Conductive	Sensorineural
External meatus	Congenital
WaxForeign bodyOtitis externaChronic suppurationDrum	Pendred’s syndrome (see p. 962)
	Long QT syndrome
	Björnstad’s syndrome (pili torti)
	End organ
	Advancing ageOccupational acoustic traumaMénière’s diseaseDrugs (e.g. gentamicin, furosemide)
Perforation/trauma
Middle ear
Otosclerosis Ossicular bone problems Suppuration (otitis media)
	Eighth nerve lesions
	Acoustic neuroma
	Cranial trauma
	Inflammatory lesions:
	Tuberculous meningitis
	Sarcoidosis
	Neurosyphilis
	Carcinomatous meningitis
	Brainstem lesions (rare)
	Multiple sclerosis
	Infarction

Weber test

A tuning fork placed on the forehead or vertex of a patient with normal hearing (or with symmetrical hearing loss) should be perceived centrally by the patient.

Weber test.

Pure tone audiometry

The patient is asked to respond to a series of pure tones presented to each ear, in turn, in a soundproof room. An audiogram is produced (see Fig. 21.2).

Perforated tympanic membrane

This arises from trauma or chronic middle ear disease where recurrent infection results in a permanent defect. Surgical repair is only indicated if the patient is symptomatic with hearing loss or recurrent discharge.

Otitis media

This is an acute inflammation of the middle ear, causing severe pain (otalgia) and conductive hearing loss. This occurs because fluid accumulation in the middle ear impairs sound conduction to the cochlea. Otitis media is often viral in origin, e.g. following a cold, and will settle within 72 hours without antibacterial treatment. In people with systemic features or after 72 hours, a systemic antibiotic, e.g. amoxicillin, should be given, particularly in the under 2 year olds. Topical therapy is of no value. Complications include infection of the mastoid bone.

Acute otitis media can spread to the mastoid area. If there is tenderness and swelling over the mastoid then an urgent ENT opinion should be obtained.

Secretory otitis media with effusion (‘serous otitis media’ or ‘glue ear’)

Secretory otitis media (glue ear). Auroscopic view of the tympanic membrane, which is dull with loss of light reflex.

This is common in children because of Eustachian tube dysfunction. The effusion resolves naturally in the majority of cases but can persist giving hearing loss, and it predisposes to recurrent attacks of acute otitis media. A grommet (tympanostomy tube) is inserted into the tympanic membrane and ventilates the middle ear cavity, i.e. takes over the Eustachian tube’s function. Grommets are extruded from the tympanic membrane as it heals (over 6 months to 2 years). Developmental outcomes are not improved by grommet insertions. In most children the middle third of the face grows around the age of 7–14 years and Eustachian tube dysfunction is rare after this.

Otosclerosis

This is usually a hereditary disorder in which new bony deposits occur within the stapes footplate and the cochlea. Characteristically seen in the second and third decades, it is commoner in females and can become worse during pregnancy. The hearing loss may be mixed, and treatment includes a hearing aid or replacement of the fixed stapes with a prosthesis (stapedectomy). The choice of treatment is dependent on the patient. Surgery is an excellent option, with very good success rates in regular stapedectomists’ hands, but it always carries a small risk of a complete hearing loss. Hearing aids, whilst safe, require the patient’s compliance if they are to afford benefit.

Presbycusis

This is the commonest cause of deafness. It is a degenerative disorder of the cochlea and is typically seen in old age. It can be due to the loss of outer hair cells (sensory), loss of the ganglion cells (neural), strial atrophy (metabolic) or it can be a mixed picture. Ageing itself does not cause outer hair cell loss but environmental noise toxicity over the years is a major factor. The onset is gradual and the higher frequencies are affected most (Fig. 21.2). Speech has two components: low frequencies (vowels) and high frequencies (consonants). When the consonants are lost, speech loses its intelligibility. Increasing the volume merely increases the low frequencies and the characteristic response of ‘Don’t shout. I’m not deaf!’

Figure 21.2 Audiogram showing presbycusis (high frequency loss).

A high-frequency-specific hearing aid will do much to ease the frustrations of both the patients and their close contacts.

Noise trauma

Cochlear damage can occur, e.g. when shooting without ear protectors or from industrial noise (see p. 935), and characteristically has a loss at 4 kHz.

This is a slow-growing benign schwannoma of the vestibular nerve (see p. 1076) which can present with progressive sensorineural hearing loss. Any patient with an asymmetric sensorineural hearing loss or sudden sensorineural hearing loss should be investigated, e.g. with an MRI scan.

Vertigo

Vertigo is usually rotatory when it arises from the ear. The presence of otalgia, otorrhoea, tinnitus or hearing loss suggests an otologic aetiology. Vestibular causes can be classified according to the duration of the vertigo. Common causes are summarized below.

