Ear, Nose and Throat Flashcards
Categories of hearing loss
There are two main categories of hearing loss: conductive hearing loss and sensorineural hearing loss.
Conductive hearing loss relates to a problem with sound travelling from the environment to the inner ear. The sensory system may be working correctly, but the sound is not reaching it. Putting earplugs in your ears causes conductive hearing loss.
Sensorineural hearing loss is caused by a problem with the sensory system or vestibulocochlear nerve in the inner ear.
Basic ear anatomy
There are three sections of the ear are:
Outer ear
Middle ear
Inner ear
The basic structures, from outside in, are:
The pinna is the external portion of the ear
The external auditory canal is the tube into the ear
The tympanic membrane is the eardrum
The Eustachian tube connects the middle ear with the throat to equalise pressure
The malleus, incus and stapes are the small bones in the middle ear that connect the tympanic membrane to the structures of the inner ear
The semicircular canals are responsible for sensing head movement (the vestibular system)
The cochlea is responsible for converting the sound vibration into a nervous signal
The vestibulocochlear nerve transmits nerve signals from the semicircular canals and cochlea to the brain
Presentation of hearing loss
Hearing loss may be gradual and insidious. Patients may present because others have noticed they are not paying attention or missing details of conversations. Sometimes patients can present with concerns about dementia, when in fact, the issue is hearing loss.
Sudden onset hearing loss (over less than 72 hours) requires a thorough assessment to establish the cause.
There may be associated symptoms alongside hearing loss, which can give clues about the potential cause:
Tinnitus (ringing in the ears)
Vertigo (the sensation that the room is spinning)
Pain (may indicate infection)
Discharge (may indicate an outer or middle ear infection)
Neurological symptoms
It is worth noting patients with hearing loss are more likely to develop dementia, and treating the hearing loss (e.g., a hearing aid) may reduce the risk.
Weber’s and Rinne’s Tests
Weber’s test and Rinne’s test are used to differentiate between sensorineural and conductive hearing loss. A tuning fork is used to perform both tests.
Weber’s Test
To perform Weber’s test:
Strike the tuning fork to make it vibrate and hum (use the palm of your hand or your knee – not the patient!)
Place it in the centre of the patient’s forehead
Ask the patient if they can hear the sound and which ear it is loudest in
A normal result is when the patient hears the sound equally in both ears.
In sensorineural hearing loss, the sound will be louder in the normal ear (quieter in the affected ear). The normal ear is better at sensing the sound.
In conductive hearing loss, the sound will be louder in the affected ear. This is because the affected ear “turns up the volume” and becomes more sensitive, as sound has not been reaching that side as well due to the conduction problem. When the tuning fork’s vibration is transmitted directly to the cochlea, rather than having to be conducted, the increased sensitivity makes it sound louder in the affected ear.
TOM TIP: The way I remember which way round these tests are, is to picture Spiderman shooting a web (Weber’s) right in the middle of someone’s face.
Rinne’s Test
To perform Rinne’s test:
Strike the tuning fork to make it vibrate and hum
Place the flat end on the mastoid process (the boney lump behind the ear) – this tests bone conduction
Ask the patient to tell you when they can no longer hear the humming noise
When they can no longer hear the noise, remove the tuning fork (still vibrating) and hover it 1cm from the same ear
Ask the patient if they can hear the sound now – this tests air conduction
Repeat the process on the other side
A normal result is when the patient can hear the sound again when bone conduction ceases and the tuning fork is moved next to the ear rather than on the mastoid process. It is normal for air conduction to be better (more sensitive) than bone conduction. This is referred to as “Rinne’s positive”.
An abnormal result (Rinne’s negative) is when bone conduction is better than air conduction. The sound is not heard after removing the tuning fork from the mastoid process and holding it near the ear canal. This suggests a conductive cause for the hearing loss. Sound is transmitted through the bones of the skull directly to the cochlea, meaning bone conduction is intact. However, the sound is less able to travel through the air, ear canal, tympanic membrane and middle ear to the cochlea due to a conductive problem.
Causes Of Sensorineural Hearing Loss
The causes of adult-onset sensorineural hearing loss are:
Sudden sensorineural hearing loss (over less than 72 hours)
Presbycusis (age-related)
Noise exposure
Ménière’s disease
Labyrinthitis
Acoustic neuroma
Neurological conditions (e.g., stroke, multiple sclerosis or brain tumours)
Infections (e.g., meningitis)
Medications
There are a large number of medications that can cause sensorineural hearing loss. Some of the more common to remember are:
Loop diuretics (e.g., furosemide)
Aminoglycoside antibiotics (e.g., gentamicin)
Chemotherapy drugs (e.g., cisplatin)
Causes Of Conductive Hearing Loss
The causes of adult-onset conductive hearing loss are:
Ear wax (or something else blocking the canal)
Infection (e.g., otitis media or otitis externa)
Fluid in the middle ear (effusion)
Eustachian tube dysfunction
Perforated tympanic membrane
Otosclerosis
Cholesteatoma
Exostoses
Tumours
Presbycusis
Presbycusis is described as age-related hearing loss. It is a type of sensorineural hearing loss that occurs as people get older. It tends to affect high-pitched sounds first and more notably than lower-pitched sounds. The hearing loss occurs gradually and symmetrically.
The causes of reduced hearing in presbycusis are complex. There are several different mechanisms, including loss of the hair cells in the cochlea, loss of neurones in the cochlea, atrophy of the stria vascularis and reduced endolymphatic potential.
Risk factors for presbycusis
Age
Male gender
Family history
Loud noise exposure
Diabetes
Hypertension
Ototoxic medications
Smoking
Exposure to loud noise over time is a key risk factor that can be addressed to potentially prevent or reduce the extent of presbycusis. Hearing protection should be worn in environments where there is exposure to loud noises for prolonged periods to reduce the risk of presbycusis, for example, in occupations such as woodworking or construction.
Presentation of presbycusis
Hearing loss in presbycusis is gradual and insidious. The gradual onset may mean patients do not notice the change in their hearing. The loss of high-pitched sounds can make speech difficult to hear and understand, particularly in loud environments. Male voices may be easier to hear than female voices (due to the generally lower pitch). Patients may present after others have noticed they are not paying attention or missing details of conversations. Sometimes patients can present with concerns about dementia, when in fact, the issue is hearing loss.
There may be associated tinnitus (ringing in the ears).
It is worth noting patients with hearing loss are more likely to develop dementia, and treating the hearing loss (e.g., a hearing aid) may reduce the risk.
Diagnosing presbycusis
Audiometry is the investigation of choice for establishing the diagnosis and extent of hearing loss. Presbycusis will give a sensorineural hearing loss pattern, with normal or near-normal hearing at lower frequencies and worsening hearing loss at higher frequencies.
Managing presbycusis
The effects of presbycusis cannot be reversed.
Management involves supporting the person to maintain normal functioning:
Optimising the environment, for example, reducing the ambient noise during conversations
Hearing aids
Cochlear implants (in patients where hearing aids are not sufficient)
Sudden sensorineural hearing loss
Sudden sensorineural hearing loss (SSNHL) is defined as hearing loss over less than 72 hours, unexplained by other causes. This is considered an otological emergency and requires an immediate referral to the on-call ENT team. The diagnosis is made when someone rapidly loses their hearing, and no conductive cause can be found.
With SSNHL, hearing loss is most often unilateral. It may be permanent or resolve over days to weeks.
Conductive causes of rapid-onset hearing loss (not classed as SSNHL) include:
Ear wax (or something else blocking the canal)
Infection (e.g., otitis media or otitis externa)
Fluid in the middle ear (effusion)
Eustachian tube dysfunction
Perforated tympanic membrane
Causes of sudden sensorineural hearing loss
Most cases (90%) of SSNHL are idiopathic, meaning no specific cause is found.
Other causes of SSNHL include:
Infection (e.g., meningitis, HIV and mumps)
Ménière’s disease
Ototoxic medications
Multiple sclerosis
Migraine
Stroke
Acoustic neuroma
Cogan’s syndrome (a rare autoimmune condition causing inflammation of the eyes and inner ear)
Investigating sudden sensorineural hearing loss
Audiometry is required to establish the diagnosis. A diagnosis of SSNHL requires a loss of at least 30 decibels in three consecutive frequencies on an audiogram.
MRI or CT head may be used if a stroke or acoustic neuroma are being considered.
Managing sudden sensorineural hearing loss
The NICE clinical knowledge summaries (updated September 2019) recommend an immediate referral to ENT for assessment within 24 hours for patients presenting with sudden sensorineural hearing loss presenting within 30 days of onset.
Where an underlying cause is found (e.g., infection), treatment can be directed at this.
Idiopathic SSNHL may be treated with steroids under the guidance of the ENT team. Steroids may be:
Oral
Intra-tympanic (via an injection of steroids through the tympanic membrane)
Eustachian tube dysfunction
Eustachian tube dysfunction is when the tube between the middle ear and throat is not functioning properly. The Eustachian tube is present mainly to equalise the air pressure in the middle ear and drain fluid from the middle ear.
When the Eustachian tube is not functioning correctly or becomes blocked, the air pressure cannot equalise properly and fluid cannot drain freely from the middle ear. The air pressure between the middle ear and the environment can become unequal. The middle ear can fill with fluid.
Eustachian tube dysfunction may be related to a viral upper respiratory tract infection (URTI), allergies (e.g., hayfever) or smoking.
Presentation of Eustachian tube dysfunction
Eustachian tube dysfunction may present with:
Reduced or altered hearing
Popping noises or sensations in the ear
A fullness sensation in the ear
Pain or discomfort
Tinnitus
Symptoms tend to get worse when the external air pressure changes and the middle ear pressure cannot equalise to the outside pressure, for example, flying, climbing a mountain or scuba diving.
Otoscopy may appear normal, but it is important to exclude other causes (e.g., otitis media).
Investigating Eustachian tube dysfunction
Often Eustachian tube dysfunction gives a typical set of symptoms and is associated with a clear cause, for example, a recent viral upper respiratory tract infection or hayfever. In this situation, investigations are not required as the symptoms will resolve with time or simple treatments.
In persistent, problematic or severe symptoms, investigations to help establish the diagnosis and cause include:
Tympanometry
Audiometry
Nasopharyngoscopy (an endoscopic camera through the nose to the throat to inspect the Eustachian tube openings)
CT scan to assess for structural pathology
Tympanometry
Tympanometry involves:
Inserting a device into the external auditory canal (ear canal)
Creating different air pressures in the canal
Sending a sound in the direction of the tympanic membrane
Measuring the amount of sound reflected back off the tympanic membrane
Plotting a tympanogram (graph) of the sound absorbed (admittance) at different air pressures
The amount of sound absorbed by the tympanic membrane and middle ear (not reflected back to the device) is known as the admittance.
Normally, sound is absorbed best when the air pressure in the ear canal matches the ambient air pressure. The ambient air pressure is equal to the middle ear pressure in healthy ears.
When there is Eustachian tube dysfunction, the air pressure in the middle ear may be lower than the ambient air pressure because new air cannot get in through the tympanic membrane to equalise the pressures. As a result, the tympanogram will show a peak admittance (most sound absorbed) with negative ear canal pressures.
Managing Eustachian tube dysfunction
Treatment options for Eustachian tube dysfunction include:
No treatment, waiting for it to resolve spontaneously (e.g., recovering from the viral URTI)
Valsalva manoeuvre (holding the nose and blowing into it to inflate the Eustachian tube)
Decongestant nasal sprays (short term only)
Antihistamines and a steroid nasal spray for allergies or rhinitis
Surgery may be required in severe or persistent cases
Otovent is an over the counter device where the patient blows into a balloon using a single nostril, which can help inflate the Eustachian tube, clear blockages and equalise pressure.
Surgery for Eustachian tube dysfunction
There are three main surgical options:
Treating any other pathology that might be causing symptoms, for example, adenoidectomy (removal of the adenoids)
Grommets
Balloon dilatation Eustachian tuboplasty
Grommets are tiny tubes inserted into the tympanic membrane by an ENT surgeon. This allows air or fluid from the middle ear to drain through the tympanic membrane to the ear canal. Grommets are usually inserted using a local anaesthetic. The procedure is relatively safe with few complications. Grommets typically fall out within 18 months.
Balloon dilatation Eustachian tuboplasty involves inserting a deflated balloon into the Eustachian tube, inflating the balloon for a short period (i.e., 2 minutes) to stretch the Eustachian tube, then deflating and removing it. This is usually done under general anaesthetic.
Otosclerosis
Otosclerosis is a condition where there is remodelling of the small bones in the middle ear, leading to conductive hearing loss. Oto- refers to the ears, and -sclerosis means hardening. It usually presents before the age of 40 years.
The development of otosclerosis is thought to result from a combination of environmental and genetic factors, although the exact mechanism is not understood. It can be inherited in an autosomal dominant pattern. However, no specific genetic mutations have been identified. It is more common in women.
Pathophysiology of otosclerosis
The auditory ossicles are the tiny bones in the middle ear that transmit sound vibrations from the tympanic membrane to the cochlea. They are the malleus, incus and stapes. The stapes is connected to the oval window (fenestra ovalis) of the cochlea, where it transmits vibrations into the cochlea, which converts them into sensory signals.
In patients with otosclerosis, these tiny bones in the middle are affected by abnormal bone remodelling and formation. This mainly affects the base of the stapes, where it attaches to the oval window, causing stiffening and fixation and preventing it from transmitting sound effectively. It causes conductive hearing loss.
Presentation of otosclerosis
The typical presentation is a patient under 40 years presenting with unilateral or bilateral:
Hearing loss
Tinnitus
It tends to affect the hearing of lower-pitched sounds more than higher-pitched sounds. Female speech may be easier to hear than male speech (due to the generally higher pitch). This is the reverse of the pattern seen in presbycusis.
Due to conductive hearing loss with intact sensory hearing, the patient can experience their voice as being loud compared to the environment (due to bone conduction of their voice). This can lead to them talking quietly.
Examining otosclerosis
Otoscopy is normal.
Weber’s test is normal if the otosclerosis is bilateral, meaning that when the tuning fork is applied to the centre of the forehead, they will hear the sound equally in both ears. If the otosclerosis is unilateral or affects one ear more than the other, the sound will be louder in the more affected ear.
Rinne’s test will show conductive hearing loss. The sound will be easily heard when the tuning fork is applied to the mastoid process (bone conduction). When the patient stops being able to hear the sound during bone conduction, and the tuning fork is removed from the mastoid process and held close to the ear canal, they will still not hear the sound (air conduction is worse than bone conduction).
Investigating otosclerosis
Audiometry is the initial investigation of choice. Otosclerosis will show a conductive hearing loss pattern. Bone conduction readings will be normal (between 0 and 20 dB). However, air conduction readings will be greater than 20 dB, plotted below the 20 dB line on the chart. Hearing loss tends to be greater at lower frequencies.
Tympanometry will show generally reduced admittance (absorption) of sound. The tympanic membrane is stiff and non-compliant and does not absorb sound, reflecting most of it back.
High-resolution CT scans can detect boney changes associated with otosclerosis, although they are not always required.
Managing otosclerosis
The options for management are:
Conservative, with the use of hearing aids
Surgical (stapedectomy or stapedotomy)
Surgical management is generally successful and can potentially restore hearing to normal. It involves lifting the tympanic membrane and some of the surrounding skin out of the way to access the middle ear through the ear canal.
Stapedectomy involves removing the entire stapes bone and replacing it with a prosthesis. The prosthesis attaches to the oval window and hooks around the incus, transmitting the sound from the incus to the cochlea in the same way the stapes normally would.
Stapedotomy involves removing part of the stapes bone and leaving the base of the stapes (the footplate) attached to the oval window. A small hole is made in the base of the stapes for the prosthesis to enter. A prosthesis is added to transmit sound from the incus to the cochlea.
Otitis media
Otitis media is the name given to an infection in the middle ear. The middle ear is the space that sits between the tympanic membrane (eardrum) and the inner ear. This is where the cochlea, vestibular apparatus and nerves are found. Bacteria enter from the back of the throat through the eustachian tube. A viral upper respiratory tract infection often precedes bacterial infection of the middle ear.
Bacteria causing otitis media
The most common bacterial cause of otitis media is streptococcus pneumoniae. This also commonly causes other ENT infections such as rhino-sinusitis and tonsillitis.
Other common causes include:
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Presentation of otitis media
Ear pain is the primary presenting feature of otitis media in adults.
It may also present with:
Reduced hearing in the affected ear
Feeling generally unwell, for example with fever
Symptoms of an upper airway infection such as cough, coryzal symptoms and sore throat
When the infection affects the vestibular system, it can cause balance issues and vertigo. When the tympanic membrane has perforated, there may be discharge from the ear.
Examining otitis media
An otoscope is used to visualise the tympanic membrane whilst gently pulling the pinna up and backwards. It may be challenging to visualise the tympanic membrane if there is significant discharge or wax in the ear canal.
A normal tympanic membrane is “pearly-grey”, translucent and slightly shiny. You should be able to visualise the malleus through the membrane. Look for a cone of light reflecting the light of the otoscope.
Otitis media will give a bulging, red, inflamed looking membrane. When there is a perforation, you may see discharge in the ear canal and a hole in the tympanic membrane.
Managing otitis media
Most otitis media cases will resolve without antibiotics within around three days, sometimes up to a week. Antibiotics make little difference to symptoms or complications. Complications (mainly mastoiditis) are rare. Simple analgesia (e.g., paracetamol or ibuprofen) can be used for pain and fever.
There are three options for prescribing antibiotics:
Immediate antibiotics
Delayed prescription
No antibiotics
Consider immediate antibiotics at the initial presentation in patients who have significant co-morbidities, are systemically unwell or are immunocompromised.
Consider a delayed prescription that can be collected and used after three days if symptoms have not improved or have worsened at any time. This can be a helpful strategy in patients pressing for antibiotics or where you suspect the symptoms might worsen.
The NICE clinical knowledge summaries (updated January 2021) suggest:
Amoxicillin for 5-7 days first-line
Clarithromycin (in pencillin allergy)
Erythromycin (in pregnant women allergic to penicillin)
Always safety-net, offering education and advice to patients on when to seek further medical attention.
Complications of otitis media
Otitis media with effusion
Hearing loss (usually temporary)
Perforated tympanic membrane (with pain, reduced hearing and discharge)
Labyrinthitis (causing dizziness or vertigo)
Mastoiditis (rare)
Abscess (rare)
Facial nerve palsy (rare)
Meningitis (rare)
Otitis externa
Otitis externa is inflammation of the skin in the external ear canal. Oto- refers to ear, -itis refers to inflammation, and externa refers to the external ear canal. The infection can be localised or diffuse. It can spread to the external ear (pinna). It can be acute (less than three weeks) or chronic (more than three weeks).
Otitis externa is sometimes called “swimmers ear”, as exposure to water whilst swimming can lead to inflammation in the ear canal. Trauma from the ear canal (e.g., from cotton buds or earplugs) is another predisposing factor. Ear wax (cerumen) has a protective effect against infection, and the removal of ear wax can increase the chances of infection.
The inflammation in otitis externa may be caused by:
Bacterial infection
Fungal infection (e.g., aspergillus or candida)
Eczema
Seborrhoeic dermatitis
Contact dermatitis
TOM TIP: Think about fungal infection in patients that have had multiple courses of topical antibiotics. Antibiotics kill the “friendly bacteria” that have a protective effect against fungal infections. This is similar to how oral antibiotics can predispose people to develop oral or vaginal candidiasis (thrush).
Bacterial causes of otitis externa
The two most common bacterial causes of otitis externa are:
Pseudomonas aeruginosa
Staphylococcus aureus
TOM TIP: It is worth remembering Pseudomonas aeruginosa. It is a gram-negative aerobic rod-shaped bacteria. It likes to grow in moist, oxygenated environments. Other than causing otitis externa, an important exam-related point to remember is that it can colonise the lungs in patients with cystic fibrosis, significantly increasing their morbidity and mortality. It is naturally resistant to many antibiotics, making it very difficult to treat in children with cystic fibrosis. It can be treated with aminoglycosides (e.g., gentamicin) or quinolones (e.g., ciprofloxacin).
Presentation of otitis externa
The typical symptoms of otitis externa are:
Ear pain
Discharge
Itchiness
Conductive hearing loss (if the ear becomes blocked)
Examination can show:
Erythema and swelling in the ear canal
Tenderness of the ear canal
Pus or discharge in the ear canal
Lymphadenopathy (swollen lymph nodes) in the neck or around the ear
The tympanic membrane may be obstructed by wax or discharge. It may be red if the otitis externa extends to the tympanic membrane. If it is ruptured, the discharge in the ear canal might be from otitis media rather than otitis externa.
Diagnosing otitis externa
The diagnosis can be made clinically with an examination of the ear canal (otoscopy).
An ear swab can be used to identify the causative organism but is not usually required.
Managing otitis externa
Mild otitis externa may be treated with acetic acid 2% (available over the counter as EarCalm). Acetic acid has an antifungal and antibacterial effect. This can also be used prophylactically before and after swimming in patients that are prone to otitis externa.
Moderate otitis externa is usually treated with a topical antibiotic and steroid, for example:
Neomycin, dexamethasone and acetic acid (e.g., Otomize spray)
Neomycin and betamethasone
Gentamicin and hydrocortisone
Ciprofloxacin and dexamethasone
Aminoglycosides (e.g., gentamicin and neomycin) are potentially ototoxic, rarely causing hearing loss if they get past the tympanic membrane. Therefore, it is essential to exclude a perforated tympanic membrane before using topical aminoglycosides in the ear. This can be difficult if the patient has discharge, swelling or wax blocking the ear canal. Patients with a blocked ear canal may need to be seen by ENT to microsuction the debris from the canal and visualise the tympanic membrane. They will also require a referral if the canal is so blocked or swollen that topical treatments cannot reach the site of infection.
Patients with severe or systemic symptoms may need oral antibiotics (e.g., flucloxacillin or clarithromycin) or discussion with ENT for admission and IV antibiotics.
An ear wick may be used if the canal is very swollen, and treatment with ear drops or sprays will be difficult. An ear wick is made of sponge or gauze. They contain topical treatment for otitis externa (e.g., antibiotics and steroids). Wicks are inserted into the ear canal and left there for a period of time (e.g., 48 hours). As the swelling and inflammation settle, the ear wick can be removed, and treatment can continue with drops or sprays.
Fungal infections can be treated with clotrimazole ear drops.
TOM TIP: The treatment for otitis externa I have seen used most often is Otomize ear spray, so this is probably the one to remember. Always check the local antibiotic guidelines when prescribing antibiotics, as they will vary in different hospitals and areas.
Malignant otitis externa
Malignant otitis externa is a severe and potentially life-threatening form of otitis externa. The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull.
Malignant otitis externa is usually related to underlying risk factors for severe infection, such as:
Diabetes
Immunosuppressant medications (e.g., chemotherapy)
HIV
Symptoms are generally more severe than otitis externa, with persistent headache, severe pain and fever.
Granulation tissue at the junction between the bone and cartilage in the ear canal (about halfway along) is a key finding that indicates malignant otitis externa.
Malignant otitis externa requires emergency management, with:
Admission to hospital under the ENT team
IV antibiotics
Imaging (e.g., CT or MRI head) to assess the extent of the infection
It can lead to complications of:
Facial nerve damage and palsy
Other cranial nerve involvement (e.g., glossopharyngeal, vagus or accessory nerves)
Meningitis
Intracranial thrombosis
Death
Ear wax
Ear wax is also called cerumen. It is normally produced in small amounts in the external ear canal. It is created from a combination of secretions, dead skin cells and any substances that enter the ear. Ear wax has a protective effect, helping to prevent infection in the ear canal. In most people, ear wax does not cause any problems.
Impacted ear wax
Ear wax can build up and become impacted and stuck to the tympanic membrane. This can result in:
Conductive hearing loss
Discomfort in the ear
A feeling of fullness
Pain
Tinnitus
Ear wax can be seen on examination with an otoscope. It may completely cover the tympanic membrane, preventing assessment of the tympanic membrane and inner ear.
Managing ear wax
In most cases, ear wax does not require any interventions. The ears should naturally regulate the amount of wax in the ear canal without any issues.
Inserting cotton buds into the ear should be avoided, as this can press the wax in further and cause impaction.
There are three main methods for removing ear wax:
Ear drops – usually olive oil or sodium bicarbonate 5%
Ear irrigation – squirting water in the ears to clean away the wax
Microsuction – using a tiny suction device to suck out the wax
Ear drops may be enough to clear the ears. If not, ear irrigation can often be performed in primary care. Where there are contraindications to ear irrigation (e.g., perforated tympanic membrane or infection), microsuction can be performed by specialist ear, nose and throat services.
Tinnitus
Tinnitus refers to a persistent addition sound that is heard but is not present in the surrounding environment. It may be described as a “ringing in the ears”, but it can also be a buzzing, hissing or humming noise.
The additional noise experienced with tinnitus is thought to be the result of a background sensory signal produced by the cochlea that is not effectively filtered out by the central auditory system. In a quiet enough environment, almost everyone will experience some background noise (tinnitus). This becomes more prominent the more attention it is given.
Causes of tinnitus
Primary tinnitus has no identifiable cause and often occurs with sensorineural hearing loss.
Secondary tinnitus refers to tinnitus with an identifiable cause. Causes include:
Impacted ear wax
Ear infection
Ménière’s disease
Noise exposure
Medications (e.g., loop diuretics, gentamicin and chemotherapy drugs such as cisplatin)
Acoustic neuroma
Multiple sclerosis
Trauma
Depression
Tinnitus may also be associated with systemic conditions:
Anaemia
Diabetes
Hypothyroidism or hyperthyroidism
Hyperlipidaemia
Objective tinnitus refers to when the patient can objectively hear an extra sound within their head. This sound can also be observable on examination by auscultating with a stethoscope around the ear. Actual additional sounds may be caused by:
Carotid artery stenosis (pulsatile carotid bruit)
Aortic stenosis (radiating pulsatile murmur sounds)
Arteriovenous malformations (pulsatile)
Eustachian tube dysfunction (popping or clicking noises)
TOM TIP: I think of primary tinnitus as the ears trying to “turn up the volume” when they cannot hear the surrounding noises as well. This is a helpful way of explaining it to patients who have tinnitus associated with hearing loss. Using hearing aids allows the ears to pick up noises better and “turn the volume down”, improving the tinnitus. The actual cause of tinnitus is not entirely understood, so this is not entirely accurate, but it is a helpful analogy.
Investigating tinnitus
The NICE clinical knowledge summaries (updated March 2020) suggest considering blood tests for possible underlying causes:
Full blood count (anaemia)
Glucose (diabetes)
TSH (thyroid disorders)
Lipids (hyperlipidaemia)
Audiology can be used to assess the hearing in detail and help establish the underlying cause.
Imaging (e.g., CT or MRI) may be rarely required to investigate for underlying causes such as vascular malformations or acoustic neuromas.
Red flags of tinnitus
Red flags that could indicate a serious underlying cause and the need for specialist assessment include:
Unilateral tinnitus
Pulsatile tinnitus
Hyperacusis (hypersensitivity, pain or distress with environmental sounds)
Associated unilateral hearing loss
Associated sudden onset hearing loss
Associated vertigo or dizziness
Headaches or visual symptoms
Associated neurological symptoms or signs (e.g., facial nerve palsy or signs of stroke)
Suicidal ideation related to the tinnitus
Managing tinnitus
Tinnitus tends to improve or resolve over time without any interventions.
Underlying causes of tinnitus can be treated, such as impacted ear wax or infection.
Several measures can be used to help improve and manage symptoms:
Hearing aids
Sound therapy (adding background noise to mask the tinnitus)
Cognitive behavioural therapy
Vertigo
Vertigo is a descriptive term for a sensation that there is movement between the patient and their environment. They may feel they are moving or that the room is moving. Often this is a horizontal spinning sensation, similar to how you feel after turning in circles then stopping abruptly.
Vertigo is often associated with nausea, vomiting, sweating and feeling generally unwell.
Pathophysiology of vertigo
The sensory inputs that are responsible for maintaining balance and posture are:
Vision
Proprioception
Signals from the vestibular system
Vertigo is caused by a mismatch between these sensory inputs.
The vestibular system is the most important sensory system to understand when learning about vertigo. The vestibular apparatus is located in the inner ear. It consists of three loops called the semicircular canals that are filled with a fluid called endolymph. These semicircular canals are oriented in different directions to detect various movements of the head. As the head turns, the fluid shifts inside the canals. This fluid shift is detected by tiny hairs called stereocilia found in a section of the canal called the ampulla. This sensory input of shifting fluid is transmitted to the brain by the vestibular nerve and lets the brain know that the head is moving in a particular direction.
The vestibular nerve carries signals from the vestibular apparatus to the vestibular nucleus in the brainstem and the cerebellum. The vestibular nucleus then sends signals to the oculomotor, trochlear and abducens nuclei that control eye movements and the thalamus, spinal cord and cerebellum. The cerebellum is responsible for coordinating movement throughout the body. Therefore, the vestibular signals help the central nervous system coordinate eye movements and other movements throughout the body.
Vertigo can be caused by either a:
Peripheral problem, usually affecting the vestibular system
Central problem, usually involving the brainstem or the cerebellum
Peripheral vertigo
There are several peripheral (vestibular) causes of vertigo. The four most common causes to be familiar with are:
Benign paroxysmal positional vertigo
Ménière’s disease
Vestibular neuronitis
Labyrinthitis
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo (BPPV) is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. They may be displaced by a viral infection, head trauma, ageing or without a clear cause. The crystals disrupt the normal flow through the canals and therefore disrupt the function of the system. The symptoms are usually positional, because movement is required to confuse the system. Therefore, attacks of vertigo are triggered by movement and can last around a minute before the symptoms settle. Often symptoms occur over several weeks and then resolve, then can reoccur weeks or months later. A special test called the Dix-Hallpike manoeuvre can be used to diagnose BPPV.
Meniere’s disease
Ménière’s disease is caused by an excessive buildup of endolymph in the semicircular canals, causing a higher pressure than normal, disrupting the sensory signals. It causes attacks of hearing loss, tinnitus, vertigo and a sensation of fullness in the ear. These attacks typically last several hours before settling. It most often occurs in middle-aged adults and is not associated with movement. The symptoms are not positional. Patients will have spontaneous nystagmus during attacks (nystagmus is discussed in more detail later). Over time, the patient’s hearing will gradually deteriorate.
Acute vestibular neuronitis
Acute vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection. Typically, the history is of acute onset of vertigo that improves within a few weeks.
Labyrinthitis
Labyrinthitis describes inflammation of the structures of the inner ear. This is usually attributed to a viral infection. Usually the history is of acute onset of vertigo that improves within a few weeks. Labyrinthitis can cause hearing loss, which distinguishes it from vestibular neuronitis.
Other peripheral causes of vertigo
There are several other peripheral causes of vertigo. These are:
Trauma to the vestibular nerve
Vestibular nerve tumours (acoustic neuromas)
Otosclerosis
Hyperviscosity syndromes
Varicella zoster infection (often with facial nerve weakness and vesicles around the ear – Ramsay Hunt syndrome)
Central causes of vertigo
Pathology that affects the cerebellum or the brainstem disrupt the signals from the vestibular system and cause vertigo. The most common pathology that results in a central cause of vertigo are:
Posterior circulation infarction (stroke)
Tumour
Multiple sclerosis
Vestibular migraine
All the central causes of vertigo will cause sustained, non-positional vertigo.
Posterior circulation infarction will have a sudden onset and may be associated with other symptoms, such as ataxia, diplopia, cranial nerve defects or limb symptoms.
Tumours in the cerebellum or brainstem will have a gradual onset with associated symptoms of cerebellar or brainstem dysfunction.
Multiple sclerosis may cause relapsing and remitting symptoms, with other associated features of multiple sclerosis, such as optic neuritis or transverse myelitis.
Vestibular migraine will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered by:
Stress
Bright lights
Strong smells
Certain foods (e.g. chocolate, cheese and caffeine)
Dehydration
Menstruation
Abnormal sleep patterns
Vertigo history
When a patient presents with “dizziness’, it is important to first distinguish between vertigo and lightheadedness. Ask whether the “room is moving” (vertigo) or whether they feel more of a lightheadedness.
Ask about symptoms that will help you differentiate between central and peripheral vertigo. The table below gives a general idea of the distinguishing features:
Peripheral Vertigo
Central Vertigo
Onset
Sudden onset
Gradual onset (except stroke)
Duration
Short (seconds or minutes)
Persistent
Hearing loss or tinnitus
Often present (except BPPV)
Usually not
Coordination
Intact
Impaired
Nausea
More severe
Mild
Key features that may point to a specific cause are:
Recent viral illness (labyrinthitis or vestibular neuronitis)
Headache (vestibular migraine, cerebrovascular accident or brain tumour)
Typical triggers (vestibular migraine)
Ear symptoms, such as pain or discharge (infection)
Acute onset neurological symptoms (stroke)
Vertigo examination
There are four things to examine when assessing a patient presenting with vertigo:
Ear examination to look for signs of infection or other pathology
Neurological examination to assess for central causes of vertigo (e.g., stroke or multiple sclerosis)
Cardiovascular examination to assess for cardiovascular causes of dizziness (e.g., arrhythmias or valve disease)
Special tests (see below)
Cerebellar examination is an important part of a full neurological examination in patients with vertigo. The components can be remembered with the DANISH mnemonic:
D – Dysdiadochokinesia
A – Ataxic gait (ask the patient to walk heel-to-toe)
N – Nystagmus (see below for more detail)
I – Intention tremor
S – Speech (slurred)
H – Heel-shin test
Special tests that may be helpful in patients with dizziness or vertigo include:
Romberg’s test (screens for problems with proprioception or vestibular function)
Dix-Hallpike manoeuvre (to diagnose BPPV)
HINTS examination (to distinguish between central and peripheral vertigo)
HINTS examination
The HINTS examination can be used to distinguish between central and peripheral vertigo. It stands for:
HI – Head Impulse
N – Nystagmus
TS – Test of Skew
Head Impulse Test
The head impulse test involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose. The head is moved slowly back to the centre before repeating in the opposite direction. Ensure they have no neck pain or pathology before performing the test.
A patient with a normally functioning vestibular system will keep their eyes fixed on the examiner’s nose.
In a patient with an abnormally functioning vestibular system (e.g., vestibular neuronitis or labyrinthitis), the eyes will saccade (rapidly move back and forth) as they eventually fix back on the examiner.
The head impulse test helps diagnose a peripheral cause of vertigo but will be normal if the patient has no current symptoms or a central cause of vertigo.
Nystagmus
Nystagmus can be demonstrated by having the patient look left and right. The eyes rapidly saccade or oscillate, meaning they shake side to side as they try to settle into place. A few beats can be normal. Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.
Test of Skew
The test of skew (also called the alternate cover test) involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner covers one eye at a time, alternating between covering either eye. The eyes should remain fixed on the examiner’s nose with no deviation. If there is a vertical correction when an eye is uncovered (the eye has drifted up or down and needs to move vertically to fix on the nose when uncovered), this indicates a central cause of vertigo.
Managing vertigo
Patients with suspected central vertigo need referral for further investigation (e.g., CT or MRI head) to establish the cause.
For peripheral vertigo, short-term options for managing symptoms include:
Prochlorperazine
Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
Betahistine may be used to help reduce the attacks in patients diagnosed with Ménière’s disease.
Epley manoeuvre can be effective in treating BPPV.
Vestibular migraine is usually managed by avoiding triggers and lifestyle changes (e.g., getting enough sleep and staying hydrated). Medical management is similar to migraines, with triptans for the acute symptoms and propranolol, topiramate or amitriptyline to prevent attacks.
The DVLA guide for medical professionals (updated March 2021) states that patients must not drive and must inform the DVLA if they are liable to “sudden and unprovoked or unprecipitated episodes of disabling dizziness”.
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo (BPPV) is a common cause of recurrent episodes of vertigo triggered by head movement. It is a peripheral cause of vertigo, meaning the problem is located in the inner ear rather than the brain. It is more common in older adults.
Presentation of BPPV
A variety of head movements can trigger attacks of vertigo. A common trigger is turning over in bed. Symptoms settle after around 20 – 60 seconds, and patients are asymptomatic between attacks. Often episodes occur over several weeks and then resolve but can reoccur weeks or months later.
BPPV does not cause hearing loss or tinnitus.
Pathophysiology of BPPV
BPPV is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal. They may be displaced by a viral infection, head trauma, ageing or without a clear cause.
The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.
Dix-Hallpike manoeuvre
The Dix-Hallpike manoeuvre can be used to diagnose BPPV (Dix for Dx – diagnosis). It involves moving the patient’s head in a way that moves endolymph through the semicircular canals and triggers vertigo in patients with BPPV. Check the patient can do the manoeuvre safely before performing it, for example, ensuring they have no neck pain or pathology.
To perform the manoeuvre:
The patient sits upright on a flat examination couch with their head turned 45 degrees to one side (turned to the right to test the right ear and left to test the left ear)
Support the patient’s head to stay in the 45 degree position while rapidly lowering the patient backwards until their head is hanging off the end of the couch, extended 20-30 degrees
Hold the patient’s head still, turned 45 degrees to one side and extended 20-30 degrees below the level of the couch
Watch the eyes closely for 30-60 seconds, looking for nystagmus
Repeat the test with the head turned 45 degrees in the other direction
In patients with BPPV, the Dix-Hallpike manoeuvre will trigger rotational nystagmus and symptoms of vertigo. The eye will have rotational beats of nystagmus towards the affected ear (clockwise with left ear and anti-clockwise for right ear BPPV).
Epley manoeuvre
The Epley manoeuvre can be used to treat BPPV. The idea is to move the crystals in the semicircular canal into a position that does not disrupt endolymph flow.
To perform the manoeuvre:
Follow the steps of the Dix-Hallpike manoeuvre, having the patient go from an upright position with their head rotated 45 degrees (to the affected side) down to a lying position with their head extended off the end of the bed, still rotated 45 degrees
Rotate the patient’s head 90 degrees past the central position
Have the patient roll onto their side so their head rotates a further 90 degrees in the same direction
Have the patient sit up sideways with the legs off the side of the couch
Position the head in the central position with the neck flexed 45 degrees, with the chin towards the chest
At each stage, support the patient’s head in place for 30 seconds and wait for any nystagmus or dizziness to settle
TOM TIP: Watch videos of the Dix-Hallpike and Epley manoeuvres and practice performing them on your friends. It is worth remembering the names, indications and interpretation, which may be tested in your MCQ exams. I would be surprised if you are asked to perform the manoeuvres in your OSCEs. However, it is worth learning how to perform them as they are not too difficult, and you can impress patients, friends, relatives or seniors if you can perform them at will.
Brandt-Daroff exercises
Brandt-Daroff exercises can be performed by the patient at home to improve the symptoms of BPPV. These involve sitting on the end of a bed and lying sideways, from one side to the other, while rotating the head slightly to face the ceiling. The exercises are repeated several times a day until symptoms improve.
Vestibular neuronitis
Vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection.
