Labyrinth It Is

Labyrinthitis
Straight to the point of care
Last updated: Jul 30, 2020

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Classification 4
Case history 5
Diagnosis 7
Approach 7
History and exam 10
Risk factors 10
Investigations 12
Differentials 15
Management 17
Approach 17
Treatment algorithm overview 18
Treatment algorithm 20
Emerging 33
Patient discussions 33
Follow up 34
Monitoring 34
Complications 35
Prognosis 36
Guidelines 37
Diagnostic guidelines 37
Treatment guidelines 37
Online resources 38
References 39
Disclaimer 43
Labyrinthitis Overview
Summary
Labyrinthitis is an inflammatory condition affecting the labyrinth in the cochlea and vestibular system of the
inner ear.
OVERVIEW
Viral infections are the most common cause of labyrinthitis. Bacterial labyrinthitis is a complication of otitis
media or meningitis.
Typical presentation includes vertigo, imbalance, and hearing loss.
Diagnosis is supported by history, physical examination, and audiometry.
Treatment is typically symptomatic and primarily involves the use of vestibular suppressants and anti-
emetics.
Definition
Labyrinthitis is an inflammatory condition caused by bacteria or viruses that affects the inner ear, which
consists of the cochlea and vestibular system. Typically, it presents with sensorineural hearing loss, vertigo,
and disequilibrium (problems with balance) and may affect one or both ears. It may be further classified as
suppurative or serous. Suppurative (bacterial) labyrinthitis follows direct microbial invasion of the inner ear
and usually presents with severe to profound hearing loss and vertigo.[1] [2] [3] Serous (viral) labyrinthitis
results from inflammation of the labyrinth only and usually presents with less severe hearing loss and vertigo
than suppurative labyrinthitis, and the hearing loss often recovers.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 30, 2020.
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Labyrinthitis Theory
Epidemiology
The actual incidence and prevalence of labyrinthitis are unknown. Viral infections are the most common
cause of labyrinthitis. They typically occur in adults, whereas purulent bacterial labyrinthitis is more common
THEORY
in children who are otitis-prone. Bacterial labyrinthitis is a rare complication of otitis media.[2] [3]
Aetiology
Viral labyrinthitis is typically associated with a preceding upper respiratory tract infection. Aetiological viral
agents include varicella zoster virus, cytomegalovirus, mumps, measles, rubella, and HIV.[4] [5] Labyrinthitis
has also been associated with autoimmune inner ear disease (e.g., Cogan's syndrome or Behcet's disease).
Bacterial labyrinthitis is associated with acute or chronic otitis media, meningitis, and cholesteatoma (a
collection of epidermal and connective tissues within the middle ear). Unlike viral labyrinthitis, the bacterial
form may affect both ears simultaneously.[2] [6] Potential bacterial causes include Treponema pallidum ,
Haemophilus influenzae , Streptococcus species, Staphylococcus species, and Neisseria meningitidis .[2]
Syphilitic labyrinthitis may follow tertiary neurosyphilis that occurs many years after the primary infection, and
is not seen with acute primary or secondary syphilis.[4]
Pathophysiology
The membranous labyrinth is surrounded by dense bone formed in utero by intramembranous and
enchondral ossification. Infections arising in the middle ear (otitis media) can spread to the inner ear
through the oval or round window. Inflammation or infectious agents can spread from the inner ear into
the internal auditory canal. Meningitis can spread to the inner ear through the cochlear aqueduct or the
cochlear modiolus.[6] Haematogenous spread of infectious agents through the labyrinthine artery to the stria
vascularis is theoretically possible but has not been demonstrated.[6]
Infection in the membranous labyrinth may result in a significant inflammatory response with resultant
intraluminal fibrosis and possible ossification (i.e., labyrinthitis ossificans).[7] [8] [9] Bacterial meningitis
is associated with a significant risk of hearing loss.[10] Auditory or vestibular symptoms, or both, may be
present in as many as 20% of children with meningitis.[11]
Classification
Types of labyrinthitis
Serous (viral) labyrinthitis:
• Caused by inflammation of the labyrinth only

• Typically presents with less severe hearing loss and vertigo than suppurative labyrinthitis; hearing loss
often recovers
• The term vestibular neuritis is often mistakenly used interchangeably with viral labyrinthitis. Patients
with either condition have vertigo and/or disequilibrium, but vestibular neuritis is not associated with
hearing loss, whereas patients with viral labyrinthitis have hearing loss.
Suppurative (bacterial) labyrinthitis:
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 30, 2020.
• Follows direct bacterial invasion of the inner ear

• Typically presents with severe to profound hearing loss and vertigo.
Meningogenic labyrinthitis:
THEORY
• Occurs in the setting of meningitis
• Typically begins at the basal turn of the cochlea adjacent to the opening of the cochlear aqueduct.
Autoimmune labyrinthitis:
• Autoimmune conditions (e.g., Cogan's syndrome or Behcet's disease) affecting the labyrinth typically
present with bilateral simultaneous or sequential hearing loss and vertigo
• Can be corticosteroid-responsive, but sometimes progress to bilateral profound hearing loss and
vestibular hypo-function.
Labyrinthitis ossificans:
• Fibrosis of the membranous labyrinth occurs within a few days of acute infection
• Ossification can occur as early as fibrosis, resulting in complete osseous replacement of the
membranous labyrinth
• Membranous labyrinth can be obstructed in up to 30% of patients with suppurative labyrinthitis.
Syphilitic labyrinthitis:
• Can follow tertiary neurosyphilis, which occurs many years after primary syphilis infection, and is not
seen with acute primary or secondary syphilis[4]
• Patients can present with progressive hearing loss and pressure- or sound-induced vertigo (Hennebert
and Tullio signs).
HIV-associated labyrinthitis:
• A variety of auditory and vestibular complaints, including labyrinthitis, have been reported in patients
with AIDS. The relative importance of the HIV infection itself as opposed to its associated opportunistic
infections requires further study.
Case history
Case history #1
A 56-year-old woman presents with a 3-week history of imbalance, right-sided hearing loss, and tinnitus.
She reports having an upper respiratory tract infection 1 week before the onset of her symptoms. Her
symptoms began with a severe episode of room-spinning vertigo with associated nausea and vomiting
that lasted all day. The next day she noticed right, high-pitched tinnitus and was unable to use the
telephone in her right ear. She now reports constant imbalance and slight vertigo with quick head turns to
the right.
5
Case history #2
A 46-year-old man presents with a 1-year history of imbalance, deafness, and tinnitus. His symptoms
began after being discharged from a prolonged admission to hospital secondary to pneumococcal
THEORY
meningitis.
Other presentations
Patients with bacterial meningitis are often critically ill and may present after resolution of the acute illness
with profound hearing loss and imbalance without a history of acute vertigo.[2] Patients with syphilitic
labyrinthitis can present with progressive hearing loss and pressure- or sound-induced vertigo (Hennebert
and Tullio signs).[4] Syphilitic labyrinthitis may follow tertiary neurosyphilis that occurs many years after
the primary infection, and is not seen with acute primary or secondary syphilis.[4] Labyrinthitis may also
be associated with autoimmune inner ear disease (e.g., Cogan's syndrome or Behcet's disease).
Labyrinthitis Diagnosis
Approach
The differential diagnosis of patients presenting with dizziness and vertigo can often be narrowed with
a thorough history and physical examination. Imaging studies are often recommended, as patients with
posterior fossa neoplasms can have a variety of presentations that can mimic other vestibular disorders.
Posterior fossa tumours include vestibular schwannomas (acoustic neuroma), meningiomas, cerebellar or
brainstem tumours, and epidermoid cysts.
Viral infections are the most common cause of labyrinthitis. They typically occur in adults, whereas purulent
bacterial labyrinthitis is more common in children who are otitis prone. Serous, as opposed to suppurative,
labyrinthitis is still far more common in both paediatric and adult patients.
History
Patients with labyrinthitis typically present with severe room-spinning vertigo and associated nausea
and vomiting. They may also have hearing loss and tinnitus (ringing in the ear). The hearing loss is
sensorineural (i.e., related to inner ear/eighth cranial nerve) rather than conductive (i.e., secondary to
middle ear causes). The acute vertigo may last up to 72 hours. Acute vertigo is typically followed by
persistent disequilibrium (problems with balance) and brief vertigo (seconds) with quick head or body
movements.
Important questions that are critical in establishing the diagnosis include:
• Describe your dizziness (e.g., room spinning, imbalance, floating, lightheaded)

