Otalgia

Pain from disease of the external ear, tympanic membrane and middle ear reaches the brain by branches of the fifth, ninth and tenth cranial nerves, together with nerves from C2 and C3 roots. Because branches of these nerves also supply the larynx and pharynx, as well as the temporomandibular joint and teeth, disease of these structures may give rise to referred pain in the ear. Therefore, if otoscopic examination is normal, examination of these other sites should be considered. In half of affected patients, the ear pain is referred.

The main causes of otalgia are listed in Box 20.1. Of the otological causes, acute infection of the cartilage of the pinna (perichondritis) can be very painful. Malignant otitis externa is not neoplastic. It is due to infection (usually Pseudomonas) and can spread to the skull base, especially in diabetic or immunocompromised individuals.

Otorrhoea

Pus draining from the ear varies in character depending on its origin (Table 20.1) A profuse mucoid discharge with pulsation suggests a tympanic membrane perforation. The length of history is important. Persistent discharge suggests chronic otitis media, with perforation (Table 20.2). Cholesteatoma usually begins with tympanic membrane retraction and blockage of migrating desquamated skin from the drum and external meatus. The retraction deepens and infection leads to destruction of middle ear structures, sometimes causing damage to the facial nerve or inner ear. The infection may spread outside the temporal bone, even causing meningitis or intracranial abscess. Bleeding from a chronically discharging ear is usually due to infection, but may rarely indicate malignant change. Cranial trauma followed by bleeding and leakage of cerebrospinal fluid (CSF) indicates fracture of the base of the skull.

Table 20.2 Classification of chronic otitis media (COM)

Hearing loss

Deafness may be gradual or sudden, bilateral or unilateral. There may be an obvious precipitating cause, such as trauma or noise exposure. There are two characteristics of hearing loss: to use the analogy of a radio, a decrease in volume, or a change in the tuning corresponding to impaired speech discrimination, so that words are not clear even with a hearing aid. Hearing loss may be conductive, sensorineural or mixed, with both conductive and sensorineural components (Box 20.2). Conductive deafness is due to disease in the external ear canal, tympanic membrane or middle ear. Characteristically, the patient retains normal speech discrimination. Sensory deafness implies pathology in the cochlea, and neural deafness implies pathology in the cochlear nerve or the central connections of hearing, but in practice this distinction is difficult to make and rarely useful, and the term sensorineural deafness is used instead. Sensorineural deafness causes impairment of speech discrimination with recruitment; the latter is an abnormal perception of the increase of intensity of sound with increasing signal volume that results from damage to the hair cells in the cochlea. This leads to a decreased functional dynamic range, so that a small increase in sound intensity is uncomfortable. The patient may also notice an apparent difference in the pitch or frequency of a tone between the two ears (diplacusis). Most hearing loss is gradually progressive and related to ageing. Deafness is often secondary to occupational or social noise exposure, and is often inherited. Many drugs are ototoxic, and there are associations between hereditary hearing loss and neurological and renal disorders. Occasionally, sensorineural hearing loss occurs suddenly. A cause is only rarely identifiable.

Tinnitus

Tinnitus is a ringing, rushing or hissing sound in the absence of an appropriate auditory stimulus. It can be caused by almost any pathology in the auditory pathways. It is strongly associated with hearing loss, although it occasionally occurs with normal hearing. It is common, affecting up to 18% of the population of industrialized countries. In a small proportion (0.5%), daily life is affected. Correction of coexisting depressive illness may be of value. Management of tinnitus includes the use of hearing aids or masking devices. It usually improves with time, but in most cases there is no specific treatment.

Vertigo

Vertigo is an illusion of movement such that the patient either feels the world moving or has a sensation of moving in the world. Patients frequently have difficulty describing the symptom. Higher centre dysfunction, as in anxiety states or drug effects, may also cause dizziness. There are therefore many causes for symptomatic ‘dizziness’ (Box 20.3). A feeling of the room spinning associated with nausea or vomiting suggests an acute labyrinthine cause, especially if there are changes in hearing or tinnitus. Fortunately, most acute vestibular events are self-limiting, because even if one vestibular system is abnormal, the central connections can ‘reset’ the system over a period of a few days. The elderly are less able to compensate. In all age groups, vertigo may cause residual vague imbalance, particularly in association with movement or after alcohol ingestion. It is important to test for positional changes, as the commonest cause of vestibular vertigo is benign paroxysmal positional vertigo (BPPV), secondary to loose debris floating in the posterior semicircular canal.

Pinna and postauricular area

First, inspect the pinna and the surrounding skin. Congenital abnormalities may be associated with accessory skin tags, abnormal cartilaginous fragments in the skin surrounding the ear or small pits and sinuses. Look also for any lymphadenopathy (associated with otis externa or scalp cellulitis) and for surgical scars. A hot, tender postaural swelling, pushing the pinna forward, suggests mastoid infection (Fig. 20.7). Incomplete development of the ear (microtia) occurs with narrowing (atresia) of the external meatus, but the auricle can also be displaced from its normal position (melotia) or pathologically enlarged (macrotia). These abnormalities may be associated with cysts or infection in a preauricular sinus.

Figure 20.7 Acute mastoiditis (A) before and (B) after incision.

External ear canal

Inspect the external auditory canal using a hand-held otoscope (Fig. 20.8). To bring the cartilaginous meatus into line with the bony canal, retract the pinna backwards and upwards. Always use the largest speculum that will comfortably fit the ear canal. Hold the otoscope like a pen between thumb and index finger, with the ulnar border of your hand resting gently against the side of the patient’s head. In this way, any movement of the patient’s head during the examination causes synchronous movement of the speculum, limiting any risk of accidental injury to the ear canal. With a young child, sit him on his parent’s lap with the head and shoulder held (Fig 20.9).

Figure 20.8 Examining the ear in an adult.

Figure 20.9 Examining the ear in a child.

Wax may be removed with a Jobson Horne probe or wax hook, or by syringing with water. Never syringe if there is a history of previous perforation or discharge. It is important to use water at 37°C lest vertigo be induced by caloric stimulation of the labyrinth. Keratin debris, pus or mucopus in the meatus can be removed, and can be sent for microbiology. Foreign bodies in the ear canal are sometimes found in children; they may be difficult to remove without a general anaesthetic.

The tympanic membrane

The hand-held otoscope is satisfactory for most examinations, but the outpatient microscope offers the best view. Be familiar with the variability in appearance of the normal drum. The most common abnormality is tympanosclerosis (Fig. 20.10), which consists of white chalky patches in the drum caused by hyaline degeneration of the fibrous layer due to previous infection. Prolonged negative middle ear pressure may cause the drum to become thinned and atelectatic (Fig. 20.11), either diffusely or with a retraction pocket. Eustachian tube dysfunction and/or acute otitis media may cause a middle ear effusion (Fig. 20.12). Fluid behind the drum is often obvious, but when the drum is opaque, increased vascularity or retraction are useful clues. Perforations of the pars tensa are either central or marginal (Fig. 20.13). Marginal perforations extend to the annulus and may be associated with cholesteatoma (Fig. 20.14), whereas with central perforations there is a rim of retained membrane between the defect and the annulus. Both are described by their position in relation to the handle of the malleus (anterior, posterior or inferior) and by their size (Fig. 20.15).

Figure 20.10 A right tympanic membrane showing marked posterior tympanosclerosis and a small anterior perforation.

Figure 20.11 A left tympanic membrane showing atelectasis and posterior retraction on to the long process of the incus.

Figure 20.12 A left tympanic membrane with a middle ear effusion.

Figure 20.13 A left tympanic membrane with an anterior central perforation.

Figure 20.14 A left tympanic membrane with cholesteatoma in the posterosuperior quadrant.

Figure 20.15 A left tympanic membrane with a subtotal perforation. The chorda tympani and long process of the incus can clearly be seen, as can the round window niche.

The fistula test is indicated if the patient is dizzy with middle ear pathology. Press on the tragus to occlude the meatus and then apply more pressure. If the labyrinth is open, this pressure change will be applied to the inner ear. The patient will be dizzy and nystagmus may be induced.

The facial nerve

Test the facial movements. Unilateral weakness is much easier to identify than bilateral weakness. A peripheral facial palsy can be graded using the House-Brackmann scale (Table 20.3). Function of the greater superficial petrosal nerve can be tested with Schirmer’s test: absorbent paper strips are applied to the inferior margin of the eye to detect tear formation (Ch. 19). Chorda tympani function can be tested by the sense of taste and by electrogustometry.

Table 20.3 The House-Brackmann facial nerve grading scale