemic antibiotics can be used if the condition is

severe

• When the problem begins to clear, it is important to check for a middle ear infection ® as this is a

common cause of otitis externa



MALIGNANT OTITIS EXTERNA

• Malignant otitis externa is a more aggressive form of otitis externa ® usually seen in the elderly &

diabetics

• The causative organism is Pseudomonas, which spreads to the bone & causes osteomyelitis of the skull

base ® this can damage the facial nerve and those exiting through the jugular foramen (CN IX, X & XI)

• This condition can be fatal ® treatment needs to be prompt, with high dose IV antibiotics and

sometimes surgical debridement

FURUNCLE OTITIS EXTERNA

• A furuncle is a painful infection of one of the hair follicles of the outer 1/3 of the EAM ® usually due to

Staphylococcus

• It usually arises after one of the hairs has been plucked, or the EAM scratched

• The main sign is of a red swelling arising from one aspect of the outer wall of the EAM bulging into the

meatus

• Treatment is with analgesia & astringents (such as glycerin & ichthammol) ® antibiotics may help in

more severe infections, when there is a lymphadenitis

BLUNT TRAUMA

• Blunt trauma is important to consider, as this can lead to a haematoma ® this blood clot, if not drained,

can cause dense scarring & thickening of the ear

• If infection occurs ® then necrosis of the cartilage & gross deformity may follow

Describe the basic pathophysiology, diagnosis & management of pinna disorders, including haematoma, infections & chondrodermatitis nodularis helicis TRAUMA

• A cauliflower ear is classically caused through a boxing or rugby injury, or during other contact sports

® it results from bleeding which strips the vascularising perichondrium from the underlying cartilage of

the external ear

• If it is not drained as a matter of urgency, it can become infected or the cartilage can become ischaemic

® this can result in perichondritis, necrosis, and later atrophy, distortion of the pinna & a cosmetic

deformity which is extremely difficult to reverse

• A perichondrial haematoma can simply be drained under local anaesthetic ® after an incision, a wick or

corrugated drain should be inserted & pressure dressing applied to the ear, as the haematoma has a

tendency to reform

• Prophylactic antibiotics should be given ® if a pressure dressing cannot be applied or tolerated, or in

cases of recurrence, the perichondrium can be held in place by sutures placed through the full thickness

of the ear, and tied over dental rolls

CHRONDRODERMATITIS NODULARIS HELICIS

• Chondrodermatitis nodularis helicis is inflammation of skin & cartilage of the ear, causing a nodule

® it is common and harmless, but can be tender when touched

• The most important factor is pressure on the skin of the ear ® usually from sleeping mainly on one side,

but can be idiopathic

• Other factors may include damage from cold & sun, or poor blood supply to the ear



• It affects middle-aged or elderly people ® more common in men than in women

• The pain can be intense but is usually short-lived ® typically, the discomfort occurs if the affected ear is

lay on in bed, when it can disturb sleep

• There is usually a single lump (often quite small, 5–10 mm), typically on the outer side of the upper part

of the rim of the ear ® it may look red & its surface can be scaly or crusty, and a small raw area or core

is often seen in the centre when the crust is removed

• The diagnosis is usually straightforward, based on the history, site & appearance of a tender lump on

the ear ® if there is doubt, the nodule can be removed under local anaesthetic & checked in the lab

• Try to avoid direct & prolonged pressure on the lesion ® try to sleep on the other side, make sure the

pillow is soft, and consider modifying it by making a hole where the tender area presses into it

• Treatments include:

o Self-adhesive ‘blister’ style dressings can be used at night to relieve the pressure over the

affected site

o Avoid too much exposure to the cold & sun

o A corticosteroid may be applied as a cream or injected into the nodule to try to reduce pain &

redness

o The lesion can be frozen off with liquid nitrogen

o The chondrodermatitis may be removed surgically, but can occasionally come back after

surgery, so it is important to avoid pressure on the ear afterwards

ENT – INNER EAR DISEASE


Describe the basic pathophysiology, diagnosis & management of noise induced hearing loss • A loud auditory stimulus can cause mild hearing loss & tinnitus that quickly resolves

• Repeated traumas of this type can cause permanent symptoms ® a similar acoustic trauma can also

arise from a very loud noise (e.g. an explosion)

• Sensorineural hearing loss most commonly results ® but conductive loss should also be considered,

due to tympanic membrane rupture or middle ear damage

• Temporary hearing loss is due to cochlear fatigue, and is called a temporary threshold shift ® this

usually occurs within 2 hours of exposure, and with further exposure a permanent threshold shift occurs

• In noise induced hearing loss, tinnitus is often a prominent feature, and the audiogram has a classical

appearance ® with the dip at 4kHz, with gradual involvement of the lower frequencies with continued

exposure

• The treatment is essentially supportive, with tinnitus counselling & provision of a hearing aid where

possible ® so prevention is most important

Describe the basic pathophysiology, diagnosis & management of tinnitus • Tinnitus can exist with a hearing loss due to any cause, but may occur even with normal hearing ®

however, it is most often a feature of sensorineural loss

• Most people will experience tinnitus at some point in their life, and it is mostly transient & a minor

problem

• Subjective (intrinsic) tinnitus is a hallucination of noises in the head or ears, and is a description of a

symptom & not a diagnosis ® it may occur on its own or be associated with hearing loss & vertigo

• Short bursts of tinnitus (<15 min) are physiological, as a result of outer hair cell activation

• Intrinsic causes include:

o Drugs

o Labyrinthitis

o Trauma

o Vascular

o Presbyacusis

o Ménière’s disease

o Noise-induced

o Otosclerosis

o Vestibular schwannoma

o Idiopathic

o Temporal lobe epilepsy

• Objective (extrinsic) tinnitus is a noise in the head or ears that can be heard by another individual ®

examples include the regular clicking of the soft palate in palatal myoclonus, or vascular bruits

• Bilateral tinnitus:

o Patients need reassurance & advice on coping strategies

o The most important is masking the tinnitus with environmental noise ® e.g. radio

• Unilateral tinnitus:

o Needs investigating, as it may be an early sign of vestibular schwannoma

o Tinnitus often starts in one ear then occurs in the other ® but tinnitus that has been unilateral

for ≥1yr should be investigated



• Counselling patients is perhaps the most important aspect of management ® for those with hearing

impairment, a hearing aid may be invaluable

• If getting to sleep is a problem ® sedation may be required

• Tinnitus maskers are also an important adjunct to therapy ® self help & support groups are useful

Describe the basic pathophysiology, diagnosis & management of Ménière’s disease • The characteristic quartet of symptoms in Ménière’s disease are episodic:

o Hearing loss

o Tinnitus

o Vertigo

o Aural fullness

• Ménière’s attacks can occur at any time, and usually give rise to acute spinning vertigo for 30min to 4hrs

® the vertigo is often disabling & very acute in onset, nausea & vomiting may occur, and nystagmus is

present during attacks

• The patient often has to remain in bed until the episode has passed, and will often feel a little off

balance for the next few days

• The hearing loss is sensorineural ® in the early stages of the disease, affects the lower frequencies

and returns to normal after the attack

• Tinnitus & a feeling of fullness or pressure in the affected ear may precede the attacks

• The disease is usually unilateral initially, but can become bilateral ® these attacks can occur in sporadic

bursts, or may occur only very occasionally

• Over the course of the condition, the hearing loss & tinnitus become permanent

• The unreliability of the attacks & their ability to render patients prostrate often leads to some anxiety ®

may seriously curtail the patient’s daily activities

• Distension of the membranous labyrinth or endolymphatic hydrops is postulated as the underlying cause

of this condition ® but the exact aetiology remains unknown

• It is thought that attacks occur due to small ruptures in Reissner’s membrane, leading to mixing of the

endolymph & perilymph ® or as a result of a sudden release to an obstruction in endolymphatic

circulation, thus causing vertigo, which settles down as the inner ear fluids stabilise once more

• Endolymphatic hydrops can also occur in other conditions of the inner ear (e.g. syphilis, labyrinthitis,

head injury & vascular occlusions) ® however, this tends to be non-progressive, unlike in Ménière’s

disease, which often follows an unremitting course until the labyrinth is non-functional

• The diagnosis is strongly suggested by the clinical history, but it is important to rule out other causes of

vertigo ® such as epilepsy, MS, tumours, vascular disease, labyrinthitis & BPPV

• In the acute phase ® treatment consists of vestibular suppressants (e.g. prochlorperazine)

• In the long term ® betahistine (a vasodilator), diuretics, avoidance of caffeine & salt, and reassurance

can reduce the number of attacks, and increase the patient’s ability to cope with attacks

• If the disease becomes debilitating, ablation may be considered ® this brings an end to the fluctuations

in vestibular function by destroying the affected labyrinth chemically with gentamicin injection, or

surgically by drilling out the inner ear or cutting CN VIII ® however, one has to hope that the condition

does not affect the other ear in future



Outline the basic physiology, diagnosis & management of vestibular schwannoma / acoustic neuroma

• Acoustic neuromas / vestibular schwannomas are benign tumours that arise from the auditory nerve

• The earliest symptom they produce is unilateral hearing loss or tinnitus

• Early diagnosis is crucial, as the morbidity & mortality from surgery is directly related to tumour size ®

removal of large tumours can compromise the blood supply to the brainstem, and preservation of the

facial nerve is only rarely possible

• Most patients with acoustic neuromas in the UK present with neurological symptoms (i.e. large tumours)

rather than with hearing loss ® a major factor is ‘doctor delay’ in referring these patients for assessment

• Investigations:

o Pure tone audiometry

o MRI / CT scanning

• Treatment:

o Gamma knife ® a sophisticated X-ray gun requiring one treatment

o Surgery is now reserved for patients with tumours >3.5 cm ® watch & wait on smaller tumours

Describe the pathophysiology, causes & management of vertigo • Vertigo is an abnormal sensation of movement ® when due to acute vestibular disease, this sensation

is often rotary in nature

• It is important to distinguish true vertigo from unsteadiness, faintness, or other types of imbalance from

the history ® cardiac & neurological disorder may give symptoms that patients describe as ‘dizziness’,

but are not actually vertiginous in nature

• Peripheral vertigo includes the ear & labyrinth ® central vertigo includes the cranial nerves & brain