• Tell me about your first episode of vertigo. How long did this episode last?
• How long are your current dizzy spells?
• Have you ever had any prior episodes of dizziness or vertigo?
• How often do you feel dizzy?
• Do you have any other associated symptoms (i.e., hearing loss, tinnitus, ear fullness, etc.)?
• Do changes in body position cause dizziness?
• Do you have any history of headaches (e.g., migraine, muscle tension)?
DIAGNOSIS
• Have you started any new or changed any medications?
• What makes your dizziness better or worse?
• Have you recently had an upper respiratory tract infection?
If the patient experiences more than one episode of room-spinning vertigo, a diagnosis of Meniere's
disease must be considered.
It is critical to evaluate for other neurological symptoms such as dysarthria, dysphagia, facial pain
or numbness, facial weakness, and extremity weakness or numbness, as these would point to a
cerebrovascular accident involving the brain stem.
Significant hearing loss with or without associated tinnitus differentiates labyrinthitis from vestibular
neuritis.[1]
Several tools, such as the Dizziness Handicap Inventory and the SF-36, can be used to assess the
impact of dizziness on patients’ quality of life.[12]
7
Physical examination
Patients who present in the acute setting may have significant difficulty walking. Spontaneous horizontal-
rotary nystagmus (rapid involuntary movement of the eyes) with the fast phase beating towards the
uninvolved ear is also frequently present.
The patient's balance should be assessed using tandem gait and Romberg's testing. Patients will
probably not be able to perform tandem gait (walking with one foot directly in front of the other foot, heel-
to-toe) and may fall with Romberg's testing (standing straight up with feet together and eyes closed).
Examination with a Weber 512-Hz tuning fork (placing the tuning fork on the forehead or maxillary teeth
and asking the patient to state in which ear the sound was louder) can quickly localise the affected ear
and determine whether the hearing loss is sensorineural or conductive. The sound will be perceived in the
affected ear when a unilateral conductive hearing loss is present or in the unaffected ear when there is a
unilateral sensorineural hearing loss. The result of this test is combined with the result of the Rinne's test
to interpret the type of hearing loss.
Rinne's testing allows the examiner to determine whether any hearing loss is secondary to middle ear
(conductive hearing loss) or inner ear/eighth cranial nerve (sensorineural hearing loss) causes. The
base of a 512-Hz tuning fork is placed on the mastoid and the patient indicates when he or she no longer
hears the sound. Once the sound is no longer audible, the tuning fork is placed in front of the ear and the
patient is asked whether he or she hears the sound. If the sound is louder when the tuning fork is on the
mastoid, then the patient has a conductive hearing loss. If the sound is louder with the fork in front of the
ear, the hearing loss is sensorineural or normal.
A thorough examination of the ear with an otoscope or microscope allows diagnosis of otitis media and
cholesteatoma. The presence of otorrhoea (ear discharge) should alert the clinician to the presence
of acute or chronic otitis media with tympanic membrane perforation. Careful inspection of the entire
tympanic membrane should identify a cholesteatoma unless there is significant debris in the ear canal
that obscures visualisation.
There should be no evidence of other neurological deficits such as upper or lower extremity weakness,
DIAGNOSIS
hoarseness, or facial weakness or numbness. The three-step bedside oculomotor exam Head-Impulse,
Nystagmus, Test-of-Skew (HINTS) has been found to identify stroke with a high degree of sensitivity
and specificity in patients with acute vestibular symptoms, and it may rule out stroke more effectively
than early diffusion-weighted magnetic resonance imaging (MRI).[13] Based on the HINTS model, one
algorithm suggests that stroke should be considered in patients presenting with acute-onset dizziness
if:[14]
• there is a central pattern of nystagmus
• there is skew deviation
• there is a negative head impulse test (in patients with nystagmus)
• there are any central nervous system signs on focused neurological examination, or
• the patient is unable to sit or walk unaided.

The presence of meningeal signs should be investigated if bacterial meningitis is a consideration. For
example, a rash is noted in 80% to 90% of patients with meningococcal meningitis, most commonly 4 to
18 hours after the initial symptoms of illness. Typically, the rash is a non-blanching petechial or purpuric
exanthem, but a few patients may initially have non-specific erythematous macular or maculopapular
lesions.
Cerebellar function should be examined by requesting the patient to perform finger to nose, heel to shin,
and rapid alternating movement tests.
Audiometry
An audiometric examination is useful to document the extent of hearing loss and to confirm the affected
ear. Hearing loss is typically of the sensorineural type. However, patients with inner ear malformations
(i.e., enlarged vestibular aqueduct) may present with similar symptoms and a mixed hearing loss with a
significant sensorineural component.
Vestibular testing with electronystagmography, rotary chair test, and vestibular-evoked myogenic
potentials is not indicated in the acute setting. However, these tests may provide additional information on
vestibular compensation and site-of-lesion testing after the patient has recovered from the acute stage of
labyrinthitis.
Laboratory tests
Patients with labyrinthitis secondary to bacterial meningitis should have appropriate cerebrospinal
fluid cultures performed. Additional serological testing for syphilis and HIV may be warranted if the
presentation is atypical or if the patient has additional risk factors.[15] If the serological tests are negative,
autoimmune conditions (e.g., Cogan's syndrome or Behcet's disease) may be suspected. For patients
who have severe nausea and vomiting, a basic metabolic panel should be evaluated to select the
appropriate crystalloid and electrolyte replacement. Check capillary blood glucose in all patients with
suspected stroke and arrange urgent neuroimaging.[16]
Imaging
Imaging can help to rule out differential diagnoses.
If an acute stroke is suspected, a computed tomography (CT) scan of the head can identify infarction
DIAGNOSIS
and provide enough information to make decisions about acute management.[16] A subsequent MRI
of the head with diffusion-weighted imaging can determine the extent of the infarct. If a temporal bone
fracture is suspected, a CT scan of the head can delineate the extent of the fracture.[17] MRI or CT scans
of the head can reveal inner ear malformations and temporal bone neoplasms. A CT scan of the petrous
temporal bones may show evidence of middle-ear or mastoid opacification, and should be ordered if
the patient is suspected of having mastoiditis. A CT scan may also be useful in patients with suspected
superior semi-circular canal dehiscence,[18] and also to confirm cholesteatoma.[19]
Any patient with an asymmetric hearing loss should undergo a retrocochlear evaluation with gadolinium-
enhanced MRI to investigate other causes of hearing loss. For example, over 10% of patients with
vestibular schwannomas (acoustic neuromas) present with sudden hearing loss. Labyrinthine
enhancement on gadolinium-enhanced MRI in the setting of meningitis is a significant predictor of hearing
loss.[20]
9
History and exam

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include viral infections, acute or chronic otitis media, meningitis, cholesteatoma, and
inner ear malformations.
vertigo (common)
• Patients typically describe 'room-spinning' (acute rotational) vertigo.
• Acute vertigo may last up to 72 hours.
dizziness (common)
• Can mean a variety of things, including floating, imbalance, disequilibrium, and impaired cognition.
nausea and vomiting (common)

• Vertigo is often associated with nausea and vomiting.
hearing loss (common)

• Typical presentation.
• May be unilateral or bilateral.
otorrhoea (common)
• Ear discharge alerts to presence of acute or chronic otitis media with tympanic membrane perforation.
Other diagnostic factors

nystagmus (common)
• Rapid side-to-side movement of the eyes is typically seen in patients with acute-onset labyrinthitis.
DIAGNOSIS
tinnitus (common)
• Possible presentation (constant noise in the ear).
vertigo-related quick head or body movements (common)

• Follow acute vertigo; indicate incomplete vestibular compensation.
influenza-like symptoms (common)

• Viral labyrinthitis may occur during an influenza-like illness or during illnesses such as measles or
mumps. Therefore, fever, sore throat, and influenza-like symptoms may be present.
otalgia (uncommon)
• Pain in the ear may be present in patients with acute or chronic otitis media.
Risk factors
Strong
viral infections
• Labyrinthitis often follows an upper respiratory tract infection.
• Other aetiological infectious agents include varicella zoster virus, cytomegalovirus, mumps, measles,
rubella, and HIV.
chronic suppurative otitis media

• Chronic middle ear infections such as chronic suppurative otitis media (CSOM, a persistent
inflammation of the middle ear or mastoid cavity), if not treated in a timely manner, may lead to
diffusion of bacterial toxins into the inner ear.
• Direct bacterial invasion into the otic capsule has been demonstrated in CSOM with or without
accompanying cholesteatoma.
acute otitis media

• Acute infections of the middle ear most typically result in serous labyrinthitis secondary to diffusion of
bacterial toxins into the membranous labyrinth.
cholesteatoma
• Direct erosion into the labyrinth or internal auditory canal by cholesteatoma (a collection of epidermal
and connective tissues within the middle ear) increases the risk of developing labyrinthitis.
meningitis
• Serous labyrinthitis results from bacterial toxins diffusing through the round window or internal auditory
canal. This can follow bacterial meningitis. Bacterial meningitis may result in labyrinthitis via spread
of infection and inflammatory mediators into the inner ear via the cochlear aqueduct. The cochlear
aqueduct connects the subarachnoid space to the scala tympani of the proximal basal turn of the
cochlea. Meningitis secondary to Streptococcus pneumoniae poses the greatest risk for labyrinthitis
and resultant hearing loss.
inner ear malformations
DIAGNOSIS
• Commonly associated with abnormal communications between the inner and middle ear.
Weak
autoimmune ear diseases
• Labyrinthitis has been associated with autoimmune inner ear disease (e.g., Cogan's syndrome or
Behcet's disease). These rare diseases cause immune-mediated inner ear damage with resultant
hearing loss and vestibular dysfunction.
syphilis
• History of sexually transmitted disease increases risk of having contracted syphilis.[3] If left untreated,
syphilis may eventually affect the central nervous system and the inner ear (tertiary neurosyphilis).
11
Investigations
1st test to order
Test Result
audiogram sensorineural hearing
loss
• Useful to document the extent of hearing loss and to confirm the
affected ear.
Weber's test sensorineural hearing
loss
• Examination with a Weber 512-Hz tuning fork (placing the tuning
fork on the forehead or maxillary teeth and asking the patient to
state in which ear the sound was louder) can quickly localise the
affected ear and determine whether the hearing loss is sensorineural
or conductive.
• The sound will be perceived in the affected ear when a unilateral
conductive hearing loss is present or in the unaffected ear when there
is a unilateral sensorineural hearing loss.
• The result of this test is combined with the result of the Rinne's test to
interpret the type of hearing loss.
Rinne's test sensorineural hearing
loss
• Allows the examiner to determine whether any hearing loss is
secondary to middle ear (conductive hearing loss) or inner ear/eighth
cranial nerve (sensorineural hearing loss) causes.
• The base of a 512-Hz tuning fork is placed on the mastoid and the
patient indicates when he or she longer hears the sound. Once the
sound is no longer audible, the tuning fork is placed in front of the
ear and the patient is asked whether he or she hears the sound. If
the sound is louder when the tuning fork is on the mastoid, then the
patient has a conductive hearing loss. If the sound is louder with the
fork in front of the ear, the hearing loss is sensorineural or normal.
DIAGNOSIS
Other tests to consider
Test Result
CT or MRI brain may be normal or
abnormal#
• Imaging can help to rule out differential diagnoses.
• If an acute stroke is suspected, a CT scan of the head can identify
infarction and provide enough information to make decisions about
acute management.[16] A subsequent MRI of the head with diffusion-
weighted imaging can determine the extent of the infarct. If a
temporal bone fracture is suspected, a CT scan of the head can
delineate the extent of the fracture.[17] MRI or CT scans of the head
can reveal inner ear malformations and temporal bone neoplasms.
A CT scan of the petrous temporal bones may show evidence of
middle-ear or mastoid opacification, and should be ordered if the
patient is suspected of having mastoiditis. A CT scan may also
be useful in patients with suspected superior semi-circular canal
dehiscence,[21] and also to confirm cholesteatoma.[19]
• Any patient with an asymmetric hearing loss should undergo a
retrocochlear evaluation with gadolinium-enhanced MRI to investigate
other causes of hearing loss. For example, over 10% of patients with
vestibular schwannomas (acoustic neuromas) present with sudden
hearing loss. Labyrinthine enhancement on gadolinium-enhanced
MRI in the setting of meningitis is a significant predictor of hearing
loss.[20]
electronystagmography may be normal or
abnormal
• Records eye movements and responses to ocular and vestibular
stimuli.
• May provide additional information on vestibular compensation after
the patient has recovered from the acute stage of labyrinthitis.
• Warm and cold air or water placed in the ear canal may show that the
affected ear has a less-robust response to caloric stimulation than the
good ear.
• Comparing results obtained from various sub-tests of an
electronystagmography evaluation assists in determining whether a
DIAGNOSIS
disorder is central or peripheral.
rotary chair test may be normal or
abnormal
• Sinusoidal harmonic acceleration or rotating chair testing involves a
variety of measurements of nystagmus on a patient who is rotated
from side to side during the procedure in a computer-controlled chair.
vestibular-evoked myogenic potentials may be normal or
abnormal
• Uses an intense, brief auditory stimulus to assess the saccule
ipsilateral to the stimulus.[22]
• If the saccule or posterior semicircular canal is affected, the
vestibular-evoked myogenic potential amplitude may be lower in the
affected ear.
syphilis serology may be normal or
abnormal
• Additional serological testing may be warranted if the presentation is
atypical or if the patient has additional risk factors.[15]
13
Test Result
• Positive titres suggest syphilis is the cause of acute or recent
deterioration in hearing.
cerebrospinal fluid Gram stain and culture gram-negative diplococci
in presence of bacterial
• Patients with labyrinthitis secondary to bacterial meningitis should
meningitis
have appropriate cerebrospinal fluid studies and cultures performed.
• Gram-negative diplococci suggest meningococcal infection in patients
with a compatible clinical illness and may provide a rapid presumptive
diagnosis.
• Gram stains are positive in 30% to 80% of patients with culture-
confirmed meningococcal meningitis.
serum HIV rapid test positive in HIV infection
• False-negatives may occur during window period immediately after
infection before antibodies to HIV have formed. Positive result should
be confirmed with a second rapid test.
basic metabolic profile (including urea and creatinine) may be normal or
• For patients who have severe nausea and vomiting, a basic metabolic abnormal
panel should be obtained before and after intravenous hydration
therapy to monitor response.
DIAGNOSIS
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Vestibular neuritis • Similar presentation to • Normal audiogram.
labyrinthitis but no hearing
loss.
• Vertigo is exacerbated by
change in head position with
respect to gravity.
Benign parox ysmal • Similar presentation to • Normal audiogram.

positional vertigo labyrinthitis but no hearing • A positive Dix-Hallpike's test
loss. (rotatory nystagmus and
reproduction of symptoms).
Meniere's disease • Fluctuating hearing loss, • Complete audiological

low-pitch tinnitus, low- evaluation.
frequency hearing loss, • Includes pure-tone air and
repeated episodes of vertigo. bone conduction, speech
audiometry, tympanometry,
and otoacoustic emissions.
• Typically reveals
sensorineural hearing
loss mainly in the low
frequencies, although other
configurations of hearing
losses may be present.
Vestibular schwannoma • Small acoustic tumours • MRI with gadolinium contrast

(acoustic neuroma) typically present as unilateral will show a tumour involving
high-frequency hearing loss the vestibulocochlear nerve
with difficulty hearing on the or eighth cranial nerve.
telephone in the affected ear.
DIAGNOSIS
Word discrimination score
is greatly reduced when
compared with pure-tone air
and bone conduction testing
(phonemic regression);
rollover phenomenon,
absent or elevated acoustic
reflexes, abnormal findings
on stapedial reflex decay,
and abnormal auditory
brainstem response.
• Hearing tests may be
normal in patients with small
vestibular schwannomas.
Posterior fossa • Ataxia, negative Romberg's • Audiogram reveals

cerebrovascular accident test, dysarthria, dysphagia, sensorineural hearing loss.
hoarseness, facial • CT scan of head.
paralysis, facial numbness,
contralateral lower extremity
weakness.
15
Condition Differentiating signs / Differentiating tests

symptoms
Temporal bone fracture • Recent head trauma. • CT scan of head delineates
extent of fracture.
Inner ear malformations • Progressive hearing loss. • MRI or CT scan of head

reveals the malformation.
Possible findings include
atresia or malformation of
ossicular chain, abnormal
incus, or missing cura of the
stapes.
Multiple sclerosis • Symptoms are often • MRI head reveals

asymmetric and involve only demyelinating lesions.
one side of the body or one Sagittal fluid-attenuated
limb. inversion recovery (FLAIR)
• Mild dragging of the foot and images distinguish
spasticity are often present. demyelinating lesions from
non-specific white matter
changes.
Labyrinthine haemorrhage • Similar presentation to • MRI T1-weighted images

labyrinthitis. without contrast will show
intra-labyrinthine hyper-
intensity.
Temporal bone neoplasm • Retro-tympanic mass, facial • MRI or CT scan of head will
nerve paresis, lower cranial show tumour.
nerve deficits.
DIAGNOSIS
Labyrinthitis Management
Approach
Treatment is symptomatic and primarily involves the use of vestibular suppressants and anti-emetics. There
is no treatment for tinnitus. Long-term therapy typically involves the use of vestibular rehabilitation with
cessation of vestibular suppressants. Most acute episodes of labyrinthitis are short-lived and self-limited, and
patients can be treated on an outpatient basis. However, they should be advised to seek further medical care
if the symptoms do not improve or if they develop neurological symptoms (e.g., diplopia, slurred speech, gait
disturbances, or localised weakness or numbness).
Viral labyrinthitis
Viral infections are the most common cause of labyrinthitis.
Symptomatic control of vertigo, nausea, and vomiting
• Symptoms of acute vertigo episodes can be treated with vestibular suppressants and anti-emetics.
Much of the effect is from the sedating action of these drugs, and patients should be warned about
driving and operating equipment while being treated. Only one agent should be used at a time.
• Commonly used treatments include antihistamines with anticholinergic properties (e.g.,

promethazine, cyclizine, dimenhydrinate) and anti-emetics (e.g., prochlorperazine, metoclopramide,
ondansetron).[23] Metoclopramide should be used for up to 5 days only in order to minimise
the risk of neurological and other adverse effects. It is not recommended for this indication in
children.[24]
• Benzodiazepines have been used historically, but dependency and delayed vestibular
compensation are significant concerns with these agents. Meclozine, an antihistamine
with anticholinergic properties, has also been used historically, but is less effective than
benzodiazepines.
• The acute vertigo symptoms typically resolve over 72 hours.
• It is important to consider fluid and electrolyte imbalances, particularly if the patient has had
prolonged nausea and vomiting. Obtaining a basic metabolic panel before and after treatment, and
initiating intravenous hydration, may be necessary in these patients.
Sudden hearing loss
• For patients with sudden sensorineural hearing loss, a short course of oral corticosteroids is
considered the standard of care.[25] The use of oral corticosteroids in meningogenic hearing loss is
controversial.
HIV-associated labyrinthitis
• A variety of auditory and vestibular complaints including labyrinthitis have been reported in
patients with AIDS. The relative importance of the HIV infection itself as opposed to its associated
opportunistic infections requires further study.
MANAGEMENT
Bacterial labyrinthitis
This may follow otitis media (middle ear infection) or bacterial meningitis. In addition to treatments for
vertigo and possible nausea and vomiting, these patients require antibiotics.
17
Acute and chronic otitis media
• If there is evidence for otitis media, such as otalgia (ear pain) and an abnormal ear examination
suggesting fluid, redness, or pus behind the ear drum, without systemic signs of infection
(i.e., fever, chills), then topical antibiotics should be prescribed. Ear drops deliver antibiotic
concentrations several orders of magnitude above minimum inhibitory concentrations that are
obtained with culture and sensitivity testing.[26] For those with tympanic membrane perforation
and purulent otorrhoea, the ear should be cleaned before topical therapy. Oral antibiotics are not
typically indicated unless the patient has systemic signs of infection (i.e., fever, chills). Following a
series of acute otitis media infections, the patient may require myringotomy (surgical incision of the
ear drum) with pressure equalisation tube placement.
Bacterial meningitis
• If intracranial infection (e.g., meningitis) is suspected, prompt treatment with intravenous antibiotics
is indicated with topical antibiotic therapy if otorrhoea is present.
Autoimmune-associated labyrinthitis
Patients with autoimmune-associated labyrinthitis (e.g., Cogan's syndrome or Behcet's disease) may
respond to oral corticosteroids. In cases of corticosteroid non-responsiveness, the use of alternative
immunomodulators may stabilise or improve hearing and balance while avoiding the adverse effects of
taking long-term corticosteroids.[27]
Syphilitic labyrinthitis
Patients with positive syphilis serology should be treated with an appropriate course of antibiotics and
may warrant a thorough evaluation by an infectious disease specialist.[4]
Persistent vestibular symptoms

Patients with persistent vestibular symptoms after treatment may be candidates for vestibular
rehabilitation.[28] [29] This therapy uses physiotherapy and occupational therapy techniques to treat
vertigo and balance disorders.
One Cochrane review found moderate-to-strong evidence that vestibular rehabilitation is safe and
effective in unilateral peripheral vestibular dysfunction. This was based on a number of high‐quality
randomised controlled trials, although a quarter of the studies may have had some risk of bias due to non-
blinding of outcome assessors and selective reporting.[29]
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
Acute ( summary )
viral: non-HIV
1st vestibular suppressant/anti-emetic#
adjunct corticosteroid
bacterial: secondary to otitis media
1st treatment of underlying condition
plus vestibular suppressant/anti-emetic
bacterial: secondary to meningitis
bacterial: syphilitic
HIV-associated
autoimmune
Ongoing ( summary )
with persistent vestibular symptoms
post-treatment
1st vestibular rehabilitation
MANAGEMENT
19
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
Acute
viral: non-HIV
1st vestibular suppressant/anti-emetic#

Primary options
» promethazine: children ≥2 years of age:

0.25 to 1 mg/kg orally/intravenously every 4-6
hours when required, maximum 25 mg/dose;
adults: 12.5 to 25 mg orally/intravenously
every 4-6 hours when required
OR
» cyclizine: children 6-11 years of age: 25

mg orally every 6-8 hours when required,
maximum 75 mg/day; children ≥12 years of
age and adults: 50 mg orally every 4-6 hours
when required, maximum 200 mg/day
OR
» dimenhydrinate: children 2-5 years of age:

12.5 to 25 mg orally every 6-8 hours when
required, maximum 75 mg/day; children
6-11 years of age: 25-50 mg orally every 6-8
hours when required, maximum 150 mg/day;
children ≥12 years of age and adults: 50-100
mg every 4-6 hours when required, maximum
400 mg/day
OR
» prochlorperazine: children 2-12 years of

age and 9-13 kg: 2.5 mg orally every 12-24
hours when required, maximum 7.5 mg/day;
children 2-12 years of age and 14-17 kg: 2.5
maximum 10 mg/day; children 2-12 years
of age and 18-39 kg: 2.5 mg orally every 8
adults: 5-10 mg orally every 6-8 hours when
required, maximum 40 mg/day
OR
» metoclopramide: adults: 5-10 mg orally/

intravenously every 8 hours when required for
a maximum of 5 days, maximum 30 mg/day
MANAGEMENT
OR
» ondansetron: children and adults: consult

specialist for guidance on dose
21
Acute
» Symptoms of acute vertigo episodes can be
treated with vestibular suppressants and anti-
emetics. Much of the effect is from the sedating
action of these drugs, and patients should be
warned about driving and operating equipment
while being treated. Only one agent should be
used at a time.
» Commonly used treatments include

antihistamines with anticholinergic properties
(e.g., promethazine, cyclizine, dimenhydrinate)
and anti-emetics (e.g., prochlorperazine,
metoclopramide, ondansetron).[23]
Metoclopramide should be used for up to
5 days only in order to minimise the risk of
neurological and other adverse effects. It is not
recommended for this indication in children.[24]
» The acute vertigo symptoms typically resolve

