The ear, nose and throat





Ear


Anatomy and physiology


The ear is the specialised sensory organ of hearing and balance. It is divided anatomically into the external, middle and inner ear.


External ear


The external ear consists of the cartilaginous pinna, the external auditory canal (cartilage in the lateral one-third, bone in the medial two-thirds) and the lateral surface of the tympanic membrane ( Fig. 9.1 ). Sound is collected and channelled by the pinna and transmitted via the external auditory canal to the tympanic membrane. The external auditory canal has an elongated S-shaped curve; hence it is important to retract the pinna when examining the ear to see the tympanic membrane clearly. The outer portion of the canal has hair, and glands that produce ear wax, which forms a protective barrier.




Fig. 9.1


The ear.

A The pinna. B Cross-section of the outer, middle and inner ear.


Middle ear


The middle ear is an air-filled space that contains the three bony, articulated ossicles: the malleus, incus and stapes. The Eustachian tube opens into the middle ear inferiorly and allows equalisation of pressure and ventilation. Vibrations of the tympanic membrane are transmitted and amplified through the ossicular chain and focused on to the smaller oval window on which the stapes sits ( Fig. 9.1B ). The malleus is attached to the tympanic membrane and can be seen clearly on otoscopy ( Fig. 9.2 ). The long process of the incus can also be visible occasionally. The tympanic membrane has a flaccid upper part (pars flaccida) and it is important to look carefully in this area, as this is where a cholesteatoma (an invasive collection of keratinising squamous epithelium) can form. The chorda tympani nerve runs through the middle ear carrying taste fibres from the anterior two-thirds of the tongue; these ‘hitch a ride’ with the facial nerve, which runs through the mastoid bone in the wall of the middle ear.




Fig. 9.2


Structures seen on otoscopic examination of the right ear.

A Main structures. B Normal tympanic membrane.


Inner ear


The inner ear contains the organs of hearing (cochlea) and balance (vestibular system). The vibration of the stapes footplate stimulates fluid within the cochlea. This results in the movement of hair cells in the cochlea, which are converted to electrical impulses along the vestibulocochlear nerve (VIII).


The vestibular system helps maintain balance, along with visual input and proprioception. The vestibular part of the inner ear contains:




  • The lateral, superior and posterior semicircular canals: these lie at right angles to detect rotational motion of their fluid (endolymph) in three planes.



  • The utricle and the saccule: their hair cells are embedded in a gel layer containing small crystals (otoliths), which are subject to gravity and enable detection of head tilt and linear acceleration.



The history


Common presenting symptoms


Pain and itching


Ask about:




  • quality of the pain



  • preceding trauma, upper respiratory tract infection (URTI)



  • associated symptoms: dysphagia/voice change (suggesting possible referred pain from a throat lesion).



Otalgia (ear pain) associated with pruritus (itching) is often due to otitis externa. Acute otitis media is common in children and otalgia often follows an URTI. Other causes of otalgia are described in Box 9.1 .



9.1

Causes and features of earache (otalgia)















































Cause Clinical features
Otological
Acute otitis externa Pain worse on touching outer ear, tragus
Swelling of ear canal
Purulent discharge and itching
Acute otitis media Severe pain, red, bulging tympanic membrane, purulent discharge if tympanic membrane perforation present
Perichondritis Erythematous, swollen pinna
Trauma Pinna haematoma, pinna laceration, haemotympanum (blood behind tympanic membrane); cerebrospinal fluid leak or facial nerve palsy may be present
Herpes zoster (Ramsay Hunt syndrome) Vesicles in ear canal, facial nerve palsy may be present; vertigo is common
Malignancy Mass in ear canal or on pinna
Non-otological
Tonsillitis
Peritonsillar abscess
Sore throat, tonsil inflammation
Trismus, soft-palate swelling in peritonsillar abscess
Temporomandibular joint dysfunction Tenderness, clicking of joint on jaw opening
Dental disease Toothache, e.g. due to dental abscess
Cervical spine disease Neck pain/tenderness
Cancer of the pharynx or larynx Associated sore throat, hoarseness, dysphagia, weight loss, neck lump



Ear discharge


Ask about:




  • purulent, mucoid or blood-stained discharge (otorrhoea)



  • associated pain.



A purulent discharge can be caused by otitis externa or acute otitis media with a perforation. A chronic offensive discharge may be a sign of cholesteatoma.