• In many cases, labyrinthine causes for imbalance can be complicated by anxiety & a global deterioration

in sight, muscle tone & joint proprioception, which all form part of the ageing process ® in such cases, a

carefully taken history (starting with the very first time the patient remembers experiencing the

sensation) is important

• Peripheral causes include:

o Labyrinthitis

o BPPV

o Ménière’s disease

o Endolymphatic hydrops from other causes

o Middle ear diseases

o Post-ear surgery

o Post-trauma

o Vascular insufficiency

o Dead labyrinth from any cause

• Central causes include:

o Vestibular neuritis

o Tumours ® e.g. acoustic neuroma

o MS

o Head injury

o Vascular occlusion

o Drug-induced



• Other causes of balance disturbance include:

o Cardiac insufficiency

o Migraine

o Cervical spine disease

o Neurological disorders

o Metabolic disorders ® e.g. diabetes

o Anaemia

o Epilepsy

Outline the difference between vertigo originating within the inner ear & vestibular nerve, or originating in the central nervous system, and presyncopal symptoms originating in the cardiovascular system

• Dizziness is a non-specific term encompassing many sensations ® e.g. vertigo, disequilibrium, light-

headedness, ataxia, diplopia, or even a psychological dissociative feeling

• It is a symptom of many disorders & diseases, and requires an especially thorough history in order to

make a differential diagnosis ® the first task is to determine which of the three types of dizziness the

patient has

CENTRAL

• This is from the vestibular nuclei, brainstem, and upwards ® it can be of a CNS or cardiovascular

origin (probably small vessel disease)



• A feeling of momentary disequilibrium or tending to veer when walking is a common symptom in the

over 60s ® this is thought to be ischaemic in origin, due to small vessel disease in the brain, and is

called presbystasis

• Presentation is extremely varied ® but usually includes:

o Ataxia

o Unsteadiness

o A gradual feeling of being off balance

o Rarely ® nausea & vomiting, hearing loss or tinnitus

• There should be other symptoms & signs of cerebellar or brainstem lesions, or of a central lesion

• Examples of central disease include:

o Space-occupying lesions

o Degenerative diseases

o Post-trauma

o Intoxication

o Vascular processes

o Vestibular neuritis

PERIPHERAL

• This involves the labyrinth (semicircular canals, saccule & utricle) and the vestibular nerve

• This is characterised by sudden episodes of vertigo ® almost always associated with nausea &

vomiting

• Hearing loss & tinnitus may be present ® pointing towards a cochlear problem

• Duration & presence or absence of hearing loss are clues towards diagnosis

• Causes include:

o BPPV

o Ménière’s disease ® triad of vertigo, tinnitus & hearing loss

o Drugs, etc.

CARDIVOASCULAR

• Feelings of faintness ® ‘weak at the knees’

• General syncopal symptoms are not uncommon in the over 60s ® they may be associated with

hypertension (or its therapy), cardiac arrhythmias, or vasovagal attacks

• Presentation includes syncope, light-headedness, faints, unsteadiness, etc.

• Common causes include:

o Postural hypotension

o Hypertension

o Arrhythmias

o Vasovagal attacks

o Drugs

o Hyperventilation



Outline the pathophysiology & management of vestibular neuritis • CN VIII leaves the inner ear via the internal auditory meatus to enter the brainstem at the

cerebellopontine angle ® in the brainstem, connections are made with the auditory & vestibular nuclei

• Disease processes may affect CN VIII during its pathway from the cochlea (hence the term

retrocochlear pathology) ® leading to hearing loss, vertigo & tinnitus

• Inflammation of the vestibular portion of CN VIII leads to vertigo (with similar symptoms to labyrinthitis),

and the hearing is usually unaffected ® a major cause of this is thought to be viral infection (e.g. herpes

zoster)

• Resolution occurs gradually over a period of weeks ® with slow compensation

• Treatment is as with labyrinthitis ® consisting of vestibular sedatives & rest

Outline the pathophysiology & management of labyrinthitis • Labyrinthitis is an acute inflammation of the inner ear that usually follows a simple URTI ® however,

infection may also spread to involve the labyrinth from:

o Middle ear infection

o Intracranial sepsis

o The bloodstream

• Vertigo is the most pronounced symptom, and may be disabling ® it can last for some days or even

weeks before beginning to settle

• Treatment of the acute event is with vestibular sedatives (e.g. prochlorperazine) & rest

• Generally there is gradual labyrinthine recovery or compensation ® this rehabilitation may be

accelerated with special Cooksey-Cawthorne exercises

• There may be some residual imbalance occurring with rapid movements for some months after the

initial episode

• In some cases, the labyrinth may never regain full function ® in such patients, short episodes of

decompensation may occur years after the original injury, particularly in challenging environments (e.g.

boat trips, uneven ground)

• If the condition is severe, hearing loss may occur ® it can even lead to total vestibular destruction (a so-

called ‘dead labyrinth’)

Outline the pathophysiology & management of benign paroxysmal positional vertigo • Benign paroxysmal positional vertigo (BPPV) is a condition characterised by episodic vertigo that

occurs when the head is moved to a certain position ® classically, it is brought on by turning in bed or

looking up at an object

• Usually lasts only for minutes ® but it can remain for hours

• The episodes of BPPV may occur regularly for weeks or months before settling slowly ® it can occur at

any age, and is probably one of the most common causes of vertigo

• Diagnosis is clinical ® the diagnostic bedside test is the Dix-Hallpike manoeuvre:



• The nystagmus of BPPV has specific characteristics:

o It is rotary towards the affected ear

o It has a latent period before starting

o The nystagmus fatigues ® slowly settles & shows adaptation, and lessens with consecutive

tests

• BPPV is thought to be caused by dislodged otoliths settling in the posterior semicircular canal ® with

certain movements causing irritation of the sensory epithelium, and therefore vertigo

• Treatment is with reassurance that the disorder invariably settles spontaneously ® vestibular sedatives

should be avoided as they retard the compensation process, and very rarely surgery on the posterior

semicircular canal may be needed

• A complex series of head movements may be used to attempt to tip the displaced otoliths out of the

semicircular canal ® known as Epley’s manoeuvre:

Outline the pathophysiology & management of presbyacusis • Presbyacusis is a degenerative disorder describing the hearing loss of old age ® it is due to the

gradual loss of outer hair cells of the cochlea

• The condition is characterised by a gradual hearing loss in both ears ® with or without tinnitus

• The loss of diversity of hair cell sound receptors leads not only to hearing loss, but also ‘confusion in

sound’ ® typically, elderly patients complain that they struggle to hear clearly in background noise

• On pure tone audiometry® the hearing less will affect the higher frequencies



• Poor hearing can make communication difficult, and tinnitus can be distressing to some patients ®

there is no cure, but a hearing aid can be of great help by amplifying sounds & masking the tinnitus

• Presbystasis ® aka disequilibrium:

o A momentary feeling of unsteadiness, particularly in elderly people ® there is no associated

nausea or vomiting

o These symptoms are thought to be due to small vessel disease in the brain

o It is usually self-limiting & may improve ® but there are no satisfactory medical treatments

Outline the pathophysiology & management of vestibular migraine • Vestibular migraine is a migraine with vestibular symptoms ® dizziness may occur before, during or

after the migraine, and typically lasts for 5–20 minutes

• This is a diagnosis of exclusion ® other problems (such as BPPV) should be excluded first

• In basilar migraines there may also be ataxia, hearing loss & tinnitus ® however, auditory symptoms

are generally rare

• Diagnostic criteria include:

o Episodic vestibular symptoms

o Current or previous migraines

o Exclusion of all other causes

o Migraine symptoms during an attack of vertigo on at least two separate occasions

• Treatment is the same as for migraines in general

Outline the clinical significance of nystagmus & how to test for it • Nystagmus is an involuntary conjugated rhythmic movement of the eyes

• It is a clinical sign of vestibular abnormality ® peripheral vestibular nystagmus can be rotary or

horizontal, while nystagmus that changes direction is always a sign of a central lesion

• If the lesion destroys the labyrinth, then the nystagmus is always away from the damaged ear ® if it is

an irritative lesion, then the nystagmus is towards the affected ear

o However, a cerebellar lesion results in a nystagmus to the ipsilateral side, and therefore

direction cannot be used to localise a lesion

• There are three degrees of nystagmus ® for example, in a sudden total vestibular failure of the right

ear:

o 1st degree ® when looking left

o 2nd degree ® when looking left & straight ahead

o 3rd degree ® when looking left, right & straight ahead

• Chronic nystagmus will gradually resolve due to compensation ® but can still be elicited if optic inputs

are abolished (e.g. using Frenzel’s glasses)

ENT – FACIAL NERVE (CN VII)


Outline the anatomy of the facial nerve & how to test its function

• The facial nerve attaches to the lateral surface of the brainstem, between the pons & medulla

oblongata

• The roots cross the posterior cranial fossa & leave the cranial cavity through the internal auditory

meatus

• The roots enter the facial canal in the petrous part of the temporal bone, where the geniculate

ganglion is formed ® at this ganglion, the greater petrosal nerve is given off, which stimulates the

secretomotor activity in the lacrimal, submandibular & minor salivary glands

• The facial nerve continues along the canal & gives off the nerve to stapedius, as well as the chorda

tympani ® provides taste to the anterior 2/3 of the tongue

• The facial nerve then emerges on the medial surface of the middle ear, before turning posteriorly to exit

the skull through the stylomastoid foramen

• It gives off the posterior auricular nerve (supplying the skin behind the ear), and then passes into the

deep substance of the parotid gland ® where it usually divides into its upper & lower trunks

• Five groups of branches are created ® these are (from superior to inferior):

o Temporal

o Zygomatic

o Buccal

o Marginal mandibular

o Cervical

• The facial nerve provides motor innervation for most of the facial muscles, so it is important to test these

groups ® such tests may include:



o Getting the patient to close their eyes tight

o Raise their eyebrows

o Whistle / pout their lips

o Clench their teeth

Describe the course & function of the facial nerve • Function:

o Motor supply to the muscles of facial expression

o Convery taste fibres from the tongue

o Convey taste fibres from the palate

o Convey cutaneous sensation from a small area of the external auditory meatus, mediated in

fibres carried by way of the vagus nerve ® these fibres are carried in a separate trunk (nervus

intermedius) in the subarachnoid space, and run with the CN VIII

• Important branches:

o Greater petrosal nerve:

§ Arises from geniculate ganglion

§ Conveys taste fibres from palate

§ Conveys preganglionic parasympathetic fibres to lacrimal gland

o Branch from ganglion:

§ Joins the lesser petrosal nerve & auriculotemporal nerve

§ Conveys secretomotor fibres to parotid gland

o Branch to stapedius muscle:

§ Motor part of stapedius reflex

§ Restricts excessive movement of the stapes due to loid noise

o Chorda tympani:

§ Conveys taste fibres from anterior 2/3 of tongue ® via the lingual nerve

§ Has branches that join the vagus & glossopharyngeal nerves

o Postauricular nerve ® motor to muscles of ear & occipital belly of occipitofrontalis

o Main trunk ® supplying muscles of facial expression:

§ Temporal ® raises eyebrows

§ Zygomatic ® closes eyes

§ Buccal ® puffs out cheeks

§ Marginal mandibular ® bears teeth

§ Cervical ® draws neck in

o Cutaneous branches:

§ Distributed with the auricular branch of the vagus nerve

§ Supplies both sides of the pinna

§ Part of the external auditory meatus & tympanic membrane

§ These fibres are carried in a separate trunk (nervus intermedius) in the

subarachnoid space, and run with CN VIII

§ Mechanism whereby pharyngeal pathology may be associated with otalgia ® e.g.

tonsillitis & tumours

§ In addition, palatal vesicles may be present with Herpes zoster of the ear canal

(herpes oticus)



Describe the signs & symptoms of Bell’s palsy • Bell’s palsy is an idiopathic lower motor palsy of CN VII ® it is a diagnosis of exclusion

• Viral infections that involve CN VII are possible one of the most common (~80%) causes of facial

weakness

• It presents with a facial palsy, usually of sudden onset ® it is often preceded by an upper respiratory

trac infection

• Increased pressure on the nerve due to swelling in its tight bony canal is thought to be the cause of the

dysfunction ® affects 2 in 10,000

• Tavener’s criteria is used for the diagnosis of Bell’s palsy:

o Acute onset

o Hemi-facial

o No CNS pathology

o No ear pathology

• If the patient presents within the first 48hrs ® treatment with high dose oral steroids should be

considered

• The majority of cases resolve completely ® but some patients are left with a residual facial weakness

• Poorer prognosis is associated with:

o Increasing age

o Associated pain

o Complete palsy

o Increased latency to onset of recovery

Outline the signs & symptoms of facial paralysis due to parotid disease • Cancers & disease of the parotid gland are uncommon ® the most common tumours are usually benign

pleomorphic adenomas, but other more concerning tumours (e.g. SCCs & adenocarcinomas) may also

occur

• Since the facial nerve enters the parotid as one fibres & splits into 5 branches within ® there are many

places where the nerve may be affected

• A large tumour or mass may compress on the entire nerve & cause a complete LMN facial palsy of that

side ® however, smaller masses may only cause paralysis of certain muscle groups, depending on

which branches are affected

• Similar problems may also occur it the nerve, or its branches, are damaged during treatment or surgical

removal

• Weakness may also occur first, and then progress to a complete palsy

Outline the signs & symptoms of skull base pathology • General signs:

o Battle’s sign ® bruising of the mastoid process of the temporal bone

o Raccoon eyes ® bruising around the eyes

o Cerebrospinal fluid rhinorrhoea

o Cranial nerve palsy

o Bleeding (sometimes profuse) from the nose & ears

o Haemotympanum

o Conductive or perceptive deafness, nystagmus, or vomitus



o In 1–10% of patients, optic nerve entrapment occurs ® causing irregularities in vision

o Serious cases usually result in death

• Skull base pathology can affect the facial nerve around the cerebellopontine angle, causing a complete

LMN facial palsy ® CN IX, X, XI & XII may also be affected

• Depending on the pathology, this also has the potential to affect taste fibres to the anterior 2/3 of the

tongue, and the posterior auricular nerve

• CN VIII also emerges at the cerebellopontine angle® hence may be associated with unilateral hearing

loss & tinnitus

• Transverse skull fractures (10–20% of fractures) have the potential to affect the facial nerve, as well as

hearing ® so may present in a similar way

• A fracture of the petrous temporal bone of the skull base often passes through the middle ear, producing

a conductive loss & a haemotympanum ® the drum appears purple in colour, and occasionally the

external auditory canal is stenosed due to a fracture of the tympanic ring

• CSF leakage is usually short-lived in a longitudinal fracture (80%), and damage to the facial nerve is

rare ® antibiotic cover is indicated

• Transverse fractures (i.e. perpendicular to the long axis of the petrous temporal bone) account for

20%, and result from frontal or occipital blows ® they are more troublesome, as they often pass through

the labyrinth or internal auditory meatus, producing a sensorineural hearing loss, vestibular damage with

vertigo, and facial nerve palsy

• Partial or delayed facial nerve palsies are likely to recover spontaneously, while complete immediate

palsies may require surgical decompression when the patient is fit for surgery

• Nystagmus can be demonstrated, and the Weber’s test localises to the unaffected ear if there is

cochlear damage® the otological symptoms are often overlooked initially because of other more life-

threatening or deforming injuries, or reduce level of consciousness

• An urgent CT scan is required to define the site of injury

• A palsy which develops after the initial injury is more common ® this is due to oedema & bruising

around the nerve, and can be managed with high dose systemic steroids

• Another complication is a CSF leak that may present as rhinorrhoea ® as the fluid drains down the

Eustachian tube

• While damage to the vestibular system causes marked vertigo, this settles as the brainstem

accommodates to the sensory information from the contralateral side ® in the elderly, this process

takes longer, and patients can remain unsteady for weeks

• Less severe head trauma can result in ‘labyrinthine concussion’, which can produce a spectrum of

symptoms including tinnitus, vertigo, permanent hearing loss & BPPV ® the majority of cases are said

to resolve within 2yrs, but ~25% of patients have more persistent trouble

Discuss the management of facial nerve paralysis • Any process that disrupts the nerve fibres of the facial nerve will lead to a partial or total weakness of

the facial muscles ® this is usually immediately apparent, and leads to the patient rapidly seeking

medical help because of the obvious cosmetic deformity

• It is important to differentiate between an UMN (above the level of the facial nucleus) & LMN palsy ®

UMN is forehead sparing (as it receives innervation from the contralateral motor cortex or pons), but

LMN causes total facial weakness



• A thorough ENT, neck & neurological examination is mandatory for any patient presenting with a

facial palsy

• Paralysis of the facial nerve can also be due to an UMN lesion in the motor cortex or pons ® such

pathologies include vascular (TIA / CVA), iatrogenic, tumour, or neurological

• Other LMN pathologies include:

o Ramsay-Hunt syndrome:

§ Herpes zoster infection

§ Causes facial palsy & pain, with the appearance of vesicles on the ear drum, canal &

pinna

§ Vertigo & deafness may occur here

§ Aciclovir treatment is needed

§ This facial weakness is usually severe & often does not recover

o Middle ear damage ® as the facial nerve runs across the medial surface, and can be

compromised during surgery, trauma or infection

• Management:

o This is always of the underlying cause of the paralysis

o The actual paralysis also needs managing ® if it is complete, then the conjunctiva may be

permanently exposed & ulcerate leading to blindness ® hence, artificial tear eye drops are

needed, along with potential surgery

o Most importantly, with anyone presenting with facial paralysis ® a full otoneurological

examination is required without delay

SPECIFIC HISTORY

• Upper or lower motor neurone lesion:

o LMN ® forehead (eyebrow raise) also affected

o UMN ® lower face involved with preservation of bilateral eyebrow raise

• Onset ® congenital, rapid or slowly progressive

• Severity ® complete or incomplete

• Symptoms related to CN VII palsy ® eye closure, drooling, hyperacusis

• Otological symptoms? ® deafness, otorrhoea, otalgia, vertigo, tinnitus

• Other neurological symptoms ® CVA, MS, Guillain-Barré, etc.

• Parotid disease? ® masses, pain

• Systemic illnesses? ® symptoms of infection, sarcoid

• Head / facial trauma ® skull base fracture, stab injuries

EXAMINATION

• CN VII ® the main facial movements to test for are:

o Raising the eyebrows

o Closure of the eyes

o Smile

• CNS ® CN V, CN VII & lower cranial nerves, and cerebellar function

• Ear ® signs of infection or tumour

• Parotid ® if mass present, malignant until proven otherwise



• Oral cavity ® look in the mouth for vesicles, palatal weakness, oropharynx, medially displaced tonsil

(deep lobe of parotid tumour)

• House-Brackmann scale ® grading of severity of CN VII palsy:

o I ® normal

o II ® slight weakness, noticeable only on close inspection

o III ® obvious weakness but not disfiguring

o IV ® severe reduction in movement, incomplete eye closure

o V ® asymmetry at rest, motion barely perceptible

o VI ® asymmetry at rest, no facial movement

INVESTIGATIONS

• Pure tone audiogram

• Stapedial reflexes

• Electroneurography ® guide to progress & prognosis

• MRI / CT ® in selected cases

CONDITIONS TO EXCLUDE

• In children:

o Congenital:

§ Moebius syndrome ® bilateral CN VI, CN VII & CN XII palsies

§ Hemifacial microsomia ® unilateral CN VII palsy with hemifacial hypoplasia

o Acquired:

§ Forceps delivery

§ Chicken pox

§ Acute otitis media

• In adults & children:

o Peripheral:

§ Trauma ® in early life, the facial nerve is more superficial & more prone to injury

§ Iatrogenic ® e.g. damage from parotid or submandibular gland surgery

§ Tumours ® malignant parotid tumours (including lymphoma)

§ Inflammatory conditions of the parotid ® e.g. sarcoidosis

o Middle ear:

§ Iatrogenic ® mastoid surgery of any kind, or ear surgery

§ Infection:

• Discharging ear & a facial palsy is a medical emergency

• A cholesteatoma must be excluded, along with mastoiditis & Ramsay-

Hunt syndrome

§ Tumours ® e.g. SCC, rhabdomyosarcoma (children), glomus jugulare / glomus

tympanicum

o Petrous temporal bone:

§ Trauma ® e.g. transverse fractures of the skull

§ Tumour ® e.g. SCC, metastases

§ Petrous apex cysts / cholesteatoma



o Intracranial:

§ Tumour ® e.g. acoustic neuroma, facial nerve neuroma, meningioma,

carcinomatous meningitis

§ Iatrogenic ® skull base surgery

§ Vascular ® stroke

§ Neurological ® e.g. MS

ENT – NASAL ANATOMY


Outline the basic nasal anatomy

• The nose can be divided into several sections ® these include:

o External nose

o Nasal vestibule & valve

o Septum

o Lateral nasal walls

o Nasopharynx (or postnasal space)

• The nose not only serves to help with respiration, but also acts to warm & humidify the air we breathe

• Stiff hairs on the vestibule help block large particles entering the nose ® whilst smaller particles are

degraded by enzymatic destruction by the epithelium

• Olfaction also gives ~85% of what we call taste ® so a loss of taste may in fact be a loss of smell

ENT – NASAL ANATOMY


THE EXTERNAL NOSE

• The upper 1/3 is made of bone attached to the frontal bone ® the lower 2/3 are cartilaginous

• The cartilage is then divided into the upper & lower cartilages, as well as the alar cartilage (that sits

behind the lower)

• This skeleton is covered in skin ® which is thin at the nasal bridge & thicker over the tip

VESTIBULE & VALVE

• The vestibule is basically the nasal entrance ® it is enclosed by the alar cartilages

• The skin bears stiff hairs called vibrissae ® the mucous membrane lies just behind these

• BCCs, SCCs & benign papillomas can be found in the vestibule

• The middle bit of skin connecting the lip to the nasal tip is called the columella

• The narrowest part of the nasal cavity is the nasal valve ® which is at the upper border of the alar

cartilage

NASAL SEPTUM

• This is the midline division between each nasal cavity, and is made of thin, flat bony sheets posteriorly

(ethmoid & vomer bones), and cartilage anteriorly

• The maxilla makes up the majority of the floor of the nasal cavities

• The covering of the cartilage is mucoperichondrium ® and the covering of the bone is mucoperiosteum

• The septum has a particularly good blood supply ® especially anteriorly, where four arteries

anastomose (Little’s area), which is the most common site for nose bleeds

LATERAL NASAL WALL

• On the lateral walls are ridges or swellings called the superior, middle & inferior turbinates ® each is

made up of a bone covered in vascular mucoperiosteum

• The space under each of these is called a meatus

• The nasolacrimal duct & paranasal sinuses drain into these spaces ® the middle meatus is

clinically most important

• The inferior turbinate can swell under autonomic control ® blocking off each nostril (to some degree) for

~4hrs each, to help prevent drying & allow regeneration

NASOPHARYNX / POSTNASAL SPACE

• The nasal cavities end as two oval spaces called the choanae ® rarely, a congenital abnormality called

choanal atresia can occur, where a thin membrane blocks these two choanae, resulting in death if an

oral airway is not given

• The Eustachian tube enters the nasopharynx on each side ® so a tumour or infected enlarged

adenoids can cause ear problems (which can be the presenting feature of a nasopharynx carcinoma)

• The dividing line between the nasopharynx & oropharynx is the soft palate

ENT – RHINOLOGICAL EXAMINATION


Describe the history & examination of a rhinology patient HISTORY

• Possible problems:

o Epistaxis

o Allergic rhinitis

o Rhinosinusitis

o Foreign body

o Anosmia

o Noisy breathing

o Malignancy ® e.g. sinonasal

o Blocked nose

• Nasal symptoms:

o Blockage

o Discharge

o Change in smell & taste

o Postnasal drip

o Facial pain

o Red flags ® unilateral, bleeding, numb face, neck lump

• Eye symptoms ® important because of sinusitis:

o Itching

o Red flags ® unilateral, proptosis, double vision, eye displacement

• Respiratory ® asthma, aspirin sensitivity

• Past medical history ® atopy, autoimmune conditions (e.g. SLE, sarcoidosis)

• Drug history ® treatments tried, decongestants

• Social history ® smoking, occupation

SINUS PAIN

• Many patients with facial pain or headaches incorrectly believe they have sinus trouble ® however,

CRS is usually painless

• Key points in the history of sinogenic pain are:

o Exacerbation of pain during a URTI

o Association with rhinological symptoms

o Pain that is worse when flying or a response to medical treatment

• Facial pain or pressure on its own without nasal symptoms or signs is highly unlikely to be due to

rhinosinusitis, and an alternative diagnosis should be considered ® such as:

o Midfacial segment pain

o Migraine

o Cluster headaches

o Atypical facial pain

• Vascular pain, such as in cluster headaches, can be associated with autonomic rhinological symptoms

such as nasal congestion & clear rhinorrhoea ® due to vasodilatation of the lining of the nose

• Traditionally, an increase in the severity of pain on bending forward has been considered diagnostic of

sinusitis ® but this finding is non-specific & can occur with many other types of facial pain

ENT – RHINOLOGICAL EXAMINATION


EXAMINATION

• Inspection:

o Look from front, bottom, back & sides ® assess aesthetically

o Looking for:

§ Deviation

§ Asymmetry

§ Landmarks

§ Systemic conditions ® e.g. malar rash, skin cancers

• Palpations ® bony going into cartilaginous:

o Pain

o Fractures

o Lumps

• Air flow:

o Screening test ® breathe on metal & look for bilateral misting

o Individual nostril ® thumb covers nostril & ask to breathe in

• Rhinoscopy using Thudicum’s speculum® looking for inflammation, polyps, septal perforations or other

pathologies

• Others:

o Eyes

o Oral cavity & palate

o Respiratory

o Cranial nerves

o Neck examination

ENT – RHINOLOGY


Differentiate between infective, allergic & non-allergic rhinosinusitis • Rhinosinusitis is an inflammatory process involving the mucosa of the nose & sinuses ® it is replacing

the term ‘sinusitis’, because inflammation of the mucosa is rarely confined to the sinuses, and there is

frequently inflammation of the whole upper respiratory tract

• Rhinosinusitis can be classified into acute (symptoms <4 weeks), subacute (4–12 weeks) & chronic

(>12 weeks) ® it can be further subdivided into:

o Infective

o Allergic

o Non-allergic

o Occupational

o Hormonal ® e.g. pregnancy

ACUTE RHINOSINUSITIS

• Acute inflammation of one, some or all of the sinuses may occur ® the maxillary sinus is the most

commonly affected, followed by the ethmoid, frontal & sphenoid sinuses

• The majority of cases follow a viral URTI, which involves all of the respiratory epithelium, including the

paranasal sinuses ® such infections cause hyperaemia & oedema of the mucosa, which can block

sinus drainage

• Stasis of secretions predisposes to secondary bacterial infection ® the most common causal organisms

are S. pneumoniae & H. influenzae

• Acute rhinosinusitis is usually readily diagnosed clinically ® it commonly follows an acute viral URTI,

with a severe, unilateral pain over the infected sinus, malaise & pyrexia

• Other symptoms include:

o Nasal obstruction

o Mucopurulent rhinorrhoea

o Poor smell

• NB: Acute facial pain without nasal symptoms is highly unlikely to be due to acute rhinosinusitis

• Sinus involvement:

o Maxillary sinus ® pain developing in the cheek or upper teeth, tends to be unilateral

o Frontal sinus ® produces pain above the eye & tenderness of the supraorbital margin

o Sphenoid sinus ® may produce retro-orbital pain or pain at the vertex of the head, but pain

can be referred to the temporal region or to the whole head

o Dental origin ® tenderness of percussion of the upper first or second molar

• Anterior rhinoscopy using an auriscope may show inflamed or oedematous nasal mucosa, and

mucopurulent secretions in the nasal cavity ® throat examination may reveal mucopurulent secretions

in the posterior oropharynx

• Investigations are rarely necessary in uncomplicated cases® plain sinus X-rays often show sinus

opacification or a fluid level in the sinus, but are rarely necessary

• Patients can try simple analgesia, steam inhalations, and a decongestant ® it can be given topically

(e.g. xylometazoline spray), but not for more than 5 days in order to avoid rhinitis medicamentosa

• Patients often expect to be prescribed an antibiotic, but there is only a 3% difference in cure rate after

one week, whether they use antibiotics or not ® in severe cases, or where symptoms are persisting or

progressing, antibiotics are recommended

ENT – RHINOLOGY


• In acute maxillary sinusitis, if there is no improvement after 3 to 5 days ® penicillin or amoxicillin for

7–14 days may be used

• ARS usually responds to medical treatment ® however, if there is progressive pain, the sinuses may

need draining with either a maxillary sinus washout or trephining of the frontal sinus, and an urgent

referral to ENT is needed

• Symptoms & signs of potential complications requiring immediate referral include:

o Periorbital cellulitis

o Severe headaches

o Focal neurology

o Signs & symptoms of meningism

INFECTIVE RHINOSINUSITIS

• Infective rhinosinusitis is the most common cause of acute rhinosinusitis

• Occasionally, secondary effects of colds can persist after the infection has passed ® such as middle

ear infection or long running sinusitis

• It can be acute (systemic upset, pyrexia, rhinorrhoea) or chronic (otherwise well, postnasal drip, muzzy

head & poor concentration)

• Presents with:

o Facial pain

o Headache

o Nasal obstruction

o Anosmia / cachosmia

• Patients with an allergic rhinitis have nasal obstruction & may have hyposmia, nasal irritation & sneezing

® often they have a slightly yellow nasal mucous due to staining with eosinophils, but this is not

indicative of active infection

• On examination, they classically have pale & swollen turbinates ® though the mucosa can be red

ALLERGIC RHINOSINUSITIS

• Allergic rhinosinusitis is the second most common type after infective rhinosinusitis

• The nasal lining becomes sensitised to allergens, which cause an IgE-mediated hypersensitivity

reaction ® this leads to mast cell degranulation & release of histamine

• Nasal effects include:

o Vascular congestion

o Oedema

o Rhinorrhoea

o Irritation

• Some patients are allergic to allergens which are only present for a particular time of year (seasonal) ®

whilst others are affected all year round (perennial)

