Anatomy

The ear (Fig. 20.1) consists of the external, middle and inner ears. The external ear consists of the pinna and external auditory canal (meatus). The cartilaginous pinna is covered with perichondrium and skin, forming the helix and antihelix. The meatus has an outer cartilaginous and an inner bony component. The skin overlying the external auditory meatus contains hair cells and modified sebaceous glands which produce wax (cerumen). Desquamated skin debris, mixed with cerumen, migrates outward from the drum and deep canal, and makes the external ear a self-cleaning system.

Figure 20.1 Anatomy of the ear.

The opaque or semitranslucent eardrum (tympanic membrane) separates the middle and external ears (Fig. 20.2). The pars tensa, the lower part of the drum, is formed from an outer layer of skin, a middle layer of fibrous tissue and an inner layer of middle ear mucosa. It is attached to the annulus, a fibrous ring that stabilizes the drum to the surrounding bone. The pars flaccida, the upper part of the drum, may retract if there is prolonged negative middle ear pressure secondary to Eustachian tube dysfunction. The malleus, incus and stapes are three small connecting bones (ossicles) (Fig. 20.3) that transmit sound across the middle ear from the drum to the cochlea. The handle of the malleus lies within the fibrous layer of the pars tensa. Within the middle ear, the head of the malleus articulates with the incus in the attic, the upper portion of the middle ear space. The long process of the incus articulates with the stapes. This articulation (the incudostapedial joint) is liable to disruption from trauma or chronic infection. The stapes footplate sits in the oval window, and transmits and amplifies sound to the fluid-filled inner ear.

Figure 20.2 A normal left tympanic membrane.

Figure 20.3 The ossicles.

The inner ear has two portions. The cochlea (Fig. 20.4), the spiral organ of hearing, is a transducer that converts sound energy into digital nerve impulses that are transmitted by the eighth cranial nerve (cochlear) to the brainstem and thence to the auditory cortex. The organ of Corti (Fig. 20.5) within the cochlea contains hair cells that detect frequency-specific sound energy: low-frequency sounds are detected in the apical region, and high-frequency sounds are detected in the basal region. The inner ear is also concerned with balance. The semicircular canals and the vestibule contain receptors that detect angular and linear motion in the three cardinal x, y and z planes. The inner ears are only one component of the balance system; visual input and proprioception from joints and muscles are also important.

Figure 20.4 Section through the cochlea.

Figure 20.5 The organ of Corti.

The facial (seventh cranial) nerve (Fig. 20.6) is important in otological practice. It runs from the brainstem through the cerebellopontine angle to the internal auditory meatus (IAM) with the cochlear and vestibular (eighth) nerves. The facial nerve passes through the temporal bone and leaves the skull through the stylomastoid foramen near the mastoid process. It may be damaged when there is suppurative middle ear disease or trauma. The chorda tympani leaves the descending portion of the facial nerve in the temporal bone to provide taste fibre innervation to the anterior two-thirds of the tongue. The facial nerve supplies the facial muscles through upper and lower divisions that arise as it passes through the parotid gland.

Figure 20.6 The course of the peripheral facial nerve.

Symptoms of ear disease

The five main symptoms of ear disease are:

Clinical examination of the ear and hearing

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.

Pure tone audiometry

A single-frequency tone is presented at standardized levels into each ear in turn. This is done in noise-free surroundings, usually in a soundproofed booth (Fig. 20.19). Air conduction is tested first through headphones. A level well above threshold, as predicted by free field testing, is chosen and the patient responds when he hears the sound. The intensity is then reduced in 10-dB steps until the patient cannot hear it. It is then increased in 5-dB steps to establish the quietest sound that can be heard – the threshold. The better ear is tested first at 1, 2, 4 and 8 kHz, then at 250 and 500 Hz (Fig. 20.20). Bone conduction tests are performed using a vibrating headset applied to the mastoid. In conductive loss, the difference is called the air-bone gap. This may be correctible by surgery to the middle ear and tympanic membrane.

Figure 20.19 Pure tone audiometry.

Figure 20.20 Pure tone audiograms: (A) normal; (B) noise-induced hearing loss; (C) presbyacusis; (D) bilateral conductive hearing loss.

