Ear, nose and throat and head and neck problems

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Chapter 2 Ear, nose and throat and head and neck problems

Sarin Wongprasartsuk, Andrew Danks, Neil Vallance

2.1 Introduction

The specialty of ear, nose and throat — head and neck (ENT — head and neck) surgery is very broad and complex. Each component is a subspecialty in itself. Addressing any problems relating to the head and neck with this in mind will allow you to systematically approach the patient’s problem. As in any aspect of clinical medicine, the initial diagnosis is made by taking a thorough history prior to a complete physical examination that is supplemented by special investigations.

History

The common symptoms in the ear are otalgia, hearing loss, vertigo, tinnitus, aural fullness, discharge, hissing, facial weakness, bleeding and blockage. Common symptoms relating to the nose and sinuses are epistaxis (bleeding nose), nasal obstruction, hyposmia (decreased smell)/anosmia (complete loss of smell), loss of taste, facial pain, post-nasal drip, facial asymmetry, diplopia (double vision), epiphora (abnormal tears due to a blocked collecting system), redness of the eye, nasal discharge, allergy, sneezing and hay fever. Common symptoms relating to the throat include pain, dysphagia (difficulty swallowing), dysphonia (abnormal voice production), reflux, referred pain, cough, haemoptysis, shortness of breath, snoring and drooling. Head and neck patients may also present with symptoms of lumps and pain.

When a patient presents with any of these symptoms (Table 2.1) it is important to characterise the symptoms in terms of site, severity, radiation, frequency, duration, exacerbating and relieving factors, associated features, the progression of symptoms and how it affects the patient’s activities of daily living. When taking a history, the past history needs to be noted, including previous surgery to the respective parts of the ear, nose and throat, head and neck and any associated conditions. A patient’s medication and adverse reactions to medication should be known, as well as their social history, including their smoking and alcohol consumption and environmental exposures such as noise, dust and any other potential allergens. The family history should be known and it is also wise to find out about any family tendencies regarding bleeding disorders and deafness.

Table 2.1 Symptoms of ear, nose and throat conditions

Ear	Otalgia, hearing loss, vertigo, tinnitus, aural fullness, discharge, hissing, facial weakness, bleeding, blockage
Nose and sinuses	Epistaxis, obstruction, hyposmia/anosmia, loss of taste, facial pain, post-nasal drip, facial asymmetry, diplopia, epiphora, red eye, nasal discharge, allergy/sneezing/hay fever
Throat	Pain, dysphagia, dysphonia, reflux, globus, referred pain, cough, haemoptysis, shortness of breath, snoring, drooling
Throat	Head and neck: lump, pain

Examination of the head and neck

As stated, a systematic approach to examining the head should recognise the principles of ENT — head and neck and include this in the examination, along with the cranial nerves. This will make a complete examination of the area. It is important to be aware of referred pain (Fig 2.1); for example, the ear is supplied by multiple nerves and ear pain can present as referred pain from intraoral or laryngeal pathology. Look for signs of redness, swelling, tenderness, increased warmth and loss of function.

Figure 2.1 Referred or non-otologic otalgia

From Dhillon & East, 2006

Ear

See section 2.2.

Nose

Based on Dhillon & East, 2006

The lymph node groups are divided into groups commonly known as 1–6. There is a seventh group but it is often not included. The groups are:

1. submental and submandibular triangle

2. upper jugular chain

3. mid-jugular chain

4. lower jugular chain

5. posterior triangle

6. anterior triangle

7. superior mediastinum.

The other areas that need to be palpated are the parotid, the posterior occipital nodes and the post-auricular region.

The lymph node groups drain specific areas of the head and neck, which in turn relates to the treatment of various head and neck cancers.

Table 2.2 outlines the process for performing a thyroid examination when thyroid disease is detected or suspected. Table 2.3 outlines an examination of the cranial nerves.

Table 2.2 Thyroid examination — performed if thyroid disease is detected or suspected

Look	Patient — hyper/hypothyroid, thyroid eye signs, proptosis — Graves’ disease, lid lag, chemosis a complication, voice — recurrent laryngeal nerve compression, goitre
Feel	Right versus left side, prominent nodules
	Percuss — retrosternal extension
	Auscultate — bruits
	Pemberton’s sign — a sign of SVC compression — raise arms above head and look for venous congestion in the head
Periphery	Pulse, reflexes

Table 2.3 Screening examination of the cranial nerves

I	Smell
II	Visual acuity, light reflex — direct and consensual, fields
III/IV/VI	Eye movements
V — V1, V2, V3	Sensation, motor — palpate jaw (masseter, temporalis)
VII	Facial movements: temporal — forehead; zygomatic — eye closure; buccal — cheek; marginal mandibular — lower lip; cervical — platysma
VIII	Tuning fork
IX/X	Gag reflex
XI	Sternocleidomastoid, trapezius — palpate
XII	Tongue mobility; palsy indicated by protrusion to affected side

A gait examination is often performed as part of the dizziness assessment and is covered in the neurologic examination.

The voroscope (Fig 2.3) has revolutionised the ENT — head and neck examination. A good headlight from theatre will often suffice. Sometimes only a light source and head mirror are available.

Figure 2.3 Voroscope

Photos courtesy of Mr Sarin Wongprasartsuk

Flexible nasal endoscopy has also revolutionised the diagnosis of ENT — head and neck conditions. It has become an integral part of the examination and enabled office-based diagnosis. There are many hidden areas in ENT — head and neck examination and the nasoendoscope has permitted access to the internal nose, sinus outflow tracts, post-nasal space, larynx, hypopharynx, tongue base and sometimes the proximal oesophagus (Fig 2.4).

Figure 2.4 Nasolaryngoscope

From Dhillon & East, 2006

After the thorough history and complete physical examination have been performed, investigations are ordered. A differential diagnosis should be considered and the mnemonic VITAMIN CID may be helpful.

Vascular

Infective: may involve bacterial, viral, fungal and parasitic problems

Tumour: subdivided into benign and malignant

Accident

Metabolic causes such as diabetes and renal impairment

Immune/autoimmune conditions

Investigations are ordered to:

• confirm the diagnosis

• rule out other diagnoses

• quantify the severity of the disease

• follow the progression of the disease

• look for complications of any therapy.

The common investigations include:

• A blood test — FBE, allergy investigations (e.g. RAST — radioallergosorbent test).

• A biopsy — always be aware of the potential for bleeding and look for any pulsations as any red lesion may be actually a vascular malformation. Lesions high in the nose should be treated with caution as there may be a communication with the CSF space.

• Fine needle aspirate (FNA) — preferred to an open biopsy of any neck lump to prevent seeding of tumour cells. Can be combined with ultrasound guidance for increased accuracy.

• Swabs can be taken to include bacterial, fungal and viral cultures.

• Radiology — includes ultrasound, X-ray, barium swallow, CT, MRI and nuclear medicine.

• The audiogram is an important component of hearing assessment.

• Vestibular function testing is often performed.

• Laryngeal videostroboscopy allows visualisation of the vocal cords.

• Rhinomanometry is used for assessment of nasal air flow.

• Clinical photographic documentation is important in assessing assaults and the preoperative assessment for some cosmetic procedures.

The last four investigations are usually ordered by ENT — head and neck specialists.

Regional and developmental anatomy

It is very important to know the regional anatomy and embryology of the structures of the ENT — head and neck. When assessing a lump in the neck consider the local anatomy of the skin, soft tissue, associated vessels, the lymph node drainage pathways, any potential nerves that may be in the area and bones. Think about the pathway for development of the thyroid, parathyroids, branchial cleft cysts, ear cysts and their appendages.

2.2 Ear

The ear has three components consisting of a number of parts listed in Table 2.4.

Table 2.4 Outer ear, middle ear and inner ear components

Outer ear	Pinna — parts
	External auditory canal — lined by skin, acts to remove accumulated squames from the tympanic membrane out of canal
	Tympanic membrane
Middle ear	Ossicles: malleus (hammer)/incus (anvil)/stapes (stirrup) — act as the chain between the tympanic membrane and the oval window membrane
	Eustachian tube — functions to aerate middle ear
	Middle ear mucosa — respiratory type
	Mastoid cells — part of the temporal bone and joined to middle ear cleft
Inner ear	Cochlea and vestibular apparatus
	Oval window — superior — part of the cochlear connection to ossicular chain
	Round window — inferior — part of the cochlea that moves in response to any hydraulic force placed on the oval window

To examine an ear, systematically investigate the outer ear followed by the middle ear and then the inner ear (Fig 2.5).

Figure 2.5 Anatomy of the ear

From Dhillon & East, 2006

For the outer ear look at the normal contour of the outer ear, the ear canal and the tympanic membrane. Sometimes it is necessary to remove the wax from the canal to get a good view. When assessing the middle ear also assess for tympanic membrane mobility using what is called pneumatic otoscopy. Check any perforation of the tympanic membrane by assessing its size, the site, associated discharge and the condition of the middle ear mucosa. The tests of the inner ear that are commonly performed are: using a 512 Hz tuning fork; testing a patient’s gait; and performing a Dix-Hallpike manoeuvre. Prior to performing a Dix-Hallpike manoeuvre the stethoscope should be used to listen for any carotid bruits because the Dix-Hallpike manoeuvre may precipitate a TIA. The stethoscope is also used to listen for pulsatile tinnitus and is placed on the mastoid tip. The Dix-Hallpike manoeuvre is diagnostic of benign paroxysmal positional vertigo (BPPV) and is performed on an examination couch. While sitting up, the patient turns their head quickly to one side while keeping the eyes wide open and focusing on a spot in the distance in the line of their eye sockets. Next, the patient lies back with their head dependent over the head of the examination bench. The examiner inspects for nystagmus, which indicates an overstimulated semicircular canal system. It is a positive result when nystagmus is elicited on the side to which the head is turned.

Facial nerve (CN VII). This nerve courses through the temporal bone then enters the internal auditory canal in the antero-superior quadrant. It then passes forwards in what is called the labyrinthine segment and passes above the cochlea, contributing to the geniculate ganglion that has branches to the petrosal nerves. It then turns back and runs between the lateral semicircular canal superiorly and the oval window that is attached to the stapes, inferiorly. After passing these two structures it courses down in the stylomastoid canal giving off two branches: first, the nerve to the stapedius and then the chorda tympani that relays taste sensation from the anterior two-thirds of the tongue. The facial nerve exits the skull base via the stylomastoid foramen. It is termed the trunk of the facial nerve at this point. It gives off its auricular branch and then separates into a superior and inferior division. The superior division has temporal, zygomatic and buccal branches and the inferior division has the marginal mandibular and the cervical branches. These braches supply the muscles of facial expression.

Vestibulocochlear nerve (CN VIII). The cochlear nerve occupies the antero-inferior quadrant of the internal auditory canal (IAC). The superior division of the vestibular nerve occupies the postero-superior quadrant of the IAC and the inferior division of the vestibular nerve occupies the postero-inferior quadrant. The cochlear nerve conducts sound and the vestibular nerve conducts the sensation of balance.

Role of the ear

The purpose of the ear is to transform sound energy into electrical impulses. Sound is conducted via the external canal, the tympanic membrane and the ossicular chain, then converted into electrical impulses by the cochlea. These impulses pass up the cochlear component of the auditory nerve.

The balance system or vestibular apparatus comprises: the lateral, posterior and superior semicircular canals; the utricle and the utricle saccule; and the endolymphatic sac. This sensory apparatus is supplied by the vestibular component of the vestibulocochlear nerve.

The cochlea and vestibular apparatus are found in the petrous temporal bone.

Nearby blood vessels

The sigmoid sinus runs from the superolateral aspect of the temporal bone coursing inferomedially to exit the skull via the jugular foramen. The internal carotid artery enters the floor of the petrous temporal bone via the carotid canal, passes below the cochlea and travels horizontally till it reaches the sphenoid and carotid siphon. The superior petrosal sinus courses along the postero-superior aspect of the temporal bone from the cavernous sinus to the transverse sinus. It lies in the outer margin of the tentorium cerebelli. The labyrinthine artery, which is a branch of the basilar artery or anterior inferior cerebellar artery, supplies the petrous temporal bone entering via the internal auditory canal.

External ear

Wax and otitis externa

Otitis externa (OE) is an inflammation of the external auditory canal (EAC). It is characterised by pain, blockage and discharge from the ear.

Predisposing factors include the following.

• Wax build up and moisture — the normal function of the EAC is to move wax produced by the ceruminous glands and keratin from the tympanic membrane and canal skin itself away from the tympanic membrane towards the opening of the EAC. Water can be trapped behind the wax and become secondarily infected resulting in an early OE.

• Cotton bud abuse — this causes damage and irritation to the skin of the EAC. This leads to build-up of debris in the canal, which can become infected.

• Diabetes/immune deficiency — this needs to be considered in all cases because skull base osteitis, which is diagnosed with a combination of CT, bone scan and white cell scan, is a severe complication of OE.

• Swimming in lakes, waterholes or community pools.

• Humid climates.

• Skin conditions.

• Posttraumatic — syringing of ears.

• Exostoses — bony growths that narrow the EAC.

The build-up of debris is subsequently infected by bacteria or fungi.

The most common bacteria is Pseudomonas aeruginosa. Fungal hyphae are seen in fungal infections.

Management

OE is best managed with one or more of the following measures:

• meticulous toileting of the external canal — this may need to be repeated as healing skin desquamates

• taking a culture of the discharge — microscopy, cultures and antibiotic sensitivities (M/C/S) and fungal

• using topical antibiotics — Ciproxin HC, Sofradex, Locacortin vioform, Otocomb

• using a pope ear wick, which is an expandable tampon that allows delivery of the medication; in moderately severe cases of OE where the EAC is completely occluded, a wick needs to be inserted and expanded with antibiotics for 24 hours prior to permitting ear toileting

• a course of oral/IV antibiotics — ciprofloxacin in non-responsive cases

• excluding skull base osteitis in severe non-responsive cases, especially in diabetic or immunocompromised patients

• excluding any predisposing factors such as cotton bud use (as a long-term measure)

• removing exostoses with an operation that drills away the bone and enlarges the ear canal.

Middle ear

Otitis media

Otitis media is an inflammation of the middle ear/mastoid cavity. Its underlying cause is an abnormality of the Eustachian tube that ceases to aerate the middle ear, leading to a range of possible complications (Figs 2.6 and 2.7). A negative pressure forms in the cleft and an effusion results. There are many causes of a dysfunctional Eustachian tube. In children, the Eustachian tube is shorter and more horizontal, therefore, more prone to blocking. Causes include: viral URTI, cleft palate and a post-nasal space tumour. The effusion may become secondarily infected resulting in acute otitis media (AOM). Common organisms are: Streptococcus pneumoniae, Haemophilus influenzae and Moraxella.

Figure 2.6 Extracranial complications of otitis media

From Dhillon & East, 2006

Figure 2.7 Intracranial complications of otitis media

From Dhillon & East, 2006

AOM presents with otalgia, fever and a red, inflamed ear drum. The treatment may include antibiotics and antipyretic analgesia. The tympanic membrane may spontaneously rupture, resulting in a discharging ear and immediate pain relief.

Otitis media with effusion (OME) presents with a conductive hearing loss and a dull ear drum. Most cases of OME in children (about 90%) will resolve within three months, as there is often a preceding URTI. In adults, a new onset effusion with no precedent URTI needs to be investigated. The post-nasal space needs to be visualised. In longstanding effusions, a middle ear ventilation tube (grommet) is inserted to resolve the effusion.

Complications of AOM are those resulting from mastoiditis and include:

• subperiosteal abscess — presents with a protruding ear; pus escapes from the mastoid cavity via a communication posterior and superior to the pinna

• intracranial complications — extradural, subdural, intracerebral abscesses; meningitis

• labyrinthitis

• facial nerve palsy

• lateral sinus thrombosis

• petrositis — infection of the apex of the petrous temporal bone; CN VI palsy; trigeminal neuralgia CN V.

CT scan findings consistent with mastoiditis are opacification of the middle ear/mastoid cleft associated with bony destruction of the normal bony trabeculae.

A chronic discharging ear for more than three months is termed chronic suppurative otitis media (CSOM). It results from chronic infection, with an associated biofilm formation or may be caused by a cholesteatoma.

A cholesteatoma is a sac of keratinised squamous epithelium that has the potential to grow and erode the surrounding structures resulting in hearing loss, discharge and potential intracranial complications.

A bacterial biofilm is a colony of bacteria that has formed a resistant matrix often on an inert surface. Bacterial biofilms result in chronic infections in the ear, nose and throat.

Inner ear

Hearing loss

There are many causes of hearing loss, as indicated in Table 2.5.

Table 2.5 Causes of hearing loss

Cause	Conductive hearing loss	Sensorineural hearing loss
Congenital	Atresia of ear, ossicular abnormalities	Prenatal: genetic, rubella
Acquired	External: wax, otitis externa, foreign body	Perinatal: hypoxia, jaundice
	Middle ear: middle ear effusion, chronic suppurative otitis media, cholesteatoma,	Trauma: noise, head injury, surgery
	Perforated drum, otosclerosis, traumatic perforation of drum	Inflammatory: chronic otitis, meningitis, measles, mumps, syphilis
	Ossicular disruption	Degenerative: presbyacusis
		Ototoxicity: aminoglycosides, cytotoxics
		Neoplastic: acoustic neuroma
		Idiopathic: Ménière’s disease, sudden deafness

Based on Dhillon & East 2006

When evaluating hearing loss, the outer ear, middle ear, inner ear and central pathways need to be considered. The time frame, whether sudden or acute versus chronic, needs to be ascertained. A prior history of trauma, noise exposure and associated symptoms is a valuable clue.

A complete examination with tuning fork tests is required and an audiogram will guide the diagnosis (Figs 2.8a and b).

Figure 2.8a Tuning fork tests

From Dhillon & East, 2006

Figure 2.8b Audiograms

From Dhillon & East, 2006

CT, MRI and other auditory tests such as stapedial reflexes (a test of middle ear function/fixation of the stapes in otosclerosis), otoacoustic emissions (a test for cochlear function) and auditory brain stem responses (ABR) (a test of the central pathway) will assist with localisation of the problem.

Vertigo

Vertigo can be disabling. The vestibular apparatus may be overactive or underactive. An imbalance between the left and right sides may result in vertigo. There are many causes (Fig 2.9).

Figure 2.9 Otologic causes of dizziness

From Dhillon & East, 2006

The most common causes of vertigo are:

• Benign paroxysmal positional vertigo (BPPV) — a disorder of the semicircular canals where otoliths (small calcium particles) float free in the semicircular canals and stimulate the ampullae of the canals. The treatment is a particle repositioning manoeuvre such as the Epley manoeuvre.

• Ménière’s — a syndrome characterised by the triad of rotatory vertigo, hearing loss and tinnitus — often associated with aural fullness. There are many theories that relate to an imbalance in the flow of endolymph in the inner ear.

• Vestibular neuronitis — often a viral aetiology, with no involvement of the auditory system.

• Labyrinthitis — often a viral aetiology involving the whole of the labyrinth and therefore both balance and hearing are affected.

When assessing a patient with a balance problem, the components of balance disorders that need to be addressed are the cardiovascular system (CVS), central nervous system (CNS)/peripheral nervous system (PNS), cerebellum, vestibular system and vision. Often the causes are irreversible and may progress. The ongoing therapy involves physiotherapy and occupational therapy to make sure it is safe for a patient to return home.

Vestibular function testing may be of assistance in diagnosing the probable cause, as is imaging. MRI is used to assess the brain, brainstem and retrocochlear region, whereas CT is used to assess the middle ear anatomy.

Tinnitus

Defined loosely as noise generated somewhere in the head, tinnitus (Fig 2.10) is annoying to the patient and can be extremely disabling.

Figure 2.10 Tinnitus

From Dhillon & East, 2006

There are many causes for tinnitus, but the most common is idiopathic.

Idiopathic tinnitus cannot be cured with an operation. It is known that if all the hearing mechanism was removed, tinnitus would still be reported by the patient because of a phenomenon known as brain plasticity — it creates the sound and amplifies it at the level of the patient’s awareness.

The treatment for idiopathic tinnitus is supportive, relying on some form of distraction therapy such as:

• having a clock radio on at night prior to going to sleep

• having a hearing aid that introduces sound (a masking sound) into the affected side

• psychological retraining — this aims to refocus a patient away from tinnitus. One can explain tinnitus to patients as likening it to tuning in to external sounds such as an air conditioning fan or a car going past. If you concentrate on it, you hear it. If you don’t concentrate on it then you don’t hear it and so with tinnitus it will stop bothering you.

Reversible causes, such as outer, middle or inner ear pathology, need to be ruled out. An audiogram is a good screening test. CT and MRI may be ordered.

2.3 Facial weakness

When a patient presents with a facial weakness a systematic approach needs to be adopted, considering the components and course of the facial nerve together with the VITAMIN CID mnemonic. Consider:

• the central nervous system — causes sparing of the forehead

• the peripheral nervous system — whole of affected side involved

• the course of the facial nerve from the internal auditory canal through the middle ear and mastoid

• the branches of facial nerve dividing in the parotid: temporal, zygomatic, buccal, marginal mandibular, cervical

• the neuromuscular junction

• muscle disorders.

Table 2.6 lists the most common causes of facial weakness.

Table 2.6 Causes of facial weakness

Site	Aetiology
Intracranial	Acoustic neuroma
	CVA*
	Brain stem tumour*
Intratemporal	Bell’s palsy
	Herpes zoster oticus
	Middle ear infection
	Trauma
	– surgical
	– temporal bone fracture
Extratemporal	Parotid tumours
Miscellaneous	Sarcoidosis, polyneuritis

Based on Dhillon & East, 2006

* Supranuclear lesions.

Management

When approaching a presentation of facial nerve palsy, the function of the branches should be considered and addressed in order of importance.

1. Zygomatic — the eye branch that normally protects the eye. Loss of function of this branch can result in severe corneal erosion and blindness. Treatment involves padding the eye closed and lubricating drops during the day and night with ophthalmological referral.

2. Buccal — this branch travels to the cheek, allowing food to be pushed into mouth. Loss of this branch results in swallowing problems.

3. Marginal mandibular — this branch stretches to the angle of the mouth. Its loss results in a cosmetic deformity.

4. Frontal — loss of this nerve results in an inability to raise the forehead, which is purely a cosmetic loss.

5. Cervical — this branch supplies the platysma; its loss is often unnoticed.

Trauma

There are many forms of trauma. Trauma to the ear may result in:

• tympanic membrane perforation — the basis of treatment is to keep the ear dry (very large holes have been known to heal spontaneously)

• ossicular chain — this can be disrupted resulting in a maximal conductive hearing loss of 60dB; treatment is middle ear reconstruction

• inner ear — cochlea: if disrupted this can result in complete deafness or ‘dead ear’; in the vestibular system, vertigo can result

• facial nerve — immediate or delayed paralysis.

2.4 Nose and sinuses

Anatomy/physiology

The nose and sinuses are made up of a number of components (Figs 2.11 and 2.12).

• The nasal airway comprises a midline septum and a lateral nasal wall. The septum has a cartilaginous component and a bony component made up of the perpendicular plate of the ethmoid and the vomer. There are also contributions from the maxilla and palatine bones.

• The lateral nasal wall comprises the ethmoid bone and its turbinates — superior and middle, the inferior turbinate, the maxilla, lacrimal and palatine bones.

• The sphenoid sits at the postero-supero-lateral aspect of the nasal airway.

• The roof of the nose comprises the ethmoid, the cribriform plate and the sphenoid.

• The floor of the nose is made up of the maxilla and the palatine bone.

• The nose and paranasal sinuses are lined by respiratory epithelium — ciliated columnar epithelium, which is secretory. The daily secretions of the nose and paranasal sinuses is in the order of 800 mL per day.

• The function of the turbinates is to warm and humidify inspired air.

Figure 2.11 Structure of lateral nasal wall

From Dhillon & East, 2006

Figure 2.12 Paranasal sinuses

From Dhillon & East, 2006

Blood supply

The blood supply is from both the external and internal carotid circulation.

The septum is supplied by the facial artery, greater palatine artery, sphenopalatine artery, anterior ethmoid artery and the posterior ethmoid artery. It has a prominent plexus called Little’s area in the centre of the cartilaginous septum.

The lateral nasal wall has its blood supply predominantly from the sphenopalatine artery, with contributions from the anterior and posterior ethmoid arteries.

Nerve supply

The nerve supply of the nose reflects its function: to smell, to warm and humidify the air that has been breathed in and to function as the airway. There are several neural components which help regulate the function.

• The area of olfaction is in the roof of the nose (the olfactory nerve has its sensory endings in the cribriform plate).

• General sensory supply of the nasal airway is from the trigeminal nerve.

• The parasympathetic nervous system contributes to nasal secretions via the sphenopalatine ganglion.

• The sympathetic nervous system gives its supply via the superior cervical ganglion. The nerves run with the blood vessels supplying the nose and sinuses.

Paranasal sinuses

There are generally four named sinuses: frontal, ethmoid, maxillary and sphenoid sinuses. They are paired — left and right. They are variable in their development and are often asymmetric. These sinuses drain via pathways that are normally 2–5 mm wide.

Epistaxis

Most commonly epistaxis is anterior and unilateral (approximately 90%) from Little’s area. Posterior epistaxis is uncommon; it presents bilaterally and is often severe from the sphenopalatine artery.