• Examination of the nose in the patients will show a damp, pale nasal lining with swollen oedematous

turbinates ® in long standing allergy, these turbinates become hypertrophied & permanently enlarged,

and lose much of their erectly ability

• Management includes avoidance of allergens, drug therapy, and occasionally turbinate surgery

• The main drugs used include steroid preparations, antihistamines & sodium cromoglycate nasal

spray (which stabilises mast cells for 4–6hrs)

ENT – RHINOLOGY


NON-ALLERGIC RHINOSINUSITIS

• Non-allergic rhinosinusitis is non-specific ® but includes:

o Vasomotor rhinitis

o Rhinitis medicamentosa

o Atrophic rhinitis

• Patients with an idiopathic rhinitis (i.e. non-infective, non-allergic) complain of nasal obstruction & clear

rhinorrhoea or postnasal discharge ® but itching & sneezing are less common than in allergic rhinitis

• NB: Chronic rhinosinusitis, allergic rhinosinusitis & idiopathic rhinitis can occur concurrently

• Vasomotor rhinitis is where patients fail to test positive for any allergens & is a diagnosis of exclusion

® treatment is much the same as with allergic rhinosinusitis

• Rhinitis medicamentosa is where there is rebound vasodilation & turbinate hypertrophy with prolonged

use of topical nasal decongestants, leading to chronic unresponsive nasal obstruction ® treatment

involves the cessation of the decongestant & instigation of topical nasal steroids, and possibly

turbinate surgery

• Atrophic rhinitis is associated with abnormal patency of the nostril, usually as a result of surgery, and

a loss of ciliated epithelium, leading to thickened secretions and a large crust with an unpleasant odour

® steam inhalation & glycerin should be used to soften the crusts, but the most effective treatment is to

surgically close off the affected nostril

• Rhinitis can also occur in pregnancy, with sexual arousal, in hot conditions, and with old age

CHRONIC RHINOSINUSITIS

• Chronic rhinosinusitis is a multifactorial disease ® contributing factors include:

o Bacterial infection

o Allergy

o Mucociliary impairment

o Swelling of the mucosa for other reasons

§ NB: Anatomical variations appear to play a minimal role

• It has a significant impact on quality of life, even when compared with chronically debilitating conditions

such as diabetes & congestive heart failure ® the disease causes significant physical symptoms, as

well as substantial functional & emotional impairment

• Chronic inflammation of the sinuses may follow an episode of acute rhinosinusitis, or may have a more

insidious onset

• The incidence of chronic infective rhinosinusitis in the UK has decreased because of improvements in

the general health of the population ® however, the incidence of chronic non-infective rhinosinusitis due

to eosinophil inflammation has increased

• The microbial pathogens present in chronic infective rhinosinusitis are significantly different to those in

ARS, and include:

o S. aureus

o Coagulase-negative staphylococcus

o Anaerobic & Gram-negative bacteria predominate

• In the majority of patients with CRS, frank purulent infection cannot be found ® many patients have

hypertrophic mucosa with tenacious secretions, and at histology the lining is replete with eosinophils

• Very occasionally, sinusitis can be secondary to dental disease, and the organisms are anaerobic,

producing a foul-smelling discharge

ENT – RHINOLOGY


• Patients with chronic rhinosinusitis have nasal obstruction & commonly a discoloured discharge for

longer than 12 weeks ® they may also experience a smell disturbance or intermittent frontal pain

• Patients should have a history of purulent secretions around the clock ® some discoloured nasal or

postnasal discharge in the mornings is common & not indicative of CRS

• The diagnosis of CRS is largely based on the history ® but physical signs such as mucosal swelling,

inflammation & discharge are needed

• Anterior rhinoscopy using an auriscope can be performed ® but viewing the middle meatus is

difficult

• Nasoendoscopy achieves much better visualisation ® but is not readily available in general practice

• Inferior turbinates are often mistaken as a nasal polyp ® but they are red & sensitive, rather than the

pale, opalescent painless swellings characteristic of a polyp

• Patients can also be asked to blow their nose to look for evidence of mucopurulent secretions

• The principle aims of treatment are to ventilate the sinuses & restore mucociliary clearance ® if a

diagnosis of CRS is made, a trial of medical therapy should be tried:

o A course of broad-spectrum oral antibiotics ® co-amoxiclav, clindamycin, or

metronidazole & penicillin is given for at least 3 weeks

o Topical nasal steroids ® such as betamethasone drops (2 drops L+R TDS) should be

given for 2 months, followed by a steroid nasal spray

o Nasal douching

• Other coexisting pathologies (e.g. allergic rhinitis / nasal polyps) should be treated accordingly

• If there is no improvement after 8 weeks of medical therapy, referral to ENT should be made ® where

the patient will undergo nasoendoscopy to confirm the diagnosis

• In persistent cases that have not responded to maximum medical treatment ® a CT scan of the

paranasal sinuses with a view to surgery may be considered

• In functional endoscopic sinus surgery ® the natural drainage pathways of the sinuses are cleared,

to allow adequate drainage & resolution of the CRS

• Chronic infective rhinosinusitis tends to be overdiagnosed ® many patients do not have an active

infection, but have developed a persistent allergic rhinitis due to perennial allergens

• Other common causes of CRS are patients with mucosal hypertrophy or polyps associated with late

onset asthma ® these patients often have hyposmia & yellow-stained secretions (due to eosinophils)

• Chronic infection is associated with green secretions throughout the day, along with nasal obstruction ®

this usually responds to the correct antibiotic regimen

• Patients with facial pain or pressure without any nasal symptoms rarely have CRS, and their pain is

usually neurological in origin ® the commonest cause of facial pain is midfacial segment pain:

o This is a symmetrical sensation of pressure that affects the face and/or, sometimes described

as ‘blockage’ ® but without any airway impairment

o It responds to low dose amitriptyline ® taking 6 weeks to work, and needing 6 months of

treatment

Describe the complications of rhinosinusitis • Complications of acute rhinosinusitis include:

o Chronic sinusitis

o Facial cellulitis

o Periorbital cellulitis

ENT – RHINOLOGY


o Mucocoele formation

o Osteomyelitis

o Meningitis

o Brain abscess

CHRONIC SINUSITIS

• Frontal sinusitis is important to recognise, as it can be life or sight-threatening

• It presents with tenderness over the forehead, especially on percussion, and can give a severe frontal

headache that becomes worse on bending

• The infection can easily spread to the orbits & cause blindness without warning

• These patients should be treated aggressively with broad-spectrum antibiotics & decongestants

• Another danger is the spread to the cranial cavity, with the formation of an extradural or intracranial

abscess

• Brain abscesses secondary to frontal sinusitis occur most commonly in the frontal lobe ® may cause

subtle changes in personality, headaches, or a grand mal seizure ® treatment requires neurosurgical

drainage or aspiration

• Extradural abscess secondary to frontal sinusitis may be found on CT scan, and is usually due to a

dehiscence of the posterior wall of the frontal sinus ® these are usually drained into the frontal sinus

• Subdural abscess secondary to frontal sinusitis is difficult to diagnose in the early stages ® patients

have general malaise, headache, neck stiffness, and signs of raised ICP ® prognosis is poor

FACIAL CELLULITIS

• Facial cellulitis may be an extension of:

o Orbital cellulitis

o Frontal sinusitis

o Maxillary sinusitis or osteomyelitis

• It is treated with high dose antibiotics & sinus drainage as necessary

PERIORBITAL CELLULITIS

• Periorbital cellulitis may be the presenting feature of an ethmoidal sinus infection ® as the infection

almost always spreads from the ethmoid sinus via the thin plate of bone (lamina papyracea)

• These patients should be managed by ENT

• This is the most common complication, and spread may be direct or bloodborne

• Treatment is high dose antibiotics & observation ® this is sight-threatening due to pressure on the

optic nerve

MUCOCOELE

• Mucocoeles are a late complication of acute sinusitis ® they are a collective of sterile mucous

occupying an obstructed sinus (usually frontal or ethmoidal)

• Over years, the sinus expands due to mucous under pressure within it ® this is usually asymptomatic

unless infection occurs, or the patient complains of facial swelling

• Treatment is by surgical drainage

ENT – RHINOLOGY


Summarise the medical & surgical treatments for rhinosinusitis and structural nasal defects RHINOSINUSITIS

• Acute rhinosinusitis:

o Simple analgesia, nasal decongestants (mx. 5 days) & steam inhalation

o Antibiotics are rarely needed

o If there are signs of complication or no improvement ® then surgical drainage of the sinus may

be indicated

• Chronic rhinosinusitis:

o Principles are to ventilate the sinuses & restore mucociliary clearance

o A broad course of antibiotics is given for 3 weeks, and topical nasal steroid drops for 2 months

® followed by a nasal steroid spray

o Any allergic element should be treated as usual

o Surgery can help those who do not improve, and involves opening the sinuses to encourage

drainage

NASAL DOUCHING

• Mix 1/2 teaspoon of salt, 1/2 teaspoon of sugar & 1/2 teaspoon of bicarbonate of soda in 2 pints of

boiled water (which has been left to cool)

• Place some of the mixture into a saucer, or draw some mixture up with a syringe

• Block off one nostril with one finger, and then sniff or squeeze the solution into the other nostril ® letting

it run out afterwards

• Topical sprays & drops should be taken after douching

PERFORATED NASAL SEPTUM

• Commonly caused by trauma (septal haematoma) or complication of septoplasty ® may also be a sign

of Wegener’s granulomatosis


o Whistling

o Crusting

o Bleeding

• Management is douching & vaseline as first line, and sufficient for most ® septal button insertion may

help some (but can cause more crusting), and surgery is only suitable for small perforations

DEVIATED NASAL SEPTUM

• This may be the result of trauma at birth or later in life ® it can lead to nasal obstruction of airflow in a

particular nostril

• The treatment is surgery to straighten the septum ® this is done by either removing the deviated

cartilage / bone, or by mobilising & repositioning the deviated cartilaginous septum (septoplasty)