Blood-stained discharge may suggest the presence of granulation tissue from infection or can be a result of trauma, with or without an associated cerebrospinal fluid (CSF) leak.


Hearing loss


Ask about:




  • sudden or gradual onset



  • precipitating factors: trauma, URTI, noise exposure, antibiotics



  • impact of the hearing loss on the patient’s function.



Hearing loss can be due to disruption in the conduction mechanism or may have sensorineural causes, such as failure of the VIII nerve or cochlea ( Box 9.2 ). Profound loss before speech acquisition affects speech development and quality.



9.2

Causes of hearing loss
















Conductive a



  • Wax



  • Otitis externa



  • Middle ear effusion



  • Trauma to the tympanic membrane/ossicles




  • Otosclerosis



  • Chronic middle ear infection



  • Tumours of the middle ear

Sensorineural b



  • Genetic, e.g. Alport’s syndrome



  • Prenatal infection, e.g. rubella



  • Birth injury



  • Infection:




    • Meningitis



    • Measles



    • Mumps





  • Trauma



  • Ménière’s disease



  • Degenerative (presbyacusis)



  • Occupation- or other noise-induced



  • Acoustic neuroma



  • Idiopathic


a Disruption to the mechanical transfer of sound in the outer ear, eardrum or ossicles.


b Cochlear or central damage.




Tinnitus


Tinnitus is an awareness of a noise in the absence of an external stimulus.


Ask about:




  • quality of tinnitus: high-pitched, ringing, pulsatile



  • intermittent or constant nature



  • whether it is unilateral or bilateral



  • associated hearing loss or other ear symptoms.



Tinnitus is usually associated with hearing loss. An acoustic neuroma (a tumour of the vestibulocochlear nerve, cranial nerve VIII) needs to be considered in unilateral tinnitus or tinnitus with an asymmetrical sensorineural hearing loss.


Vertigo


Vertigo is a sensation of movement relative to one’s surroundings. Rotational movements are most common and patients often have associated nausea, vomiting and postural or gait instability. Vertigo can originate peripherally or, less often, centrally (brainstem, cerebellum). Patients will often say they are ‘dizzy’ when describing the illusion of movement: that is, vertigo. It is very important to clarify exactly what they mean by this. Lightheadedness is not a vestibular symptom, but unsteadiness may be.


Ask about:




  • duration and frequency of episodes



  • aggravating or provoking factors (position, head movement)



  • associated ‘fullness in the ear’ during the episode (Ménière’s disease)



  • associated focal neurology (cerebrovascular event)



  • fluctuating hearing loss or tinnitus



  • associated headaches, nausea or aura (migraine)



  • previous significant head injury; previous URTI.



The most common causes of vertigo include benign paroxysmal positional vertigo (attributed to debris within the posterior semicircular canal), vestibular neuritis (also known as vestibular neuronitis, a viral or postviral inflammatory disorder) and Ménière’s disease (caused by excess endolymphatic fluid pressure). Other causes include migraine, cerebral ischaemia, drugs and head trauma. Discriminating features are described in Box 9.3 .



9.3

Diagnosing vertigo

















































Benign paroxysmal positional vertigo Vestibular neuritis Ménière’s disease Central vertigo (migraine, MS, brainstem ischaemia, drugs)
Duration Seconds Days Hours Hours – migraine
Days and weeks – MS
Long-term – cerebrovascular accident
Hearing loss ++
Tinnitus ++
Aural fullness ++
Episodic Yes Rarely Recurrent vertigo; persistent tinnitus and progressive sensorineural deafness Migraine – recurs
Central nervous system damage – usually some recovery but often persistent
Triggers Lying on affected ear Possible presence of upper respiratory symptoms None Drugs (e.g. aminoglycosides)
Cardiovascular disease

MS, multiple sclerosis.



Nystagmus


Nystagmus is an involuntary rhythmic oscillation of the eyes, which can be horizontal, vertical, rotatory or multidirectional. It may be continuous or paroxysmal, or evoked by manœuvres such as gaze or head position. The most common form, ‘jerk nystagmus’, consists of alternating phases of a slow drift in one direction with a corrective saccadic ‘jerk’ in the opposite direction. The direction of the fast jerk is used to define the direction of nystagmus ( Box 9.4 ). Pendular nystagmus, in which there is a sinusoidal oscillation without a fast phase, is less common. Nystagmus may be caused by disorders of the vestibular, visual or cerebellar pathway.