Seconds to minutes – benign paroxysmal positional vertigo

Minutes to hours – Ménière’s disease

Hours to days – labyrinthine or central pathology.

Benign paroxysmal positional vertigo (BPPV)

BPPV is thought to be due to loose otoliths in the semicircular canals, commonly the posterior canal. Positional vertigo is precipitated by head movements, usually to a particular position, and often occurs when turning in bed or on sitting up. The onset is typically sudden and distressing. The vertigo lasts seconds or minutes and the phenomenon becomes less severe on repeated movements (fatigue). There is no serious underlying cause but it sometimes follows vestibular neuronitis (see p. 1079), head injury or ear infection.

Diagnosis

Diagnosis is made on the basis of the history and by the Hallpike manoeuvre (Fig 21.3). A positive Hallpike test confirms BPPV, which can be cured in over 90% of cases by the Epley manoeuvre. This involves gentle but specific manipulation and rotation of the patient’s head to shift the loose otoliths from the semicircular canals.

Figure 21.3 Hallpike manoeuvre for diagnosis of benign paroxysmal positional vertigo. This can be done in the outpatient department. (a) The patient sits on a couch, his head is turned towards one ear. (b) The head is supported by the examiner while the patient lies down so that his head is just below the horizontal. Nystagmus (following a latent interval of a few seconds) is commonly noted when the head has been turned towards the affected ear. This can be repeated with the patient’s head turned towards the other ear.

A differential diagnosis is a cerebellar mass, but here positional nystagmus (and vertigo) is immediately apparent (no latent interval) and does not fatigue.

Ménière’s disease

This condition is characterized by recurring episodic rotatory vertigo lasting 30 minutes to a few hours; attacks are recurrent over months or years. Classically, it is associated with a low frequency sensorineural hearing loss, feeling of fullness in the affected ear, loss of balance, tinnitus and vomiting. There is a build-up of endolymphatic fluid in the inner ear, although its precise aetiology is still unclear.

Treatment

Vestibular sedatives, e.g. cinnarizine, are used in the acute phase. Preventative measures, such as a low-salt diet, betahistine and avoidance of caffeine, are useful. If the disease cannot be controlled, then a chemical labyrinthectomy, perfusing the round window orifice with ototoxic drugs such as gentamicin, is used. Gentamicin destroys the vestibular epithelium; therefore the patient has severe vertigo for around 2 weeks until the body compensates for the lack of vestibular input on that side. The patient will happily trade occasional mild vertigo when the balance system is challenged to the unpredictable, severe and disabling attacks of vertigo of Ménière’s disease.

Labyrinthine or central causes of vertigo (see Table 22.4)

These are managed with vestibular sedatives in the acute phase. Most patients will settle over a few days but continuous true vertigo with nystagmus suggests a central lesion. A patient with a deficit of vestibular function due to viral labyrinthitis or neuronitis should be able to cease vestibular sedatives within 2 weeks; long-term use can give parkinsonian side-effects, delay central compensation and thus prolong the vertigo. Vestibular rehabilitation by a physiotherapist or audiological scientist can speed up the compensation process, although most patients will be able to do this themselves with time.

Tinnitus

This is a sensation of a sound when there is no auditory stimulus. It can occur without hearing loss and results from heightened awareness of neural activity in the auditory pathways. Patients describe a hissing or ringing in their ears and this can cause much distress. It usually does not have a serious cause but vascular malformation, e.g. aneurysms, or vascular tumours can be associated. Tinnitus occurs due to awareness of neural activity in the auditory pathways that our brains are made more conscious of.

Treatment

This is difficult. A tinnitus masker (a mechanically produced continuous soft sound) can help. Specialist audiological services are of use and rehabilitate patients well.

The nose

Anatomy and physiology (Fig. 21.4)

The function of the nose is to facilitate smell and respiration:

Smell is a sensation conveyed by the olfactory epithelium in the roof of the nose. The olfactory epithelium is supplied by the first cranial nerve (see p. 1071).

The nose also filters, moistens and warms inspired air and in doing so assists the normal process of respiration.

Figure 21.4 The anatomy of the nose in longitudinal section. IT, inferior turbinate; MT, middle turbinate; ST, superior turbinate; a, internal ostium; b, respiratory region; c, choanae.

The external portion of the nose consists of two nasal bones attached to the rest of the facial skeleton and to the upper and lower lateral cartilages. The internal nose is divided by a midline septum that comprises both cartilage and bone. This divides the internal nose in two, from the external nostril to the posterior choanae. The posterior choanae are in continuity with the nasopharynx posteriorly. The paranasal sinuses open into the lateral wall of the nose and are a system of aerated chambers within the facial skeleton.

The blood supply of the nose is derived from branches of both the internal and external carotid arteries. The internal carotid artery supplies the upper nose via the anterior and posterior ethmoidal arteries. The external carotid artery supplies the posterior and inferior portion of the nose via the superior labial artery, greater palatine artery and sphenopalatine artery. On the anterior nasal septum is an area of confluence of these vessels (Little’s area) (Fig. 21.5a).

Figure 21.5 (a) Blood supply of Little’s area on the septum of the nose. (b) Nasal pack.

Examination

The anterior part of the nose can be examined using a nasal speculum and light source. Endoscopes are required to examine the nasal cavity and postnasal space.

Common disorders

Epistaxis

Nose bleeds vary in severity from minor to life-threatening. Little’s area (Fig. 21.5a) is a frequent site of nasal haemorrhage. First aid measures should be administered immediately, including external digital compression of the anterior lower portion of the external nose, ice packs and leaning forward. The patient should be asked to avoid swallowing any blood running posteriorly as this causes gastric irritation and then nausea and vomiting.

Not infrequently, small recurrent epistaxes occur and these may require a visit to the emergency clinic for an examination and simple local anaesthetic cautery with a silver nitrate stick. If the bleeding continues profusely then resuscitation in the form of intravenous access, fluid replacement or blood, and oxygen can be administered. If further intervention is necessary, consideration should be given to intranasal cautery of the bleeding vessel, or intranasal packing using a variety of commercially available nasal packs (Fig. 21.5b). In addition to direct treatment of the epistaxis, a cause and appropriate treatment of a cause should be sought (Table 21.2).

Table 21.2 Aetiology of epistaxis

Local	Idiopathic
	Trauma – foreign bodies, nose-picking and nasal fractures
	Iatrogenic – surgery, intranasal steroids
	Neoplasm – nasal, paranasal sinus and nasopharyngeal tumours
General	Anticoagulants
	Coagulation disorders
	Hypertension
	Osler–Weber–Rendu syndrome (familial haemorrhagic telangiectasia)

Rhinitis

See page 808.

Nasal obstruction

Nasal obstruction is a symptom and not a diagnosis. It can significantly affect a patient’s quality of life. Causes include:

Rhinitis (see p. 808). If an allergen is identified, then allergen avoidance is the mainstay of treatment. Topical steroids and/or antihistamines can be tried. If severe, then oral antihistamines or referral to an allergy clinic for immunotherapy is warranted.

Septal deviation. Correction of this deviation can be undertaken surgically.

Nasal polyps. This condition occurs with inflammation and oedema of the sinus nasal mucosa. This oedematous mucosa prolapses into the nasal cavity and can cause significant nasal obstruction. In allergic rhinitis (see p. 798) the mucosa lining the nasal septum and inferior turbinates are swollen and a dark red or plum colour. Nasal polyps can be identified as glistening swellings which are not tender. Treatment with intranasal steroids helps but if polyps are large or unresponsive to medical treatment then surgery is necessary.

Foreign bodies. These are usually seen in children who present with unilateral nasal discharge. Clinical examination of the nose with a light source often reveals the foreign body, which requires removal either in clinic or in theatre with a general anaesthetic.

Sinonasal malignancy. This is extremely rare. The diagnosis must be considered if unusual unilateral symptoms are seen, including nasal obstruction, epistaxis, pain, epiphora, cheek swelling, paraesthesia of the cheek and proptosis of the orbit.

Sinusitis

Sinusitis is an infection of the paranasal sinuses that either is bacterial (mainly Streptococcus pneumoniae and Haemophilus influenzae) or is occasionally fungal. It is most commonly associated with an upper respiratory tract infection and can occur with asthma. Symptoms include frontal headache, purulent rhinorrhoea, facial pain with tenderness and fever. It can be confused with a variety of other conditions such as migraine, trigeminal neuralgia and cranial arteritis.

Treatment

Treatment for a bacterial sinusitis includes nasal decongestants, e.g. xylometazoline, broad-spectrum antibiotics, e.g. co-amoxiclav because H. influenzae can be resistant to amoxicillin, anti-inflammatory therapy with topical corticosteroids such as fluticasone propionate (nasal spray) to reduce mucosal swelling, and steam inhalations.

If the symptoms of sinusitis are recurrent (Box 21.2) or complications such as orbital cellulitis arise, then an ENT opinion is appropriate and a CT scan of the paranasal sinuses is undertaken. Plain sinus X-rays are now rarely used to image the sinuses.

Box 21.2

Types of sinusitis

Acute	Symptoms lasting 1 week to 1 month
Recurrent acute	>4 episodes of acute sinusitis per year
Subacute	Symptoms for 1–3 months
Chronic	Symptoms for >3 months