• It is important not to excise the anterior or dorsal septum ® since this provides support for the nose &

cosmetic deformities may occur

EXTERNAL NASAL SKELETON

• Trauma to the external nose is common ® a fractured nose is a common reason for ENT referral

• It is important to take a holistic approach ® consider of the patient is suffering from cervical spine injury,

any head injuries and/or any other facial injuries

ENT – RHINOLOGY


• Important symptoms include:

o Epistaxis

o CSF rhinorrhoea ® basal skull fracture

o Obstruction

o Septal haematoma

• It should also be considered if any legal action may occur ® in which case an X-ray may be relevant

• Acute management ® may need epistaxis intervention or treatment of a septal haematoma

• Septal haematoma is a bilateral fluctuant swelling of septum, which needs to be distinguished from

septal deviation (which is unilateral & hard) ® requires drainage under GA & antibiotic cover

• 5–7 days post-injury will need to be seen in clinic, which allows soft tissue swelling to settle so the bony

nose can be assessed ® manipulation of bony deformity can then be done under local anaesthetic

Describe the management of epistaxis • There may be many causes for epistaxis ® including:

o Spontaneous

o Trauma / foreign body

o URTI

o Clotting disorders / HHT

o Drugs ® anticoagulants & NSAIDs

• Initial first aid should include getting the patient to sit forward & pinch the fleshy part of the nose for 10

minutes ® the patient should avoid swallowing the blood, and an ice pack on the nasal bridge may be

helpful

• Resuscitation may be needed in severe epistaxis ® e.g. assessing blood loss, pulse, BP, getting IV

access, setting up an infusion, FBC, coagulation, and group & save

• Further management includes examining the nose and looking for a point of bleeding ® if visible, then

spray the area with 5% lidocaine & attempt nasal cautery ® if severe, then the nose may need

packing

• Advice on discharge:

o No heavy lifting or bending

o No hot showers or drinks

o No picking

o Gentle nose blowing

o Vaseline

o Vestibulitis ® common S. aureus infection of vestibule, treated with muciprocin ointment or

naseptin cream

BLOOD SUPPLY

• Blood supply mainly comes from the external carotid artery ® from this, the maxillary branch supplies

the septum & palate

• The internal carotid artery also gives off the ophthalmic artery, which branches into anterior & posterior

ethmoid arteries ® these supply the ethmoid & part of the septum

• This means there is a collateral supply to the nose ® called Little’s area or Klesselbach’s plexus

ENT – RHINOLOGY


CAUTERISATION

• Apply cotton buds soaked in 1:200,000 adrenaline or 5% lidocaine solution to the area ® apply

pressure for at least 2 minutes

• Take a silver nitrate cautery stick, which should be applied for 1–2 secs at a time ® provides AgOH &

nitric acid

• Start a few mm away from the bleeding point & work in a circle to cauterise the feeder vessels before

attempting to cauterise the main point ® if unsuccessful, then reapply pressure & pack the nose

• Never cauterise heavily active bleeding vessels ® can cause chemical burns to other parts of the face

or throat

NASAL PACKING

• When cautery cannot be done (e.g. a posterior bleed) then the nose needs to be packed ® the idea is

to put pressure on the blood vessels to prevent active haemorrhage & allow thrombotic mechanisms to

act

• These packs are usually left in for 24–48 hrs, and are secured anteriorly to prevent them prolapsing

back into the airway

• Most doctors will give prophylactic antibiotics whilst the packing is in place

• The packing can be uncomfortable, so the patient may be admitted & lightly sedated ® should usually

only be used unilaterally at first, but bilateral may help by applying pressure to the other side

Outline the treatment of obstructive sleep apnoea & snoring • Snoring is common and is caused by vibration of one or more areas of the upper airway ® sleep

apnoea is an increased upper airway resistance, resulting in cessation of breathing, sleep disruption,

and resultant daytime sleepiness

• Aetiology of snoring & sleep apnoea:

o Age ® increased chance with older age up to 7th decade

o Sex ® males are 2–5 times more likely to suffer

o Obesity ® the most important risk factor (70% of those with BMI >40), but neck & hip

measurements are better

o Obstructed upper airway

o Social habits ® smoking & alcohol

o Other risk factors ® family history, sedating drugs, neuromuscular disease, chronic lung

disease

OBSTRUCTIVE SLEEP APNOEA

• Obstructive sleep apnoea (OSA) is a particular subtype of sleep apnoea ® where there is repeated

collapse of the upper airway, usually associated with desaturation

• Chest movements continue but to no avail, and blood oxygen saturations falls ® when hypoxia occurs,

a central impulse causes a slight lightening of consciousness and in increased respiratory effort to

overcome the obstruction

• Not all people who snore have sleep apnoea ® but all people who have sleep apnoea will snore

• Sleep apnoea is broadly defined as 30 or more episodes of cessation of breathing, each lasting at least

10 seconds, occurring over a 7hr period of sleep

ENT – RHINOLOGY


• Symptoms associated with OSA include:

o Excessive daytime sleepiness

o Impaired consciousness

o Snoring

o Unrefreshing sleep

o Choking episodes during sleep

o Witnessed apnoea

o Restless sleep

o Irritability / personality change

o Nocturia

o Decreased libido

• There are many different ways to assess a patient with OSA, but the main reasons are to assess where

the cause is & what the actual diagnosis is ® methods include sleep studies with various monitoring, or

invasive endoscopies with probes to detect vibrations

• Sleep studies should be conducted in patients with COPD or respiratory problems, people who work as

drivers or with dangerous machinery, and patients who are being considered for surgery

• Unlike adults, the incidence in children is similar in both sexes & does not increase with age ® peak

incidence is between 2–5 yrs (when the adenoid & tonsils are largest), and children often show signs of

failure to thrive & may be overactive rather than sedated

• Over the long term, OSA may lead to pulmonary hypertension & right ventricular strain, and finally cor

pulmonale

• Management can be through lifestyle changes, medical intervention & surgery:

o Lifestyle changes include weight loss & reducing alcohol consumption (and any other sedative)

o Medically, the patient may use drugs that reduce the amount of REM sleep (where these

episodes are more common) or respiratory stimulants to maintain an increased effort

o Continuous positive airway pressure (CPAP) involves wearing a mask that gives a higher

end pressure than normal, and this acts as a split to keep the airway open ® this is often

poorly tolerated

o The surgical option for children is adenotonsillectomy

o In adults, surgery has to be focussed on the area that is actually responsible for the collapse ®

this can vary from nasal polyps or a deviated septum, to the soft palate or lateral pharyngeal

bands

ENT – UPPER AIRWAY OBSTRUCTION


Outline the diagnostic features, causes, signs & symptoms, and management of upper airway obstruction

• Causes:

o Allergic reactions ® in which the trachea or throat swell close

o Chemical burns & reactions

o Epiglottitis ® infection of the structure separating the trachea from the oesophagus

o Fire or buns from breathing in smoke

o Foreign bodies

o Infections of the upper airway

o Injury to the upper airway

o Peritonsillar abscess

o Retropharyngeal abscess

o Throat cancer

o Tracheomalacia ® weakness of the cartilage that supports the trachea

o Vocal cord problems

• Symptoms of upper airway obstruction:

o Noisy breathing

o Increased shortness of breath

o Change in voice ® hoarseness

o Potentially local pain

o Possibly dysphagia

• Signs of upper airway obstruction:

o Stridor

o Breathlessness:

§ Increased RR

§ Suprasternal retraction

§ Use of accessory muscles for inspiration

§ Restlessness

o Voice change

o Drooling

o Subcutaneous emphysema

• First aid measures should be applied ® if in respiratory arrest, then clear mouth & oropharynx of vomit,

dentures or foreign bodies

• If cyanosed & still breathing, give heliox (80% helium & 20% oxygen) ® then consider which

management option is most suited to the situation

• Airway options are:

o Adjunct ® nasopharyngeal, oral or laryngeal mask

o Intubation

o Cricothyroid puncture

o Tracheostomy under local anaesthetic

• Endotracheal intubation vs tracheostomy ® the choice should depend on the nature of the obstruction,

the severity, the expertise available, the equipment available, and the anxiety of the patient

• Treatment most consists of fixing the upper airway obstruction once the patient has been stabilised & an

airway secured



Outline the diagnostic features & differentiate between stridor & stertor STERTOR

• Stertor is a low-pitched noise produced at the level of the oropharynx / nasopharynx ® i.e. snoring

• It can manifest as heavy snoring when in a coma or deep sleep, and is sometimes due to obstruction of

the upper airways (e.g. with enlarged tonsils or choanal stenosis)

STRIDOR

• Stridor is defined as noisy breathing which can be on inspiration, expiration or both

• The inspiratory phase is most likely to be at the laryngeal level, whilst expiratory is the wheeze of

asthma in the bronchi or bronchioles ® a mixed type can also occur, which involves the trachea or

larynx & lower airways

• Stridor is typically high in pitch & is a sign of respiratory obstruction ® such as croup, a foreign body,

abscess, or allergic reaction

• Stridor can have many different causes ® the more common of which are:

o Congenital:

§ Laryngomalacia

§ Vocal cord palsy

§ Vocal cord web

§ Subglottic stenosis

o Acquired:

§ Trauma

§ Foreign body

§ Angioedema

§ Epiglottitis

§ Croup

§ Vocal cord palsy

§ Laryngeal carcinoma

§ Subglottic stenosis

§ Laryngeal papillomata

§ Large laryngeal polyps

/ cysts

§ External compression

® e.g. a thyroid mass

• Management consists of taking a basic history & giving first aid as required ® the severity of the stridor

should be assessed, and the airway should be improved or secured as necessary

• The severity of stridor can be assessed by the patient’s general appearance, and the following

categories can be used:

o Only present on exertion

o Only present on deep inspiration

o Audible all the time but able to hold a conversation

o Has to talk in short phases

o Only able to get odd words out as concentrating on breathing

o Unable to talk & using accessory muscles

o Cyanosed

o Respiratory arrest

• Finally, the underlying cause should be investigated & treated



Outline the indications, management & complications of a tracheostomy • A tracheostomy is an operation where a small hole is made through the skin over the lower part of the

neck & into the trachea ® a breathing tube is then inserted to bypass any obstruction above & allow

ventilation

• However, by doing this, the humidifying & warming function of the nose & upper airway is removed ®

these functions can be replaced artificially and are very important

• The tube also bypasses the vocal cords, and hence prevents speech ® various valves can be fitted to

allow expired air to pass through these

• Indications for a tracheostomy:

o Obstruction ® e.g. infections, cancers, anaphylaxis, foreign bodies

o Oedema:

§ To prevent breathing problems due to tissue swelling after an operation

§ The air passage through the larynx is relatively narrow ® so a small amount of

swelling can cause a substantial obstruction

o Secretions:

§ To allow easier removal of secretions from the air passages & prevent scarring of the

larynx from long-term artificial respiration

§ Initially patients may be intubated, but this means the patient is unable to cough up

mucous and hence this may cause a chest infection

§ Although mucous can be removed by suction, it is much easier with a tracheostomy,

and these also protect the delicate lining of the larynx

o Prevent overspill:

§ To prevent overspill of secretions into the lungs

§ Certain neurological conditions affect the ability to cough & swallow ® meaning

aspiration is a risk

§ A cuffed tracheostomy prevents this

o Laryngectomy:

§ To provide an alternative means of air entry into the lungs after a laryngectomy

§ This is a special type of tracheostomy where the trachea is cut across & the lower end

is brought into a permanent stoma

§ The swallowing passage is then recreated

o Ventilation:

§ T reduce airway pressure in someone who requires airway support

§ It reduces airways pressures as it allows oxygen to enter the airway lower down in the

respiratory tract

§ Used in patients e on long-term ventilation (e.g. ICU)

• There are two main types of tracheostomy:

o End tracheostomy ® performed as part of a laryngectomy

o Side tracheostomy ® the larynx is left in place & an airway is put through the skin over the

trachea

• A patient may only need to spend 5–10 days in hospital, depending on why the tube was inserted ® the

inner tube will need to be changed at 5 days, and the patient should be confident on how to look after

the tube whilst at home



• Risks & complications:

o Early ® tube displacement, blocked tube from dry secretions, pneumothorax, local infection,

dysphagia, surgical emphysema

o Late ® tracheocutaneous fistula on removing the tube, tracheo-oesophageal fistula, and

tracheal stenosis

• Outcome:

o Often the tracheostomy can be removed at a later date ® depending on the reason for it

o It is important to check the patient is able to breathe for themselves normally ® the tube is

often blocked off for 24–48hrs to check this

o Later, a large occlusive dressing is applied over the hole ® it has to be airtight to heal

• Elements of a tracheostomy tube:

o Cuff ® allows seal for ventilate & to prevent aspiration

o Fenestration ® allows air to pass from lung up through larynx for speech

o Reservoir ® allows cuff pressure to be estimated

o Inner tube ® can be removed regularly for cleaning

o Speaking valve ® flap valve which opens & allows air flow to lungs on inspiration and closes

on expiration, directing air through the larynx for speaking

o Temporary tubes are often plastic ® but long-term tubes are made of an inert silver

ENT – VOICE DISORDERS


Outline the anatomy & function of the larynx

LARYNX

• The main function of the larynx is to act as a sphincter, to protect the lower airways from contamination

by food, liquid & secretions ® it also allows for an effective cough, and provides the ability to produce

speech

• The larynx is essentially a tube made up of a series of cartilage & bone which are held together by

interconnecting membranes, ligaments & muscles ® superiorly it connects to the pharynx, and inferiorly

to the trachea

• The larynx consists of:

o Cricoid cartilage

o Thyroid cartilage

o Epiglottis

o Arytenoid cartilages (x2)

o Cuneiform cartilages (x2)

o Corniculate cartilages (x2)



• The cricoid cartilage is the most inferior cartilage of the larynx & is signet ring in shape ® it provides

an attachment for the arytenoid cartilages & the thyroid cartilage

• The thyroid cartilage is the largest of the laryngeal cartilages, and connects with the cricoid cartilage &

hyoid bone ® it also provides a site of attachment for the epiglottis & the vocal ligament

• The epiglottis is attached to the posterior aspect of the thyroid cartilage at the angle, and projects

posterosuperiorly from its attachment ® its main function is to protect the airway when swallowing

• The arytenoid cartilages are pyramidal shaped cartilages & attach to the vocal cords, and they are

responsible for adduction & abduction of the ligaments ® they also attach the vestibular ligament

superiorly (the false cord)

• During swallowing, the food bolus is propelled backwards by the tongue, and from here it enters two

channels called the pyriform fossa, which are grooves that run downwards & backwards around the

laryngeal inlet (epiglottis) and lead into the oesophagus ® during this process, the larynx is drawn

upwards, and this has the function of tilting the laryngeal inlet & bringing it closer to the tongue base &

epiglottis, which act like a lid

VOCAL CORDS

• The vocal folds are sometimes called the glottis, and lie suspended in the airway by the arytenoid &

thyroid cartilages

• The vocal cords themselves have a complex structure consisting of many layers ® which allows the

superficial coverings to be relatively mobile while the body remains stiffer

• The glottis divides the larynx into the supraglottis & the subglottis

• The supraglottis has sensation supplied by the internal branch of the superior laryngeal nerve, whilst

the external branch carries motor fibres to the cricothyroid muscles ® these help adjust the tension of

the vocal cords, and is the only laryngeal muscle on the outside of the larynx

• The recurrent laryngeal nerve carries sensation to the subglottis and supplies all other laryngeal

muscles ® this is a branch of the vagus nerve and has a relatively long course (especially on the left),

making it prone to injury in the neck or chest

• There are several laryngeal muscles, and they are all involved with the adjustment of the vocal cord

position & tension ® the posterior cricoarytenoid muscle is the only muscle that abducts the cords,

and is often described as the most important muscle in the body

• The glottis acts as a sort of watershed in the larynx ® the supraglottis drains to nodes in the neck,

whilst the subglottis drains into paratracheal nodes (the cords themselves have very limited drainage)

Describe the diagnostic features & causes of laryngeal malignancy • Then most common malign tumour of the larynx is a squamous cell carcinoma

• The most important aetiological factor is smoking ® the greater the number smoked & the longer the

time period equates to a higher risk

• Heavy alcohol intake can increase this risk even further, as well as a genetic predisposition

• The primary symptom of carcinoma of the vocal cords is hoarseness ® so it is important to always

consider laryngeal carcinoma in patients with persistent hoarseness lasting >6 weeks

• Since a small lesion in the larynx will cause symptoms early, and because of this area’s poor lymphatic

drainage, the prognosis is good ® 5yr survival is 95%

• Cancers in the supraglottis & subglottis unfortunately do not have such definite & early symptoms ®

they may cause irritation in the throat, a cough, referred otalgia, or may present with a node in the neck



o NB: It is usually not until later when the airway or voice is compromised

• Other symptoms include difficulty swallowing & cervical lymphadenopathy

• The larynx may present with a raised, thickened, irregular mass, with leucoplakia & redness ® there will

also be narrowing of the airway, and potentially fixation of the vocal cord on visual examination

• The primary options are endoscopic removal, radiotherapy, and radical surgical excision

(laryngectomy) ® however, it must be noted that surgery can have a significant impact on the voice,

and may result in a tracheostomy being needed after the laryngectomy

Outline the diagnostic features & causes of recurrent laryngeal nerve palsy • The recurrent laryngeal nerve is a branch of the vagus nerve (CN X) ® it has an unusually long course,

especially on its left side, where it runs around the arch of the aorta before passing upwards over the

pleura & into the neck ® here it runs in a groove between the trachea & oesophagus before finally

entering the larynx

• Because of this long route, it is commonly damaged by disease or, or surgery to, any structures close to

it ® e.g. lungs, oesophagus, thyroid

• There is generally a rule of thirds for vocal cord palsy ® 1/3 idiopathic, 1/3 surgery, 1/3 neoplasia

• Possible causes of recurrent laryngeal nerve palsy include:

o Surgical trauma (23%) ® e.g. thyroidectomy

o Malignant disease (22%):

§ Bronchus

§ Thyroid

§ Oesophagus

o Idiopathic (16%)

o Neurological disorders (4%) ® e.g. brain tumour

o Miscellaneous (35%) ® other trauma or CVA

• In more central pathologies, phonation is less important than protection of the airway ® many of the

patients with extensive brain injury die of pneumonia as a result of aspiration

• Symptoms:

o Weak voice

o Tired on prolonged talking

o Perilaryngeal discomfort

o Choking with fluids

o Higher pitched voice

o Diplophonia ®’two tone’ voice

o Weak ‘bovine’ cough

• Vocal cord palsies affect the left side in 75%, the right side in 15%, and both in 10% ® of the malignant

diseases, the most common is cancer of the bronchus

• When investigations of a vocal nerve palsy are done, the cause should be assumed to be malignant

unless proven otherwise

• A CXR is mandatory ® also a CT scan (skull base to mid thorax) if the CXR shows nothing abnormal

• Other investigations may include an USS of the thyroid, and rigid endoscopy of the aerodigestive

tract under GA



• It is also important to consider that the vocal cords may be paralysed for other reasons (e.g. the

cricoarytenoid joint may become fixed due to severe RA or reflux) ® here, direct laryngoscopy is

recommended under GA

• Most management is awaiting recovery (up to 1yr) as the disease is self-limiting ® however, voice

therapy & vocal cord medialisation may also help recovery

Outline the diagnostic features & causes of muscular tension dysphonia • Muscular tension dysphonia is the commonest cause of voice disorders seen in secondary care ® it

is caused by an imbalance of ‘pull’ in the cords, which results in excessive tension of the paired

laryngeal muscles

• There are many multifactorial aetiologies ® including:

o Stress

o Anxiety

o Depression

o Conversion disorders

o Neck / back problems

o Poor vocal hygiene

o Lifestyle ® vocal abuse, not enough fluids, tea / coffee / fizzy drinks, etc.

o A secondary mechanism ® e.g. structural defect of cords or poor respiratory function

• It presents as a variable hoarseness, and can range from normal to no voice ® the voice usually

worsens with use, and may be a little deeper or higher for the expected age & sex ® the voice is

unstable, and there is dryness / uncomfortable sensation in the throat

• Signs include a croaky / hoarse, breathy, bizarre or aphonic voice ® the voice quality can vary & may

sometimes be normal

• The cough is often normal ® even with aphonia

• Vocal folds appear normal in appearance & movement ® but there is either constriction of false cords,

anteroposterior constriction, or extreme sphincter closure when the vocal folds disappear from view

beneath the false cords

• Treatment involves:

o Vocal hygiene

o Lifestyle advice

o Voice therapy

o Addressing the underlying causative factors

Outline the diagnostic features & causes of benign vocal cord lesions NODULES

• The most common cause of nodules is voice abuse, shouting, talking above background noise & reflux

• Mostly seen in young adults (<40yrs) ® much more common in women


o Husky voice that worsens with use

o Loss of higher range of voice

o Perilaryngeal discomfort

• Bilateral swellings in mid-membranous portion of the vocal fold give an hourglass appearance

• Treatment ® voice therapy or surgical excision if unresponsive



POLYPS

• The most common cause of polyps is shouting when suffering with a cold or extra-oesophageal reflux

• More common in men than women ® affects people 30–60 yrs


o Husky voice which worsens with use ® may be deeper

o Voice cuts out during speaking

o Choking episodes if very large

• Usually unilateral grey or haemorrhagic swelling arising from mid-membranous portion of the vocal fold

® has a smooth edge

• Treatments:

o Surgical excision

o Medical treatment

o Voice therapy

REINKE’S OEDEMA

• The most common cause of Reinke’s oedema is smoking ® however, talking a lot & extra-

oesophageal reflux can contribute

• Equally common in men & women ® but more noticeable in women

• Present with deep-pitched gravelly voice ® if severe, may cause choking episodes

• Usually bilateral grey or erythematous swellings along whole length of membranous portion of the vocal

fold

• Treatments:

o Smoking cessation

o Surgical reduction ® of polypoid swelling

o Medical treatment ® of reflux

o Voice therapy

CYSTS

• The cause of cysts is unknown ® some may develop after laryngeal inflammation, and some may be

congenital

• There are 2 types of cysts:

o Mucous retention cysts

o Epidermoid cysts


o Husky voice

o Pitch breaks

o Loss of range of voice

o Increased effort to produce voice

• Signs ® unilateral nodular swelling or localised bulge or stiffness of vocal fold

• Treatments:

o Voice therapy ® can help reduce secondary muscle tension

o Surgical excision



Outline the diagnostic features & causes of reduced or absent vocal cord mobility • Reduced or absent vocal cord mobility can result in the cords coming to rest laterally or medially ® if

lateral, the voice will be poor but the airway good, and if medially, the voice will be good but the airway

poor

• The major causes are:

o Viral infection

o Tumours of the cord / joint ® benign or malignant

o Tumour of the nerve

o Damage from intubation

o Laryngeal reflux

o Functional dysphonia

o Laryngitis

FUNCTIONAL DYSPHONIA

• Functional dysphonia is a diagnosis that includes a wide variety or non-organic voice problems

• The patient may present with a weak or hoarse voice that tires easily & is abnormally pitched ® these

problems can be attributed to laryngeal dysfunction resulting from vocal strain, stress & psychological or

psychiatric problems

• The patient may have experienced some form of stress or life event at the time of onset, and it is not

infrequent that a family member / friend has recently developed a serious throat condition

• Firm reassurance is necessary, and speech therapy can relieve laryngeal tension ® on rare occasions,

the help of a psychiatrist may be needed

ACUTE LARYNGITIS

• The larynx can become inflamed in isolation or as part of a general infective process, as well as due to

irritant substances (e.g. cigarette smoke or alcohol fumes) ® when only the larynx is affected, it may be

due to vocal abuse or voice strain

• A hoarse voice is the most common complaint, but occasionally complete aphonia may occur ® the

patient may also complain of pain on speaking & swallowing

• If there is an infective element ® then general malaise & slight pyrexia may be present

• The vocal cords appear read & oedematous, and often the whole larynx is inflamed, with swelling of the

arytenoids & false cords ® movement of the cords is restricted, but symmetrically & without paralysis

• Treatment is largely supportive, and includes:

o Steam inhalation

o Voice rest

o Simple analgesia

o Gentle warmth applied to the anterior neck

o Cough suppressant may help if this is a prominent feature

• Forced vocalisation of an already inflamed larynx can lead to haemorrhage into the vocal fold, and the

resulting fibrous reaction can lead to permanent vocal disorder

EPIGLOTTITIS

• Epiglottitis is an acute & life-threatening condition caused be H. influenzae ® it must always be

considered in pyrexial children with a sore throat



• It can start with features of an URTI and rapidly progress to total airway obstruction within hours ®

usually occurs in children, but can also affect adults where the whole supraglottis is usually involved

• Features include:

o Difficulty swallowing

o Drooling

o Change in voice

o Change in child’s cry

o High grade pyrexia

o Inspiratory stridor

• Avoid lying the patient down as this can lead to a collapse of the airway ® the patient will usually be

sitting up & using their accessory muscles for respiration

• No intra-oral investigations should be performed without the equipment for intubation or emergency

tracheostomy

• Treatment is rapid IV antibiotics ® ceftriaxone

CROUP

• Croup (laryngotracheobronchitis) is usually viral in origin ® parainfluenza mainly, but RSV &

adenovirus can also cause it

• It causes diffuse inflammation of the airways ® not just the supraglottis

• It tends to have a longer course than epiglottitis, and can be serious or even fatal

• A low grade URTI is common, followed by a rise in temperature & presence of inspiratory stridor ® a

generalised deterioration ensures, and the child quickly becomes toxic

• Treatment is with IV antibiotics (if bacterial) & nebulised adrenaline ® a period of ventilation may be

necessary in serious cases

LARYNGEAL DIPHTHERIA

• Extremely rare in the UK ® but early treatment with antibiotics & antitoxin is needed

• The symptoms are a hoarse voice, cough & late stridor which can progress to total airway obstruction ®

it can also affect the oral cavity & pharynx, causing erythema & swelling

• Damage to the myocardium & peripheral nerve from the toxin can occur

CHRONIC LARYNGITIS

• This is often multifactorial, but the most important aetiological factor is smoking ® but patients can often

trace things back to a nasty URTI, and since this they have been hoarse

• Once inflammation has occurred, it is sustained due to a combination of factors ® such as:

o Vocal abuse

o Chronic bronchitis

o Sinusitis ® leading to postnasal drip

o Environmental pollutants

o Acid reflux

o Alcohol fumes

• Rarely, TB, syphilis & fungal infections can be a cause

• The patient complains of a hoarse voice ® examination will show erythematous cords which may be

thickened & oedematous



o NB: Even a small amount of oedema in Reinke’s space will be slow to resolve due to the poor

lymphatic drainage of the area

• Chronic inflammation can lead to dysplasia & carcinoma in situ ® so this must be watched

• Management consists of intensive speech therapy and the removal of causative factors ® surgery is

more diagnostic now, so has been largely abandoned

Outline the diagnostic features & causes of common voice disorders • Common voice disorders include:

o Laryngitis

o Muscular tension dysphonia

o Nodules

o Polyps

o Reinke’s oedema

o Cysts

o Papillomata

o Carcinoma

o Cord palsy

• Dysphonia ® any impairment in the voice or difficulty speaking

• Dysarthria ® imperfect articulation of speech due to disturbances of muscular coordination

• Dysphasia ® impairment of speech & verbal comprehension or production when associated with brain

injury

• Hoarseness ® a perceived rough, harsh or breathy quality to the voice

• Voice problems can be categorised into one of the following causes ® one may lead to another, and

more than one may be present at once:

o Inflammation

o Muscle tension imbalance

o Structural / neoplastic

o Neuromuscular

• Assessing a voice problem should include:

o History

o Listening to the voice:

§ If rough ® implies a problem with the way the vocal folds are vibrating, or false cords

being used

§ If breathy ® implies problems bringing vocal folds together (e.g. vocal cord palsy)

o Visualise the larynx

o Palpate the neck

o Identify any contributing factors

• Treatment depends on the condition causing the dysfunction ® however, injecting materials to change

the position of the cords & laryngeal framework surgery (thyroplasty) are used to medialise a

lateralised cord

• It must be mentioned that surgeons usually like to wait 6 months before operating (unless urgent) ® as

sometimes vocal cord function can return

• Thyroplasty:

o Performed under local anaesthetic, so voice can be assessed during operation

o This involves a small neck incision & exposure of the thyroid cartilage

o An oblong window is cut into the cartilage below the level of the vocal cord, and then a silastic

shim is inserted to manually reposition the cords



o Alternatively, a thick fluid can be injected lateral to the cord, and hence push it closer to the

midline

• If the cords are medialised and need lateralising ® then the cords can either be manually repositioned

as above, or a section of cord can be removed to improve breathing

List the key features & common symptoms that help distinguish benign from malignant causes of hoarseness HISTORY

• Could the patient have cancer? ® risk factors include:

o Smoker, ex-smoker or are exposed to smoke occupationally / socially

o Difficulty breathing or swallowing

o Family history of throat / laryngeal cancer

o Complaining of pain or referred otalgia

o Have a lump in the neck

• If yes to any ® refer on the 2 week wait cancer pathway

• Could the patient have infective laryngitis?

• Are there other symptoms & signs of an upper respiratory tract infection?

• Is the voice problem related to voice use / abuse and/or poor vocal hygiene?

• What does the patient do for a living, socially, or domestically with their voice?

• What is their lifestyle & diet like?:

o How much tea / coffee / fizz do they drink?

o Do they drink any water?

o Do they eat irregularly or late at night, or have large meals before going to bed?

o Eat a lot of spicy / fatty food?

o Suffer from heartburn, indigestion, reflux, coughing or choking episodes?

• Has the voice problem persisted for >6 weeks? ® they need referring for laryngeal examination

ASSESSMENT OF A VOICE PROBLEM

• History

• Listen to voice:

o Rough or breathy?

o Constant / variable?

o Pitch too low or too high?

o Voice too loud or difficulty hearing it?

• Visualise the larynx:

o Fibreoptic or rigid telescopes, or laryngeal mirror

• Stroboscopy ® allows wave motion of mucosa to be observed

• Identify contributing factors

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