9.4

Characteristics of nystagmus









































Nystagmus type Clinical pathology Characteristics
Fast phase Maximal on looking
Jerk:
Peripheral Semicircular canal, vestibular nerve Unidirectional
Not suppressed by optic fixation
Patient too dizzy to walk
Dix–Hallpike fatigues on repetition
Away from affected side
Central Brainstem, cerebellum Bidirectional (changes with direction of gaze)
Suppressed by optic fixation
Patient can walk (even with nystagmus)
Dix–Hallpike persists
To either side
Dysconjugate (ataxic) Interconnections of III, IV and VI nerves (medial longitudinal bundle) Typically affects the abducting eye To either side
Pendular Eyes, e.g. congenital blindness No fast phase Straight ahead



Past medical history


Ask about:




  • previous ear surgery, trauma



  • recurrent ear infections



  • systemic conditions associated with hearing loss (such as granulomatosis with polyangiitis)



  • any significant previous illnesses such as meningitis, which can result in significant sensorineural hearing loss.



Drug history


The aminoglycoside antibiotics (such as gentamicin), aspirin, furosemide and some chemotherapy agents (cisplatin) are ototoxic.


Family history


Some causes of sensorineural hearing loss and otosclerosis are congenital. Otosclerosis causes a conductive hearing loss due to fixation of the stapes footplate.


Social history


The patient’s occupation should be noted, as well as any significant previous exposure to loud noise.


The physical examination




Examination sequence


Inspection





  • Pinna skin, shape, size, position, scars from previous surgery/trauma, deformity.



Palpation





  • Gently pull on the pinna and push on the tragus to check for pain.



  • Gently palpate over the mastoid bone behind the ear to assess for pain or swelling.



Otoscopy





  • Use the largest otoscope speculum that will comfortably fit the meatus.



  • Explain to the patient what you are going to do.



  • Hold the otoscope in your right hand for examining the right ear (left hand to examine left ear). Rest the ulnar border of your hand against the patient’s cheek to enable better control and to avoid trauma if the patient moves ( Fig. 9.3 ).




    Fig. 9.3


    Examination of the ear using an otoscope.



  • Gently pull the pinna upwards and backwards to straighten the cartilaginous external auditory canal. Use the left hand to retract the right pinna ( Fig. 9.3 ).



  • Inspect the external auditory canal through the speculum, noting wax, foreign bodies or discharge. You should identify the tympanic membrane and the light reflex anteroinferiorly (see Fig. 9.2 ).




Congenital deformities of the pinna, like microtia ( Fig. 9.4A ) or low-set ears, can be associated with other conditions such as hearing loss and Down’s syndrome. Children can also have protruding ears that occasionally require corrective surgery (pinnaplasty). Trauma can result in a pinna haematoma ( Fig. 9.4B ) and subsequent ‘cauliflower ear’ due to cartilage necrosis if untreated. Trauma may also cause mastoid bruising (‘Battle’s sign’), suggesting a possible skull-base fracture. Lesions on the pinna are relatively common and can be related to sun exposure; they include actinic keratosis, and basal cell and squamous cell cancers ( Fig. 9.4C ).




Fig. 9.4


The pinna.

A Microtia. B Haematoma. C Squamous cancer (arrow) .


If discharge is noted on otoscopy and the tympanic membrane is intact, otitis externa is the likely cause ( Fig. 9.5A ). The canal can reveal exostoses, abnormal bone growth due to cold water exposure, often seen in surfers ( Fig. 9.5B ).




Fig. 9.5


Auditory canal abnormalities.

A Otitis externa. B Exostosis of the external auditory meatus. C Cholesteatoma.