Contributing factors include:

• hypertension

• coagulopathy

• being elderly — having thin, friable mucosa

• rhinitis

• trauma

• deviated nasal septum causing airway turbulence.

Treating epistaxis is based on the following principles.

• Cover up — protect yourself with gloves, masks, gowns and eye protection. Blood anywhere in the upper aerodigestive tract can stimulate a cough reflex that the patient cannot control.

• Assistance — ask for help with equipment, handling tongue depressors, suckers and packing.

• General first aid — apply pressure.

• Ensure you have a good light source to work by.

• Inspection — clear all clots with a nasal sucker (Frazier type) and Killian nasal speculum.

• Active bleeding is often not amenable to cautery and requires direct pressure. A pack situated at the bleeding point is preferable. Removing a clot during active bleeding helps because a clot is like jelly and provides no pressure on the bleeding point.

• Nasal pack (anterior pack) — Kaltostat, expandable tampon, gauze impregnated with antibiotic paste. Always admit the elderly. Prescribe oral antibiotics to reduce the theoretical potential for toxic shock.

• Posterior pack post-nasal space balloon — use a Foley catheter filled with 10 mL of water in combination with an anterior pack. The Foley needs to be secured at the nostril to prevent the balloon slipping backwards and occluding the airway. All patients with posterior packing need admission and close observation. Care needs to be taken to protect the nostril from trauma caused by the clip securing the balloon catheter.

• Ensure adequate fluid resuscitation.

• Correct any underling predisposing causes such as coagulopathy and hypertension.

• Cautery — using silver nitrate or electrocautery.

• Arterial ligation — sphenopalatine, anterior and posterior ethmoid, maxillary, external carotid artery.

• Greater palatine foramen injection of vasoconstrictor — 3 mL leuer lock syringe with 25/27 gauge needle. Aspirate prior to injection to create vasoconstriction of sphenopalatine artery.

• Embolisation.

Nasal obstruction

Often when we refer to the nose we actually mean the nose and paranasal sinuses. Patients will often present with the complaint of a blocked nose and pain around the area of their sinuses. Associated symptoms include hyposmia, anosmia and loss of taste. More sinister symptoms might be facial sensory loss — V1 or V2, or diplopia.

The cause of nasal obstruction can relate to anatomical, mucosal and pathologic factors. Remember the nasal airway extends from the skin of the nostril to the post-nasal space.

Anatomical factors include deviated nasal septum, nasal bones, anatomical variants of the normal sinus outflow tracts and adenoid hypertrophy.

Mucosal factors include turbinate mucosal hypertrophy. The turbinates have a blood and nerve supply and the epithelium is respiratory with glandular elements. Therefore, they shrink and enlarge in response to conditions that affect:

• blood flow — posture in bed, exercise, vasoconstrictors or vasodilator, heat or cold

• neurologic inputs — sympathetic and parasympathetic responses

• glandular activity — allergy, irritants.

Pathological factors may include:

• vascular lesions — vascular malformations

• infective processes — viral, bacterial and fungal: viral factors lead to a transient blockage, whereas bacterial and fungal infections often become chronic

• tumours — benign and malignant. Polyps are a common cause of nasal obstruction. There are many theories about the cause of polyps — they may be caused by infective processes — viral, bacterial, fungal; airflow turbulence; allergy; or part of a multistep developmental progression towards cancer in which the polyp acquires malignant cellular characteristics.

Beware of new onset unilateral nasal hypertrophy in adults — you must rule out a tumour. There are certain conditions to watch out for:

• nasopharyngeal carcinoma in Asian males, especially those of Cantonese origin

• juvenile angiofibroma in teenage males

• inverting papilloma

• accident (posttraumatic) — fractured and displaced nasal/facial bones and septum

• secondary to systemic conditions — metabolic, immune-related, nutritional, drug-related

• congenital — cysts, abnormal development of the nose/paranasal sinuses, choanal atresia.

Sinusitis/nasal polyps/allergy

Sinusitis often develops as a complication of nasal obstruction. Secretions build up secondary to obstruction of the normal sinus outflow tract and infection often develops. This causes the symptoms of pressure-type pain in the face, fever and discharge. Maxillary sinus pain occurs in the cheek, ethmoids (midface, between the eyes), frontals (forehead) and sphenoid (the vertex of the skull).

Complications of sinusitis include:

• maxillary — subperiosteal abscess — cheek swelling

• ethmoid (eye presentations) — cellulitis of the eye lid (pre-septal) orbital cellulitis (post-septal), subperiosteal abscess, intraorbital abscess, cavernous sinus thrombosis

• frontal — subperiosteal abscess

• sphenoid — cavernous sinus pathology, cranial neuropathy V1 and V2, decreased visual acuity.

Intracranial complications of the ethmoid, frontal and sphenoid sinuses include meningitis, extradural abscess, subdural abscess, subarachnoid abscess and intra-cerebral abscess.

The following points are also worth noting.

• A patient presenting in the middle of the night with the worst headache they’ve ever experienced is not simple sinusitis. Exclude an intracranial lesion such as a cerebral aneurysm.

• In immune-compromised patients (diabetes, leukaemia) beware of fungal sinusitis, which can often be invasive and life-threatening.

• Ask patients if their sinus symptoms get worse in the setting of a cold or nasal obstruction. This will help differentiate between sinus-related pain and other causes of headache.

If sinus pain is unable to be resolved, a CT scan is indicated, including the axial, coronal and parasagittal views. If pus is present, a swab is taken for M/C/S. An MRI should be ordered if there is concern regarding intracranial problems.

Treatment

Treatment relates to addressing the underlying obstructing factors including:

• treating the infection with oral or intravenous antibiotics

• nasal douching — using a saline solution to reduce the inflammatory load

• prescribing topical/oral decongestants to reduce mucosal swelling (topical decongestants should only be used for five days, otherwise a rebound effect called rhinitis medicamentosa occurs)

• prescribing intranasal/oral steroids to reduce polyps

• analgesia

• performing surgery to correct anatomical abnormalities.

2.5 Throat

Tonsils and adenoids

Figure 2.13 depicts the framework of the larynx and Table 2.7 lists the spaces and anatomy related to the throat.

Figure 2.13 Laryngeal framework

From Dhillon & East, 2006

Table 2.7 Related spaces and anatomy

Parapharyngeal space	Inferior: hyoid
	Anterior: pterygomandibular raphe
	Posterior: prevertebral fascia
	Medial: superior constrictor
	Lateral: parotid, mandible and lateral pterygoid
	Styloid process divides into: pre-styloid and post-styloid compartments
	Pre-styloid: fat, LN, IMA, inferior alveolar, lingual and auriculotemporal nerves
	Post-styloid: ICA, IJV, sympathetic chain, IX, X,XI,XII
	Superior: BOS
Retropharyngeal space	Superior: BOS
	Inferior: T4 where space is obliterated through fusion of oesophagus to prevertebral layer
	Anterior: pharynx and oesophagus
	Posterior: alar fascia
	Lateral: carotid sheath
	Above superior constrictor: Eustachian tube and pharyngobasilar fascia
	Between superior and middle constrictor: tongue, stylopharyngeus, styloid process, stylohyoid ligament, lingual nerve

Microbiology/pathology

A number of organisms may be found in the tonsils, as listed in Table 2.8.

Table 2.8 Organisms found in the tonsil

Establishment of N flora of URT begins at birth	First 6–8/12 Actinomyces, Fusobacterium nucleatum, Nocardia fusobacterium increase after first dentition
	Follow: Bacteroides, Leptotrichia, Propriobacteria, Candida
	AnO₂: O₂ — 10:1 due to [O₂]
Pathogenic bacteria found in healthy patients	Streptococcus pneumoniae 19%
	Haemophilus influenzae 13%
	Group A streptococci 5%
	Moraxella 36%
	First three most common causative pathogens for recurrent tonsillitis
Chronic illness: change of pathogens	Staphylococcus aureus
Chronic illness: change of pathogens	Gram-negative

Infectious mononucleosis

This is a disease characterised by fever, sore throat, LN and atypical lymphocytes. These are T cells reacting against B cells infected by Epstein-Barr virus (EBV). The condition is associated with a rising titre of antibodies against EBV. The disease is associated with a high titre of heterophilic (reacting with cells of another species) antibodies: sheep, horse and beef red blood cells.

The typical age for infectious mononucleosis is 15–40 years, often without a history of any recurrent tonsillitis.

History and examination

The typical patient will present for the first time with a tonsillitis-like episode that does not respond to antibiotics. They are often adolescent or young adults who are socially active. The typical examination findings include:

• bilateral Cv LN –75%

• sore throat with inflamed oral and pharyngeal surfaces, follicular tonsillitis

• morbilliform rash, HA and eye signs

• palpable splenomegaly — 50%, hepatomegaly 15%

• jaundice

• ECG/CNS changes

• lymphoma-like proliferation.

Diagnosis

The typical investigations include:

• pleomorphic atypical lymphocytosis (10–20×10⁹/L)

• heterophile antibodies: Paul-Bunnell test — to sheep RBC antigen (Ag)

• monospot test — to horse RBC Ag

• EBV serology — EBV antibodies (Ab) are produced against EBV capsid Ag; IgG develops early (2–3 weeks); IgM — develops early and disappears (2–3 months versus EBV nuclear antigen, which develops later)

• at 2–6 months, persistence of the antibodies can suggest chronic infection.

Medical treatment

Penicillin is the first-line choice for treating bacterial tonsillitis (Fig 2.14) and is used for 10 days as a minimum to avoid possible complications relating to systemic streptococcal infections. Beware of prescribing amoxicillin in undiagnosed infectious mononucleosis as this can cause a rash. Treating viral pharyngitis and glandular fever is supportive. Patients with glandular fever should be counselled against participating in contact sports to avoid splenic injury.

Figure 2.14 Bacterial tonsillitis

From Dhillon & East, 2006

A quinsy (Fig 2.15) is a peritonsillar collection of pus, which is one of the most common complications of bacterial tonsillitis. It is managed through recognition and drainage.

Figure 2.15 Quinsy

From Dhillon & East, 2006

Surgical treatment

The indications for tonsillectomy include recurrent episodes of tonsillitis, typically seven episodes in one year, five in two consecutive years or three in three consecutive years, having more than two weeks off school or work, any associated upper airway obstruction or any suspected tumour.

The complications of tonsillitis include:

• a quinsy or peritonsillar abscess

• retropharyngeal or parapharyngeal space abscesses

• systemic problems such as nephritis and rheumatic fever

• lung abscesses or pneumonia after inhaling discharged pus

• otitis media (by association).

2.6 Airway emergencies and tracheostomy

The upper airway is any point that conducts air between the nostrils and the trachea. Any infection or mass in the mouth and oropharynx and neck can potentially compress the upper airway. Assessment of the airway should be performed clinically prior to sending a patient for any radiological investigation such as a CT scan as this can have disastrous consequences.

Assessing an airway obstruction comprises:

• taking a history — acute, chronic or recent infection, fever, how well the patient can talk

• conducting an examination — obs: pulse, looking for tachycardia, temperature, looking for a febrile/infective cause, respiratory rate — laboured breathing, blood pressure

• inspecting for intercostal recession, tracheal tug, distress, asymmetry or induration of the neck

• listening for stridor — biphasic stridor may indicate a fixed obstruction.

A flexible nasal endoscope is certainly helpful and a portable lateral neck X-ray may also assist. It is important to lie the patient down before a CT scan, to see if they can tolerate lying in the CT scanner.

Performing a tracheostomy

A tracheostomy is a surgical opening in the trachea indicated by an upper airway obstruction. It prevents aspiration of saliva and protects the lower airway as well as permitting long-term ventilation and avoiding the complications of prolonged endotracheal intubation.

The technique used to perform a tracheostomy is as follows.

1. Make a transverse skin incision halfway between the cricoid and sternal notch.

2. Expose the trachea by retracting the strap muscles and thyroid isthmus, which may be divided.

3. Identify the second and third tracheal rings.

4. Puncture this area, creating an opening large enough to insert a tracheostomy tube (Fig 2.16).

5. Secure the tracheostomy tube with sutures or ties.

Figure 2.16 Tracheostomy tubes

From Dhillon & East, 2006

Tube types

Single versus double lumen: Double lumen tubes permit regular cleaning of the tracheostomy airway without having to change the tube. Single lumen tubes require regular changing of the tube.

Cuffed versus uncuffed: A cuffed tube permits maintenance of positive end expiratory pressure and is required for long-term ventilation. The problem with a cuff is that it may lead to pressure necrosis of the tracheal mucosa. Low pressure cuffs have been created.

Nonfenestrated versus fenestrated: a fenestrated tube permits the tracheostomy tube opening to be occluded during expiration that will allow air to pass the vocal cord and mouth to generate speech.

Complications

Complications from performing a tracheostomy can include:

• bleeding — local skin; erosion of minor vessels (thyroidea ima) or major vessels (innominate artery)

• infection — skin and soft tissue

• perichondritis and subglottic stenosis from trauma to the trachea with subsequent scar tissue

• subcutaneous emphysema, pneumothorax, pneumomediastinum

• scarring

• tracheo-oesophageal fistula

• aspiration

• tracheocutanous fistula

• tracheomalacia

• dysphagia

• tracheal stenosis

• occlusion of the tracheostomy tube from dry secretions that have not been cleared (if an occlusion has not been detected, this can be fatal)

• dislodgement of the tracheostomy tube — completely or partially

• postoperative dysphonia — nerve damage — recurrent laryngeal nerve (RLN), superior laryngeal nerve (SLN).

Avoiding complications

Patients should be located on wards where the nursing staff are experienced in caring for tracheostomies.

Humidified air/oxygen should be administered and regular suctioning performed to prevent tube occlusion. The inner cannula should be regularly changed and cleaned; single lumen tubes should be regularly changed. The tube should be reviewed at least twice daily, ideally during each nursing shift.

2.7 Snoring and obstructive apnoea

Snoring and obstructive sleep apnoea (OSA) belong under the broad classification of upper airway restriction. Snoring is at one end of the spectrum and severe OSA is at the other, with mild to moderate grades of OSA in between.

There are several sites for upper airway obstruction:

• nose, paranasal sinuses and post-nasal space

• mouth and oropharynx — tonsils, uvula, hard palate and tongue

• hypopharynx, tongue base and larynx.

The diagnosis of severe OSA should be ruled out prior to any elective surgery on the upper airway. This is achieved with a thorough history and physical examination. A sleep study is also arranged (Fig 2.17). This involves an overnight stay in hospital with the patient being monitored.

Figure 2.17 Sleep study in obstructive sleep apnoea

From Dhillon & East, 2006

Problems associated with OSA are:

• oxygen desaturation resulting in poor sleep and daytime somnolence because of waking during the night to try to obtain more oxygen

• cardiac arrhythmia, hypertension, earlier heart failure and respiratory failure

• neurologic impairment

• increased risk of stroke associated with secondary polycythaemia and hypertension

• social impairment

• (in children) poor growth, poor energy levels and poor feeding.

Treatment

The treatment for OSA is continuous positive airway pressure (CPAP). In this procedure, air is pumped and delivered via a mask, which makes breathing easier. Upper airway obstructions need to be addressed either through:

• nasal surgery

• oral/oropharyngeal surgery — uvulopalatopharyngoplasty (UPPP)

• hypopharynx — a tongue base advancement often achieved with a dental mandibular advancement splint

• tracheostomy (the gold standard, but often impractical).

2.8 Voice/dysphonia/hoarse voice

The larynx has three main functions:

• breathing — conduction of air

• protecting the lower airway during swallowing

• phonation — generating the voice.

The larynx consists of the laryngeal cartilages, bone, ligaments, membranes and muscles (Fig 2.18, Box 2.1).

Figure 2.18 The larynx

From Epstein et al, 2008 (courtesy of Wonersh Surgery)

True vocal fold has five layers:

• stratified squamous epithelium (SSE)

• superficial layer of lamina propria (LP) — Reinke’s layer

• Intermediate lamina propria — elastic fibres

• deep layer of LP — collagen fibre

• vocalis muscle.

The true vocal fold functionally has three layers:

• the cover — SSE and superficial LP

• the transitional zone — intermediate and deep LP

• the body — vocalis.

Nerve supply

The larynx is supplied by two branches of the vagus nerve:

• superior laryngeal nerve

• recurrent laryngeal nerve.

Dysphonia

The course of the vagus nerve in the neck (Fig 2.19) is from the jugular foramen travelling down in the carotid sheath between the internal carotid artery and internal jugular vein. On the right side, it gives off the recurrent laryngeal nerve, which passes around the right subclavian artery, while on the left side it curls around the arch of the aorta.

Figure 2.19 Course of vagus nerve and potential causes of vagus palsy/hoarseness

From Dhillon & East, 2006

Dysphonia is the term used to describe an abnormality of a person’s normal voice; its cause can be both organic and non-organic (Table 2.9). Aphonia is the complete absence of voice production.

Table 2.9 Organic and non-organic causes of dysphonia

Like any disorder, a systematic approach considering the factors associated with voice production is required. Intelligible voice production begins centrally with the language centres. It requires adequate respiratory reserve and exhalation to create airflow past the vocal cords. Sound is modulated by the mouth, nose and paranasal sinuses.

Disease processes affecting the lower respiratory system should be studied from the usual medical texts.

Concentrating on disorders involving the larynx, the usual systematic evaluation should be made considering the VITAMIN CID mnemonic as well as:

• the central nervous system — tumours, systemic conditions

• the peripheral nervous system — motor and sensory (nerve injury) vagus nerve, recurrent laryngeal nerve

• the neuromuscular junction

• muscle disorders

• joint disorders (arthritis)

• vocal fold disorders — cover level: epithelium — nodules, leukoplakia, carcinoma; middle/transitional layer — cysts and Reinke’s oedema;

deep layer — conditions affecting the vocalis muscle.

Videostroboscopy also has a role in diagnosing vocal fold disorders.

More common benign lesions include polyps, cysts, granulomas, recurrent papillomas, haemangiomas, laryngocoele, contact ulcers and lymphangiomas.

2.9 Dysphagia

There are three phases to swallowing:

• oral phase

• pharyngeal phase

• oesophageal phase.

Dysphagia is an abnormality of swallowing (Ch 7.12). Odynophagia is pain on swallowing. When assessing dysphagia, the three stages of swallowing need to be addressed. A dynamic contrast study (barium swallow) is often performed.

2.10 Congenital anomalies

Thyroglossal cysts often present as midline cysts that develop along the pathway of the thyroid, anywhere between the foramen caecum and the site of the thyroid. Cysts can be single or multiple.

The investigations performed are an ultrasound, FNA, nuclear study (to ensure that this is not the only functioning thyroid tissue) and a CT neck study with contrast (after the nuclear study). The administration of contrast will delay the nuclear scan because it may reduce the thyroid’s normal uptake of iodine and give a false result.

The treatment of choice is a Sistrunk’s procedure in which the thyroglossal cyst is removed with the body of the hyoid. This reduces cyst recurrence as it is easier to remove any residual thyroglossal tract.

The types of branchial cysts are listed in Box 2.2.

Box 2.2

Branchial cysts

First branchial cysts, sinuses and fistulae — these are associated with the ear and may be intimately related to the facial nerve

Second branchial cysts (most common) — often related to the tonsils, enlarging during an episode of tonsillitis. They present as lumps from the level of the tonsil, run across the carotid sheath into the neck.

Third and fourth branchial cleft cysts and sinuses are uncommon.

Vascular malformations

These are classified as:

• haemangiomas

• vascular malformations — low flow (venous) and high flow (arteriovenous)

• lymphatic.

Depending on their size and site, they may be of either cosmetic or clinical significance. Some may affect the airway and others may affect vision; some may be associated with intracerebral vascular malformations such as Sturge-Weber syndrome.

Nasolabial cyst/dermoids/cleft lip and palate

Facial cysts form along lines of fusion of the face. The facial bones and skull are formed from processes — frontal, maxillary and mandibular — and sometimes cysts form at these sites. Examples of these are nasolabial cysts and dermoids. Intranasal lesions seen to be arising from the roof of the nose should not be biopsied without adequate imaging as there may actually be an associated meningocele or encephalocele.

Failure of fusion of these facial processes results in conditions such as cleft lip and cleft palate.

2.11 Foreign bodies

Foreign bodies of the ear, nose and throat often have a history of some contact with the foreign object. In young children, prevention is the most important aspect and vigilance the key. Having access to the correct equipment to diagnose and remove a foreign body are vital aspects in successful treatment. In young children it is often better to allow an experienced clinician to remove the foreign body because in the emergency department setting, a child will often permit one attempt prior to losing all confidence in the medical staff.

The paradigm of history, examination, investigation and treatment should be followed.

Microalligator forceps can assist, as well as good ear suction. Trauma to the EAC is a cause of pain and this should be avoided. The TM needs to be inspected after the procedure and an audiogram should be obtained prior. If this is impractical, tuning fork tests should be documented and, if the child is too young, part of the consent should include mentioning that the patient’s hearing will need to be followed up and that the foreign body may have caused injury to the hearing apparatus. After successfully removing the foreign body from one ear, the other ear should always be inspected.

You must elicit the symptoms consistent with a perforation and abscess formation or mediastinitis: fever, chest pain, subcutaneous emphysema.

The exact nature of the foreign body needs to be obtained. A history of ingestion of a disc battery should hasten all management as a perforation of the oesophagus with subsequent life-threatening mediastinitis may result from delayed removal.

Examination

Examination should include careful inspection of the mouth, oropharynx, tonsils and tongue base in combination with a fibre-optic nasal endoscopy of the larynx and hypopharynx.

For fish bones, the wiggle test is useful. Start by grasping (in order) the hyoid, thyroid, cricoid, then trachea. At each level, move the structure from side to side and, if there is an impacted fish bone, pain will be elicited.

Investigation

Investigation is usually by:

• lateral neck X-ray

• chest X-ray — looking for complications of a perforation

• CT scan — fine cuts.

Treatment

Endoscopic removal is commonly used in treatment. Disc batteries need to be removed as soon as possible to lessen the risk of perforation of the oesophagus. This is potentially a life-threatening complication that can result in mediastinitis because of infective saliva passing into the mediastinum.

2.12 Head and neck cancer

Most head and neck cancers (about 90%) are squamous cell cancers (SCC). Treating any tumour depends on its stage. Staging is performed clinically and radiologically by CT, MRI or PET scan. The upper aerodigestive tract needs to be assessed and this is achieved by performing a triple endoscopy: direct laryngoscopy, oespohagoscopy and bronchoscopy. Biopsies are taken to confirm the diagnosis and also determine the extent of any surgery. An FNA is taken to assess lymph node involvement. This avoids the potential spread of tumour cells to the surrounding tissues of the neck with more invasive biopsies such as a core biopsy.

The tumour classification system often employed is the TNM classification: Tumour size, Nodal status, Metastases (Table 2.10). Depending on the TNM classification of a tumour, it is then classified as stage I, II, III or IV. Early tumours are classified stage I and II. Advanced tumours are classified stage III or IV. Generally, stages I and II have no nodal involvement — N0, stage III has early nodal involvement (N1) without distant metastases (M0) and stage IV has advanced nodal status (N2 or N3) and/or distant metastases (M1).

Table 2.10 TNM

TX	Primary tumour cannot be assessed. In these instances, patients present with lymphadenopathy of the head and neck with no obvious primary site tumour
T0	No evidence of primary tumour
NX	Regional lymph nodes cannot be assessed
N0	N0 — no regional lymph node metastases
MX	Distant metastasis cannot be assessed
M0	No distant metastasis

Therapy involves one or more of surgery, radiotherapy and chemotherapy. Often in sites where surgical access is difficult, a combination of chemo-radiotherapy is used. The nasopharynx is one such site.

Tables 2.11 to 2.14 indicate staging for a variety of head and neck cancers. Figure 2.20 depicts a carcinoma of the tonsil.

Table 2.11 Staging for lip and oral carcinoma

T1 T2 T3 T4	≤ 2 cm >2–4 cm >4 cm Invades adjacent structures
N1 N2 N2a N2b N2c N3	Ipsilateral single node ≤ 3 cm Nodes 3–6 cm Ipsilateral single >3–6 cm Ipsilateral multiple nodes ≤ 6 cm Bilateral, contralateral nodes ≤ 6 cm Nodes >6 cm

Table 2.12 Staging for oropharyngeal carcinoma

T1 T2 T3 T4	≤ 2 cm >2–4 cm >4 cm Invades adjacent structures
N1 N2 N2a N2b N2c N3	Ipsilateral single node ≤ 3 cm Nodes 3–6 cm Ipsilateral single >3–6 cm Ipsilateral multiple nodes ≤ 6 cm Bilateral,contralateral nodes ≤ 6 cm Nodes >6 cm

Table 2.13 Staging for hypopharyngeal carcinoma

T1 T2 T3 T4	≤ 2 cm and limited to one subsite >2–4 cm or more than one subsite >4 cm or with laryngeal fixation Invades adjacent structures
N1 N2 N2a N2b N2c N3	Ipsilateral single node ≤ 3 cm Nodes 3–6 cm Ipsilateral single >3–6 cm Ipsilateral multiple nodes ≤ 6 cm Bilateral, contralateral nodes ≤ 6 cm Nodes >6 cm

Table 2.14 Staging for nasopharyngeal carcinoma

T1 T2 T2a T2b T3 T4	Limited to nasophayrnx Soft tissue of oropharynx and/or nasal fossa Without parapharyngeal extension With parapharyngeal extension Invades bony structures and/or paranasal sinuses Intracranial extension, involvement of cranial nerves, infratemporal fossa, hypopharynx orbit
N1 N2 N3a N3b	Unilateral metastasis in node/s ≤ 6 cm, above supraclavicular fossa Bilateral metastasis in lymph node/s ≤ 6 cm above supraclavicular fossa >6 cm In supraclavicular fossa

Figure 2.20 Carcinoma of tonsil

From Dhillon & East, 2006

2.13 Larynx

Most of the cancers of the larynx are SCC. For the purposes of tumour staging, the larynx is divided into three anatomical regions: the glottis (true vocal cords, anterior and posterior commissures); the supraglottis (epiglottis, arytenoids and aryepiglottic folds, and false cords); and the subglottis.

Tables 2.15 to 2.18 outline the staging for these cancers, as well as cancer affecting the salivary gland.

Table 2.15 Staging for supraglottic carcinoma

T1	One subsite, normal mobility of vocal cord
T2	Involving mucosa of more than 1 adjacent subsite of supraglottis or glottis or adjacent region outside the supraglottis without fixation
T3	Limited to larynx with vocal cord fixation or invades postcricoid area, pre-epiglottic tissues, base of tongue
T4	Extends beyond larynx

Table 2.16 Staging for glottic carcinoma

T1	Limited to vocal cord/s, normal mobility
T1a	Unilateral vocal cord involvement, normal mobility
T1b	Bilateral vocal cord involvement, normal mobility
T2	Extending to supraglottis, subglottis, impaired vocal cord mobility
T3	Vocal cord fixation
T4	Extends beyond larynx

Table 2.17 Staging for subglottic carcinoma

T1 T2 T3 T4	Limited to the subglottis Extends to the vocal cords with normal/reduced cord mobility Cord fixation Extends beyond larynx
N1 N2 N2a N2b N2c N3	Ipsilateral single node ≤ 3 cm Nodes 3–6 cm Ipsilateral single >3–6 cm Ipsilateral multiple nodes ≤ 6 cm Bilateral, contralateral nodes ≤ 6 cm Nodes >6 cm

Table 2.18 Staging for salivary gland carcinoma

T1 T2 T3 T4	≤ 2 cm, without extraparenchymal extension >2–4 cm, without extraparenchymal extension Extraparenchymal extension and/or >4–6 cm Invades base of skull, seventh nerve and/or >6 cm
N1 N2 N2a N2b N2c N3	Ipsilateral single node ≤ 3 cm Nodes 3–6 cm Ipsilateral single >3–6 cm Ipsilateral multiple nodes ≤ 6 cm Bilateral, contralateral nodes ≤ 6 cm Nodes >6 cm

2.14 Parotid and salivary glands

In the head and neck there are three paired major salivary glands and many minor salivary glands that are part of the mucosa.

The major salivary glands are the parotid, submandibular and sublingual. The submandibular and sublingual glands contribute 60% of saliva production and the parotid contributes about 30%.

The parotid gland drains via Stensen’s duct opposite the second upper molars. The submandibular and sublingual glands drain via Warton’s duct, which opens either side of the tongue frenulum. The facial nerve is an inherent part of the parotid gland and needs to be identified during any parotid surgery. The submandibular gland has the marginal mandibular, lingual and hypoglossal nerves in close proximity, and these need to be avoided during surgery.

Examination of the gland involves careful inspection of it and the duct orifice, palpation of the gland and massage to see the nature of the expressed secretions, whether clear or pus. Cervical lymph nodes should be examined to assess for malignancy. The associated nerves also need to be tested.

All salivary glands can be affected by the same pathologic processes.

Sialadenitis is acute inflammation of a salivary gland. Managing acute sialadenitis involves regular massage of the involved gland, massaging in the line of the duct, oral hygiene, maintaining hydration status by drinking lots of water, using sialagogues such as lemon juice to stimulate saliva production, adequate analgesia and antibiotics (flucloxacillin or clindamycin).

Calculi can present as intraglandular or intraductal and cause a build-up of saliva with subsequent swelling of the affected gland. This fluid has potential to become infected, often by Staphyloccus aureus.

Investigations

Investigations include:

• plain X-ray — 60 % of submandibular calculi are radio-opaque versus only 30% of parotid calculi

• sialogram — contrast is injected via the salivary duct, looking for stones, duct dilatation and constriction

• CT scan — differentiation between stones and tumours; however, does not always detect stones.

Systemic conditions that may affect the salivary glands are:

• mumps — presents as bilateral parotitis

• Sjögren’s syndrome — results in dry eyes and enlargement of the salivary glands

• alcoholism — results in bilateral enlargement of the parotids.

As a general rule, 80% of tumours in major salivary glands are benign and 20% are malignant. In minor salivary glands, 20% of tumours are benign and 80% are malignant.

Benign tumours include:

• monomorphic adenoma

• Warthin’s — also known as adenolymphoma, which are often bilateral and found in smokers

• pleomorphic adenoma — accounting for about 80% of benign tumours. These tumours need to be excised with a margin of tissue to prevent recurrence as they have bosselations that are out pouchings of the lesions. There is a long-term risk of malignant change if they are not excised.

Malignant tumours comprise:

• SCC — metastatic — from associated skin lesions, primary

• adenoid cystic carcinoma

• carcinoma ex pleomorphic — arise from pleomorphic adenomas

• mucoepidermoid carcinoma

• lymphoma

• adenocarcinoma

• acinic cell carcinoma — almost exclusively confined to the parotid gland.

2.15 Thyroid/parathyroid

Goitre

The most common presentation of thyroid disease is an enlargement of the gland (goitre). Abnormalities of endocrine function may coexist. Morphologically goitre has three types: general enlargement (either diffuse or multinodular) or a solitary nodule. Physiological enlargement of the thyroid occurs at puberty and the normal thyroid gland is frequently visible and palpable in slender individuals on either side of the trachea as a soft, smooth, bilobed fullness that moves upwards when the patient swallows. In thick-necked individuals the normal gland can be neither felt nor seen.

Thyroid enlargement involving the whole gland is usually easy to recognise — the gland’s characteristic shape of two lobes on either side of the trachea joined by an isthmus and its movement with the larynx on swallowing and speech are unmistakable signs. A localised discrete lump in the thyroid will also be confined by the pretracheal fascia and will move on swallowing. All forms of goitre affect women more frequently than men.

Common causes

I. General enlargement

1. Multinodular goitre: euthyroid or toxic

2. Diffuse toxic goitre (Graves’ disease)

3. Thyroiditis

4. Anaplastic carcinoma

II. Single nodule

1. Dominant nodule in a multinodular goitre

2. Adenoma

3. Colloid nodule, cyst or haematoma

4. Carcinoma

III. Recurrent goitre after surgery

Clinical features

History

Most swellings are chronic and painless. Pain over the swelling, particularly when accompanied by acute enlargement, strongly suggests acute haemorrhage, thyroiditis or occasionally carcinoma. Symptoms suggesting compression of local structures should be sought — tracheal compression may cause dyspnoea, wheeze and stridor, particularly at night or on tilting the head to one side. Flushing of the face on exertion or on arm elevation suggests venous obstruction. A recent voice change suggests recurrent laryngeal nerve involvement. Sometimes extrathyroid manifestations of malignancy, such as a lymph node swelling, can be the primary presenting problem.

Hormonal imbalance can cause protean symptoms because thyroid hormones exert effects on most body tissues. In young patients, ocular and general systemic manifestations are common; in older patients, symptoms are predominantly cardiac. A typical history is of anxiety, weight loss without loss of appetite and heat intolerance. Hypothyroidism is often iatrogenic. A history of previous thyroid surgery or antithyroid drug intake should be sought.

Table 2.19 sets out the process of examining a goitre.