Speech audiometry

A pure tone audiogram does not test discrimination. A speech audiogram measures the patient’s ability to recognize words from phonetically balanced lists delivered at different sound levels to the test ear from a tape recording. The percentage of words correctly repeated by the subject is noted at each level. With normal hearing, all words are heard (100% optimal speech discrimination – ODS) at a sound intensity of 40 dB. Patients with sensorineural deafness are often unable to achieve 100% ODS and, in particular, patients with neural/retrocochlear loss have poor ODS (Fig. 20.21).

Figure 20.21 Speech audiogram.

Tympanometry

An earpiece is inserted into the external meatus through which pass three channels. The first delivers a continuous tone into the ear canal during the test (probe tone); the second has a microphone to record the sound intensity level within the ear canal; the third channel connects to a manometer so that the pressure within the canal can be altered (Fig. 20.22).

Figure 20.22 A tympanogram being performed.

The external meatus is a rigid tube with a compliant end (the drum). Normally the middle ear and ear canal pressures are equal, and most of the sound introduced into the meatus is transmitted into the ear; only a minimum of sound energy is reflected back and measured by the microphone. Changing the pressure difference between the external and the middle ear causes the tympanic membrane to become less compliant. This increases the sound energy reflected back to the probe. These changes are plotted graphically on a tympanogram (Fig. 20.23). The test also measures the volume of the canal: a large volume indicates a tympanic perforation. Impedance (the reciprocal of compliance) is increased when the tympanic membrane is thickened or the middle ear has fluid, and is decreased when the drum is hypermobile or atrophic. Tympanometry is an objective test. It has particular value in children in the assessment of glue ear.

Figure 20.23 A tympanogram.

Otoacoustic emissions

When a click or tone-burst is played into the ear, a very small noise is emitted in return, probably arising from the outer hair cells. These emissions are particularly prominent in neonates but become increasingly difficult to elicit with age. Testing does not require cooperation. When there is hearing loss there is no response. The technique is valuable in the screening of neonates and forms the backbone of the Universal Neonatal Hearing Screen programme.

Evoked-response audiometry

A click presented to the ear causes a nerve impulse to be sent to the auditory cortex via the brainstem. If a large number (>2000) of responses are averaged, then evoked responses in brainstem and cortex can be seen and amplitudes and latencies measured. The auditory brainstem response is not affected by sedation and the main indication is in the establishment of hearing thresholds, especially in infants. Cortical-evoked responses are less widely used. They require an awake and alert patient.

Radiological examination

Computed tomography (CT) scanning is the investigation of choice, but is not a substitute for clinical assessment of chronic ear disease. It is not specifically diagnostic of cholesteatoma (Fig. 20.26), but is useful in cranial trauma (Fig. 20.27) and in the evaluation of temporal bone neoplasia. Magnetic resonance imaging (MRI) is more useful in identifying soft tissue abnormalities in the cerebellopontine angle, especially vestibular schwannoma (Fig. 20.28). These present with asymmetric sensorineural hearing loss. MRI also helps assess tumour spread outside the temporal bone. MR angiography helps assessment of pulsatile tinnitus and vascular lesions. Formal angiography is useful for embolization of vascular tumours.

Figure 20.26 CT scan of left ear showing a fistula of the lateral semicircular canal in a patient who had previously undergone a mastoidectomy.

Figure 20.27 CT scan of a right ear showing a fracture across the middle ear. The incus is seen and is lying in a displaced position.

Figure 20.28 MRI scan demonstrating a large left vestibular schwannoma with brainstem compression.

Anatomy

The nose (Box 20.4) is formed by the two nasal bones, which articulate with the nasal process of the maxilla on each side. The lateral cartilages provide support for the nostrils, especially in inspiration (Fig. 20.29). The nasal cavity is divided by the nasal septum, formed of cartilage anteriorly and bone posteriorly (Fig. 20.30). The lateral wall of the nose is formed by the three nasal turbinate bones; inferior, middle and superior (Fig. 20.31). Under each turbinate is a corresponding meatus. The nose constantly produces mucus – a pint a day – which is constantly propelled backwards by the cilia to the posterior choanae, whence it is swallowed, usually unnoticed.

Figure 20.29 The external nose.

Figure 20.30 The nasal septum.

Figure 20.31 The lateral wall of the nose.

The paranasal sinuses are air-filled spaces in the bones of the facial skeleton (Figs 20.31 and 20.32). They comprise the paired maxillary, frontal and ethmoid sinuses and the unpaired but bisected sphenoid sinus, and form the structure of the adult face. The ethmoidal cells or labyrinth comprises a number of small bony cells. The sinuses open into the nose via small drainage channels (ostia). Their mucus is swept by cilia through the ostia to be mixed with mucus secreted by the nose. The middle meatus is the common pathway for drainage from the maxillary, the anterior ethmoid and the frontal sinuses. The anterior ethmoids are important because disease in these areas will compromise maxillary and frontal sinus drainage. Blockage of the ostia due to inflammation in the nose, with retention of mucus and secondary infection, is the presumed mechanism for sinus infection (rhinosinusitis). The upper teeth are closely related to the floor of the maxillary sinus: infection here may lead to sinus problems.

Figure 20.32 Cross-section through the sinuses (semischematic).

The olfactory neuroepithelium of the nose is located in the roof of the nasal cavity. Neurones run through the cribriform plate to the olfactory bulb lying on the floor of the anterior cranial fossa. The postnasal space contains the adenoids, which are lymphoid tissue, part of Waldeyer’s ring, which includes the palatine tonsils. These are largest in childhood and regress from the age of about 8 years onwards, although rarely they may persist into adult life. The inferior opening of the Eustachian tube is on the lateral wall of the postnasal space.

Symptoms of nasal disease

The important symptoms of nasal and sinus disease are:

Examination of the nose and face

Inspect the nose and face from the front, side and back in a good light. Note the colour of the skin and any asymmetry of facial contours. Observe for scars and pigmentary changes. With age, the tip of the nose tends to droop. Deformities of the nasal bone and cartilage, such as saddle deformity, often follow a nasal fracture or other destructive disorders of the bony or cartilaginous septum. Palpate the nose and facial skeleton, especially the orbital margins, noting tenderness and any swelling, expansion or depression of bone. Facial swelling is unusual in maxillary sinusitis, but occurs with dental root infections and in carcinoma of the maxillary antrum. Inspect and palpate the palate and alveoli from inside the mouth using a gloved finger.

Examine the nasal vestibule and intranasal contents by gently pushing the tip of the nose upwards with a finger, preferably using reflected illumination from a head mirror. The nasal vestibule is lined with skin and contains vibrissae (thicker hairs): these become prominent in older men. Inspect the anterior nasal cavity with Thudicum’s nasal speculum or an otoscope (Fig. 20.33). The nasal septum is rarely completely straight but should not be so bent that it is not possible to see the anterior end of the inferior turbinate. The majority of nasal resistance to airflow occurs in the front of the nose. Look for any area of granulation on the nasal septum and for any perforation (Fig. 20.34). Perforations may be secondary to cocaine snorting, digital trauma (nose-picking), surgical trauma, granulomatous conditions or inhalation of industrial dusts, notably nickel and chrome.

Figure 20.33 Examining the nose.

Figure 20.34 A septal perforation.

Nasal polyps are usually easily identifiable by their pale colour (Fig. 20.35) and their softness and lack of sensitivity to probing. In a child, an apparent polyp may be seen arising from the roof of the nose: this should not be probed as it may be the intranasal presentation of a meningocele. In children and adults, airflow through a patent nostril causes misting on a cold metal tongue depressor or mirror held at the nose. In a neonate, nasal patency is best estimated by observing any movement of a wisp of cotton wool held in front of each nostril, after blocking each in turn with the thumb. Nasal endoscopy (Fig. 20.36), after applying a topical decongestant such as xylometazoline with topical lidocaine anaesthesia, allows inspection of the middle meatus for oedema, draining pus or polyps. The postnasal space and the opening of the Eustachian tube (Fig. 20.37) can be seen, with the fossa of Rosenmuller, the site of origin of postnasal space carcinomas, lying directly above and behind. In children and young adults, look for adenoidal swelling.

Figure 20.35 A large polyp in the right nasal cavity.

Figure 20.36 Rigid nasal endoscopy.

Figure 20.37 Endoscopic view of the Eustachian tube orifice and the postnasal space.

Special tests

Radiological examination

Plain X-rays are unreliable in the management of sinus disease but may be helpful in the absence of more specialized tests. A lateral X-ray may be useful in estimating the degree of adenoidal hypertrophy in young children (Fig. 20.38). Endoscopic nasal examination and CT scanning are the investigations of choice for sinus disease (Fig. 20.39). CT is useful in the management of chronic infection, trauma and neoplasia. However, there is a radiation dosage to the eyes and the investigation should be used only when the diagnosis is uncertain or to provide accurate anatomical information before surgery. MRI is less useful in sinus disease because of difficulties in interpretation. MRI is highly sensitive to changes in the mucosal lining of the sinuses. However, it tends to overdiagnose and interpretation requires caution. It does have value in assessing spread of sinus neoplasia.

Figure 20.38 Lateral X-ray of the nasopharynx demonstrating adenoidal hypertrophy (arrowed).

Figure 20.39 Coronal CT scan of the nose showing an opaque right maxillary antrum and anterior ethmoid cells.

Anatomy

The throat includes the oral cavity, the pharynx (oropharynx, nasopharynx and hypopharynx), the larynx and the major salivary glands. The oral cavity extends from the lips to the anterior faucial pillars. The oral cavity proper is bounded by the teeth laterally, the tongue and floor of the mouth inferiorly and the hard and soft palate superiorly. The pharynx extends from the base of the skull to the cricopharyngeal sphincter (Fig. 20.40). The oropharynx is bounded above by the soft palate and below by the upper surface of the epiglottis. Its anterior margin is defined laterally by the anterior faucial pillar, containing the palatoglossus muscle, and by the posterior third of the tongue. The posterior pharyngeal wall is its posterior boundary. The palatine tonsils are situated laterally between the anterior and posterior pillars of the fauces. The base of the tongue contains the lingual tonsils. This lymphoid tissue, together with the adenoids and the tubal tonsil (lymphoid tissue around the Eustachian tube opening), makes up Waldeyer’s ring, an important line of immunological defence. The hypopharynx consists of the posterior pharyngeal wall, the piriform fossae and the postcricoid area. The piriform fossae, which comprise the lateral walls of the pharynx adjacent to the larynx, are the routes by which food is passed into the upper oesophagus. The larynx is a rigid structure consisting of cartilages, the most prominent of which are the paired thyroid cartilages, which articulate with the cricoid cartilage below. The epiglottis is attached to the inner surface of the thyroid cartilage and aids the separation of air and food passages during swallowing. The larynx consists of three compartments (Fig. 20.41): glottis, supraglottis and subglottis. The glottis is formed by the vocal folds. The glottis has poor lymphatic drainage, which may help to delay the spread of malignancy from this area. The epiglottis extends from the false cords below to the hyoid bone above. It has a rich lymphatic drainage, and therefore malignancy in this area is more frequently associated with metastatic disease. The subglottis is the narrowest part of the upper respiratory tract and extends from the glottis to the lower border of the cricoid.

Figure 20.40 Midline sagittal section demonstrating the pharynx.

Figure 20.41 The divisions of the larynx.

The prime function of the larynx is to separate breathing and swallowing, thereby protecting the airway. Voice production is a secondary function that has arisen with evolution. Phonation occurs with movement of the vocal folds into the midline (Fig. 20.42). Changes in volume of the voice are caused by alterations in the subglottic pressure, whereas alterations in pitch are due to modification of the length and tension of the vocal folds. The quality of this basic laryngeal sound is modulated by resonance in the pharynx, air sinuses, mouth and nose.

Figure 20.42 The mechanism of phonation.

The pharynx is innervated from the pharyngeal plexus (cranial nerves IX, X and XI). Interruption of this nerve supply by lesions at the jugular foramen leads to swallowing problems and severe morbidity. All the muscles of the larynx except the cricothyroid are supplied by the recurrent laryngeal branch of the vagus (cranial nerve X). In the chest, this nerve loops around the arch of the aorta on the left and the subclavian artery on the right, before running up to enter the larynx. The long course of the left recurrent laryngeal nerve means it is more frequently affected by disease. The cricothyroid is supplied by the external branch of the superior laryngeal nerve (cranial nerve X).

There are three paired major salivary glands (Fig. 20.43). The parotid gland lies anterior to the ear. Its duct opens opposite the second upper molar tooth. The submandibular gland lies far posterior in the floor of the mouth and may be palpated in the neck, under the mandible. Its duct opens anteriorly in the floor of the mouth adjacent to the frenulum of the tongue. The smaller sublingual gland lies anteriorly in the floor of the mouth and its duct joins the submandibular duct.

Figure 20.43 The major salivary glands.

The lymph nodes of the head and neck (Fig. 20.44) provide a barrier to the spread of disease, whether inflammatory or neoplastic. Enlargement implies that there is either primary disease within the nodes or that they have become involved secondary to pathology in the areas they drain. Occasionally they may become involved by pathology below the clavicle.

Figure 20.44 The cervical lymph node groupings.

Symptoms of throat disease

Patients with throat disorders present with:

Occasionally lesions in the upper airway may present with overspill of food and fluids into the upper trachea or nose, or with weight loss. Malignant mouth, throat and airway disease is very strongly associated with smoking, with alcohol intake an important synergistic factor.

Dysphonia

Dysphonia or hoarseness covers a range of symptoms, from subtle changes noticed by professional voice users to aphonia, when there is no voice. It may be caused by structural problems affecting the vocal fold, or by neurological disease (Box 20.8). Hoarseness followed by increasing airway obstruction is the typical presentation of a laryngeal neoplasm (Fig. 20.45). Damage to the recurrent laryngeal nerve anywhere along its course usually leads to hoarseness, although compensation from the unaffected side will limit symptoms. A lesion of the vagus above the exit of the superior laryngeal nerve produces a more breathy voice, as there is also loss of cricothyroid function. Acute vocal abuse and acute inflammation causes dysphonia, which is usually self-limiting. Long-term vocal abuse may lead to a number of changes of the vocal folds: singer’s nodules, polyps (Fig. 20.46) or Reinke’s oedema. These will often respond to speech therapy, although surgery may be necessary. It is also worth considering whether gastro-oesophageal (laryngopharyngeal) reflux may be implicated. Malignancy should be considered in any patient with dysphonia of more than 4 weeks’ duration.

Box 20.8 Causes of dysphonia

Inflammatory

Acute and chronic laryngitis

Smoke inhalation

Neoplasia

Carcinoma

Laryngeal papillomatosis

Recurrent laryngeal nerve

Post thyroidectomy

Carcinoma of lung/breast

Neurological

Myasthenia gravis

Spasmodic dysphonia

Systemic: hypothyroidism, rheumatoid arthritis

Habitual dysphonias

Reinke’s oedema

Singer’s nodules

Vocal cord polyps

Vocal process granuloma

Gastro-oesophageal/laryngopharyngeal reflux

Psychogenic

Musculoskeletal tension

Ventricular

Dysphonia

Conversion disorders

Mutational falsetto (pubophonia)

Figure 20.45 Laryngeal carcinoma at the anterior commissure with hyperkeratosis of the right vocal cord.

Figure 20.46 A traumatic right vocal cord polyp.

Examination of the mouth and throat

With practice it is possible to inspect all of the oral cavity, the pharynx and the larynx. Use a headlight or a head mirror to ensure adequate illumination and keep both hands free for the manipulation of instruments. First check the lips, teeth and gums, the floor of the mouth and the openings of the submandibular and parotid ducts. Observe the corners of the mouth for cracks or fissures (angular stomatitis or cheilitis). In children, this is usually due to bacterial infection, but poor dentition in the elderly leads to cracks and candidiasis (thrush). This may also be seen in severe iron-deficiency anaemia and in vitamin B₂ (riboflavin) deficiency. Grouped vesicles on the lips on a red base with crusted lesions are seen in herpes simplex labialis. This viral infection is acute and the lack of induration and ulceration serves to distinguish it from malignancy. If salivary gland pathology is suspected, bimanual palpation, with one gloved finger in the mouth and synchronous palpation of the gland, may help to define pathology. Palpation is also valuable for examining the cheeks, tongue and even the tonsils on occasion. Tongue mobility (cranial nerve XII) should be assessed by protrusion and side-to-side movement. Look for wasting or fasciculation. Depress the tongue to inspect the tonsillar pillars, the palatine tonsils, soft palate and uvula. The tonsils and soft palate should be nearly symmetrical. Check the gag reflex (cranial nerve IX). The more distant portions of the pharynx can be inspected only with a laryngeal mirror or fibreoptic laryngoscope. For indirect laryngoscopy (Fig. 20.47), remove any dentures; gently hold the protruded tongue and ask the patient to take slow deep breaths. With the mouth opened wide, a warmed or demisted laryngeal mirror is introduced gently but firmly to the soft palate. Displace the soft palate upwards and backwards with the mirror and instruct the patient to say ‘ee’ or ‘ah’. The larynx elevates towards the examining mirror. The vallecula, epiglottis, supraglottis and glottis are examined in turn. The whole length of each vocal fold should be clearly visible and the mobility of each side noted. Vision can be helped in the gagging patient by using a 2% lidocaine anaesthetic spray. If an inadequate view is obtained (this depends upon the skill of the examiner), the flexible fibreoptic nasal endoscope (Fig. 20.48) allows a good view in almost every case. If available, the flexible endoscopic examination is mostly used due to the superior view, and recording the examination for clinical review. Videolaryngostroboscopy (Fig. 20.49) is a specialized endoscopic examination, useful for detailed visualization of the vocal folds. In this technique, stroboscopic light is used through the endoscope to visualize the mucosal wave of the vocal fold and heighten diagnostic capabilities.

Figure 20.47 Indirect laryngoscopy.

Figure 20.48 Flexible fibreoptic nasendoscopy.

Figure 20.49 (A) Videolaryngostroboscopy and (B) the image.

Examination of the neck

This is part of the routine assessment of any patient with suspected or proven disease in the throat. The neck is exposed and inspected from the front and side before the examiner stands behind the patient (Fig. 20.50) and follows a well-rehearsed routine so that no area is missed. Start by palpating the nodes in the posterior auricular region, and then progressively feel for the nodes on the anterior border of the trapezius muscle down to the supraclavicular fossa. The latter area is palpated from behind forwards. The examining fingers then pass up the jugular vein, where the most important groups of nodes in the head and neck are situated, towards the ear. The jugular, parotid and preauricular areas are then examined, followed by submandibular and submental nodes. Finally, the nodes associated with the anterior jugular chain are examined. This brings the fingers to the thyroid gland (details of thyroid examination are in Ch. 16). Midline lumps should also be assessed with the patient protruding the tongue. Movement suggests attachment to the base of the tongue and implies the presence of a thyroglossal cyst (Fig. 20.51). The larynx should be mobile from side to side, and if the thyroid cartilage is held between thumb and first finger and gently moved against the cervical spine, it should grate. This laryngeal crepitus is a normal phenomenon. It may be reduced or abolished by hypopharyngeal pathology or a mass in the prevertebral space displacing the larynx away from the cervical spine. Finally, auscultate the carotid arteries and the thyroid gland.

Figure 20.50 Examination of the neck.

Figure 20.51 Thyroglossal cyst.

Radiological examination

A soft-tissue lateral neck X-ray is not a sensitive investigation, even for detecting foreign bodies. A barium swallow is a dynamic investigation and can locate obstruction in the oesophagus or demonstrate incoordinate swallowing. It can be combined with video recording (videofluoroscopy). It is less helpful in evaluating the hypopharynx, where endoscopy under a general anaesthetic is the preferred investigation. Endoscopy is also helpful in taking biopsies in suspected malignancy. Ultrasound is useful for the evaluation of neck masses and the thyroid gland. Doppler ultrasound assesses the cervical vasculature. CT scanning helps to stage neoplastic disease and may demonstrate metastatic spread that has eluded palpation (Fig. 20.52). MRI complements CT as an imaging technique.

Figure 20.52 CT scan of neck demonstrating a large metastatic lymph node with central necrosis.