Scarring on the tympanic membrane (tympanosclerosis) can be caused by previous grommet insertion or infections. Tympanic membrane perforations can be central or marginal, and the position and size of the perforation should be noted as a percentage ( Fig. 9.6A ). A severe retraction pocket of the pars tensa can mimic a perforation ( Fig. 9.6B ). A retraction of the pars flaccida can contain a cholesteatoma, which may cause an offensive discharge and erode the bony ossicles, resulting in a conductive hearing loss ( Fig. 9.5C ). Fluid behind the tympanic membrane is called otitis media with effusion (OME or ‘glue ear’, Fig. 9.7A ), and a fluid level may be seen ( Fig. 9.7B ). This commonly affects children and can be treated surgically with insertion of a ventilation tube or grommet (see Fig. 9.6C ). If persistent OME is seen in adults, the postnasal space needs to be examined by a specialist to exclude a lesion in that site. Acute otitis media presents with pain; the tympanic membrane can become inflamed ( Fig. 9.7C ), and may bulge and eventually perforate.




Fig. 9.6


Tympanic membrane abnormalities.

A Tympanic membrane perforation (arrow) . B Retraction pocket of the pars tensa (arrow) . C Grommet in situ.



Fig. 9.7


Otitis media.

A With effusion. B Fluid level behind the tympanic membrane (arrow) . C Acute otitis media.


Testing hearing


Whispered voice test




Examination sequence





  • Stand behind the patient.



  • Start testing with your mouth about 15 cm from the ear you are assessing.



  • Mask hearing in the patient’s other ear by rubbing the tragus (‘masking’).



  • Ask the patient to repeat a combination of multisyllable numbers and words. Start with a normal speaking voice to confirm that the patient understands the test. Lower your voice to a clear whisper.



  • Repeat the test but this time at arm’s length from the patient’s ear. People with normal hearing can repeat words whispered at 60 cm.




Tuning fork tests


A 512-Hz tuning fork can be used to help differentiate between conductive and sensorineural hearing loss.


Weber’s test




Examination sequence





  • Strike the prongs of the tuning fork against a hard surface to make it vibrate.



  • Place the base of the vibrating tuning fork in the middle of the patient’s forehead ( Fig. 9.8 ).




    Fig. 9.8


    Weber’s test.



  • Ask the patient, ‘Where do you hear the sound?’



  • Record which side Weber’s test lateralises to if not central.




In a patient with normal hearing, the noise is heard in the middle, or equally in both ears.


In conductive hearing loss the sound is heard louder in the affected ear. In unilateral sensorineural hearing loss it is heard louder in the unaffected ear. If there is symmetrical hearing loss it will be heard in the middle.


Rinne’s test




Examination sequence





  • Strike the prongs of the tuning fork against a hard surface to make it vibrate.



  • Place the vibrating tuning fork on the mastoid process ( Fig. 9.9A ).




    Fig. 9.9


    Rinne’s test.

    A Testing bone conduction. B Testing air conduction.



  • Now place the still-vibrating base at the external auditory meatus and ask, ‘Is it louder in front of your ear or behind?’ ( Fig. 9.9B ).




With normal hearing, the sound is heard louder when the tuning fork is at the external auditory meatus. That is, air conduction (AC) is better than bone conduction (BC), recorded as AC > BC. This normal result is recorded as ‘Rinne-positive’.


In conductive hearing loss, bone conduction is better than air conduction (BC > AC); thus the sound is heard louder when the tuning fork is on the mastoid process (‘Rinne-negative’). A false-negative Rinne’s test may occur if there is profound hearing loss on one side. This is due to sound being conducted through the bone of the skull to the other ‘good’ ear. Weber’s test is more sensitive and therefore the tuning fork will lateralise to the affected ear in conductive hearing loss before Rinne’s test becomes abnormal (negative). In sensorineural hearing loss, Rinne’s test will be positive, as air conduction is better than bone conduction.


Tuning fork test findings are summarised in Box 9.5 .



9.5

Tuning fork tests































Weber test Rinne test
Bilateral normal hearing Central AC > BC, bilateral
Bilateral symmetrical sensorineural loss Central AC > BC, bilateral
Unilateral or asymmetrical sensorineural loss LEFT Louder right AC > BC, bilateral a
Unilateral conductive loss LEFT Louder left BC > AC, left
AC > BC, right
Bilateral conductive loss (worse on LEFT) Louder left BC > AC, bilateral

AC, air conduction; BC, bone conduction.

a Patients with a severe sensorineural loss may have BC > AC due to BC crossing to the other better-hearing cochlea that is not being tested (false-negative Rinne test).




Testing vestibular function


Testing for nystagmus



Dec 29, 2019 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on The ear, nose and throat
Premium Wordpress Themes by UFO Themes
%d bloggers like this: