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