Table 2.19 Physical examination of the thyroid

Examination	At what	Significance
Look, look, look!/inspect/listen	General body habitus Hyperthyroid — proptosis, weight loss, eye signs, lid lag Hypothyroid — overweight Goitre, ask to swallow with water Redness, scarring Other neck swelling Stick out tongue Voice — ask name, stridor Finger nail changes	Indicates hyper/hypothyroid Size of thyroid Thyroiditis, previous surgery Cervical node metastases Thyroglossal cyst Recurrent laryngeal nerve palsy airway compromise
Feel	Goitre size, nodularity, consistency, tenderness, warmth Tethering Pulse Warmth of periphery	Thyroid lesion Carcinoma may tether gland Hyperdynamic circulation Hyper versus hypothyroid
Percuss	Sternum	Retrosternal extension
Auscultate	Bruit	Hyperdynamic circulation
Dynamic manoeuvres	Pemberton’s sign Reflexes Kocher’s test	SVC compression Brisk hyperthyroid Sluggish hypothyroid Evokes stridor

Examination of the neck should always begin with a frontal inspection of the patient’s exposed entire head, neck and upper chest in repose, then while swallowing water from a glass. Any scars of previous operations and visible swellings are noted. The patient should sit comfortably and swallow first with the neck in a neutral position and then slightly extended to throw the gland into more prominence. The effects of lateral neck flexion and of raising both arms above the head are noted. Obstruction of the superior vena cava (SVC) may be precipitated by arm-raising, causing facial flushing and venous congestion (Pemberton’s sign). Vascular pulsation may be apparent; visible jugular veins and the level and symmetry of the jugular venous pulse and pressure waves are noted. The lower limits of lateral lobe swelling are often visible on swallowing. The position of the anatomical landmarks of the thyroid cartilage, hyoid bone and trachea are noted.

If an enlargement of the gland is noted, its size, consistency and vascularity, together with its local and systemic effects, must be assessed. The examiner first stands behind the patient and identifies the trachea by palpation and notes any displacement. The limits of the gland are outlined with the finger pulps and, as the patient swallows, the gland is allowed to slip between the fingers. The lateral lobes, isthmus, pyramidal lobe and lower boundaries of the gland are assessed and nodules defined. To evaluate each lobe more precisely, each sternomastoid in turn is retracted by one hand and the exposed gland palpated from behind by the other hand passed across the midline.

Finally, the gland is palpated from in front. Each lobe is palpated between the thumb in front and the fingers crooked behind the posterior edge of the sternomastoid: the right hand palpates the left lobe and vice versa. Each lobe is made more prominent for palpation by displacing and rotating the trachea towards the side being examined, so the lobe is brought more anteriorly, using the thumb of the other hand placed on the trachea.

If a lower lobe’s boundary is neither visible nor palpable by these manoeuvres, it is probably retrosternal and should be further assessed by percussion over the sternum. Tracheal compression may be exposed by compressing the lateral lobes of the thyroid between both hands (Kocher’s test) to see if stridor is evoked. Fixation or attachment of the goitre to the sternomastoid muscles, the trachea and carotid vessels is assessed. Benign swellings, even when very large, displace but do not obscure the vessels; cancers can wrap around them (Berry’s sign). Examine the neck for enlarged nodes, particularly looking for prelaryngeal (Delphic) or pretracheal nodes, as well as those of the deep cervical chain and posterior triangle. Finally, listen for bruits: evidence of hyperthyroidism within the gland is established solely on this basis. If surgery is to be undertaken or if carcinoma is suspected, examination of the goitre is not complete until the cords have been assessed by indirect laryngoscopy. Paralysis of the recurrent laryngeal nerve causes an immobile cord and is usually indicative of carcinoma and occasionally of thyroiditis or previous surgery.

Signs of hyperthyroidism outside the neck are next assessed: these may be obvious or occult. One must be alert for eye signs, cardiovascular manifestations and peripheral signs.

A longstanding nodular enlargement involving the whole gland without endocrine disturbance is, in most cases, associated with dietary deficiency and hyperplasia (involution sequence) or with goitrogens in the diet. Toxicity may develop in older patients, in whom symptoms are predominantly cardiac. Tracheal compression and intrathoracic extension are also common complications. Dyspnoea, wheeze and stridor develop, particularly when lying on one side at night.

2 Graves’ disease

This is common in young women and combines signs of overactivity with a smooth diffuse vascular enlargement. Eye signs and systemic effects may predominate with no visible or palpable goitre. Some patients present because of associated symptoms such as diarrhoea or amenorrhoea.

3 Hashimoto’s thyroiditis

This is the most common form of thyroiditis. It is much more common in women. Association of a nodular goitre with mild hypothyroidism in a middle-aged patient is very suggestive of Hashimoto’s thyroiditis. The gland may also be painful, tender and initially associated with clinical and laboratory signs of thyrotoxicosis progressing to hypothyroidism.

Acute or subacute thyroiditis (De Quervain’s thyroiditis) is suggested by sudden onset of swelling with severe pain, fever and a diffusely enlarged, firm and a very tender gland. It often follows an upper respiratory tract infection and is related to infection with mumps or Coxsackie virus infection. Riedel’s thyroiditis is a rare fibrotic condition of the thyroid associated with hypothyroidism and tracheal compression.

4 Anaplastic carcinoma

This occurs in older patients and is suggested by a hard, irregularly enlarged gland with signs of fixation to surrounding structures and local lymph node spread.

Single nodule

A single-nodule goitre is depicted in Figure 2.21.

Figure 2.21 Goitre — single nodule

A: dominant nodule in a multinodular goitre; B: benign adenoma; C: celloid nodule within a haemorrhagic cyst; D: carcinoma (papillary) with nodes

The differential diagnosis includes: dominant nodule in an unrecognised multinodular goitre; adenoma; colloid nodule or haemorrhagic cyst; papillary or follicular carcinoma; and lobular thyroiditis. The main question to be answered is whether the lesion is benign or malignant. Pressure effects and toxicity are much less common as complications of a single nodule. A single thyroid nodule is more likely to be cancer in a man than in a woman and in a young patient than in an old one.

Benign lesion

A short history suggests a haemorrhagic cyst or thyroiditis; an abrupt onset of a tender nodule is typical of haemorrhage into a cyst. Tenderness on palpation is the main feature of thyroiditis. Benign adenomas are usually nontender. Careful palpation is essential to exclude multinodular goitre, but it is often difficult to be sure that a nodule is truly single.

Carcinoma

Papillary carcinoma is the most common thyroid cancer and usually presents in young adult women. Initial spread is typically lymphatic and the disease may present as a lateral or medial lymph node swelling in the neck (the primary lesion being impalpable). The tumour is well differentiated histologically and can be difficult to distinguish from normal thyroid tissue. Thyroid tissue obtained from cervical nodes was considered for some time to be aberrant thyroid tissue, but it is now realised that these findings imply a small and often impalpable, primary cancer in the thyroid. The classification and staging of thyroid carcinoma is listed in Box 2.3.

Box 2.3

Thyroid carcinoma classification and staging

T1 ≤ 2 cm

T2 >2–4 cm

T3 >4 cm

T4 Extends beyond gland

N1 Regional lymph node metastases

N1a Ipsilateral cervical nodes

N1b Bilateral, midline, contralateral or mediastinal nodes

Follicular carcinoma accounts for about 20% of malignant thyroid tumours. Follicular carcinoma can be very difficult to distinguish from a benign follicular adenoma (Box 2.4). Capsular invasion, if present, is indicative of malignancy. Follicular tumours occur more often than papillary tumours in older patients and have a greater tendency for blood-borne spread. The prognosis is therefore not as good as for papillary carcinoma.

Box 2.4

Staging: papillary (follicular) carcinoma

Medullary carcinoma is an uncommon form of thyroid cancer. It is a solid hard tumour that secretes calcitonin and occurs as part of the familial multiple endocrine adenomatosis syndrome.

Undifferentiated or anaplastic thyroid carcinoma is uncommon and of poor prognosis (Box 2.5).

Box 2.5

Staging: undifferentiated (anaplastic) carcinoma

Staging and prognosis for differentiated thyroid cancer is made in terms of 20-year survival versus five-year survival rates for head and neck SCC. Having a differentiated thyroid cancer is, therefore, a relatively good prognosis. From the 20-year perspective, it means that thyroid cancer should continue to be under surveillance once diagnosed. Prognostic scoring systems do not account for local lymph node metastases, as these relate to recurrence rather than long-term survival.

Table 2.20 Thyroid carcinoma outcome statistics

The US-based Mayo Clinic classifies carcinoma according to the acronym MAICS (Table 2.21):

Table 2.21 The Mayo Clinic carcinoma classification system

Metastasis yes = 3, no = 0

Age <39 = 3.1, >40 = 0.08 × age

Invasion yes = 1, no = 0

Completeness of resection yes = 1, no = 0

Size 0.3 × size in centimetres.

The Lahey Clinic, also in the US, bases its classification system on the acronym AMES (Table 2.22):

Table 2.22 The Lahey Clinic’s AMES classification system

	Low risk	High risk
Age	<41 male, <51 female	>41 male, >51 female
Metastases	No	Yes
Extent	Intrapapillary thyroid, follicular with minor capsular invasion	Extracapsular
Size	<5 cm	>5 cm