over 72 hours.
» It is important to consider fluid and electrolyte

imbalances, particularly if the patient has had
prolonged nausea and vomiting. Obtaining
a basic metabolic panel before and after
treatment, and initiating intravenous hydration,
may be necessary in these patients.
adjunct corticosteroid
Treatment recommended for SOME patients in
selected patient group
Primary options
» prednisolone: children: 1 mg/kg/day orally;

adults: 60 mg/day orally
» For patients with sudden sensorineural hearing

loss, corticosteroids are considered the standard
of care.[25]
» Treatment course: 10 to 14 days with a 5-day

taper.
bacterial: secondary to otitis media
» If there is evidence for otitis media, such

as otalgia (ear pain) and an abnormal ear
examination suggesting fluid, redness, or pus
behind the ear drum, without systemic signs
of infection (i.e., fever, chills), then topical
MANAGEMENT
antibiotics should be prescribed.
» Ear drops deliver antibiotic concentrations

several orders of magnitude above minimum
inhibitory concentrations that are obtained with
culture and sensitivity testing.[26]
Acute
» For those with tympanic membrane perforation
and purulent otorrhoea, the ear should be
cleaned before topical therapy.
» Oral antibiotics are not typically indicated

unless the patient has systemic signs of infection
(i.e., fever, chills).
» Following a series of acute otitis media

infections, the patient may require myringotomy
(surgical incision of the ear drum) with pressure
equalisation tube placement.
» Please refer to our topic on Acute otitis media

for more information.
Treatment recommended for ALL patients in
Primary options

OR

OR

400 mg/day
OR

MANAGEMENT

23
Acute
OR

OR


used at a time.


over 72 hours.

bacterial: secondary to meningitis
» If intracranial infection (e.g., meningitis) is

suspected, prompt treatment with intravenous
antibiotics is indicated.
» Topical antibiotics are recommended if

otorrhoea is also present.
MANAGEMENT
» Please refer to our topic on Bacterial

meningitis for more information.
Acute
Primary options

OR

OR

400 mg/day
OR

OR

OR
MANAGEMENT


25
Acute
used at a time.


over 72 hours.

bacterial: syphilitic
» Patients with positive syphilis serology

should be treated with an appropriate course
of antibiotics and may warrant a thorough
evaluation by an infectious disease specialist.[4]
» Please refer to our topic on Syphilis infection

Primary options

OR

MANAGEMENT

OR
Acute

400 mg/day
OR

OR

OR


used at a time.

MANAGEMENT

over 72 hours.
27
Acute
HIV-associated
» Patients with HIV-associated labyrinthitis

should be referred to a physician with experience
in managing HIV patients.
» Please refer to our topic on HIV infection for

more information.
Primary options

OR

OR

400 mg/day
OR
MANAGEMENT

Acute
OR

OR


used at a time.


over 72 hours.

autoimmune
» Patients with autoimmune-associated

labyrinthitis (e.g., Cogan's syndrome or Behcet's
disease) may respond to oral corticosteroids.
MANAGEMENT
» In cases of corticosteroid non-responsiveness,

the use of alternative immunomodulators may
stabilise or improve hearing and balance while
avoiding the adverse effects of taking long-term
corticosteroids.
29
Acute
» Consult specialist for guidance on dose.
» Please refer to our topic on Behcet's syndrome

Primary options

OR

OR

400 mg/day
OR

OR
MANAGEMENT

OR
Acute


used at a time.


over 72 hours.

MANAGEMENT
31
Ongoing
with persistent vestibular symptoms
post-treatment
1st vestibular rehabilitation
» Physiotherapy and occupational therapy

techniques are used to treat vertigo and balance
disorders.[28] [29]
» One Cochrane review found moderate-to-

strong evidence that vestibular rehabilitation
is safe and effective in unilateral peripheral
vestibular dysfunction. This was based on a
number of high‐quality randomised controlled
trials, although a quarter of the studies may have
had some risk of bias due to non-blinding of
outcome assessors and selective reporting.[29]
» A simple home programme of vestibular

habituation head movement exercises reduces
symptoms of imbalance during stance and
gait.[29]
» One 2015 study has demonstrated that a

virtual reality-based vestibular rehabilitation
programme had equivalent outcomes but was
more enjoyable than conventional balance
exercises.[30]
MANAGEMENT
Emerging
Tumour necrosis factor-alpha inhibitors
Tumour necrosis factor (TNF)-alpha is a pro-inflammatory cytokine that increases the production of
prostaglandins, thromboxanes, and leukotrienes by activating phospholipase A2. These autocoids are
typically released by neutrophils, platelets, and endothelial cells. Data from an animal study suggest that
TNF-alpha is involved in meningitis-induced hearing loss and cochlear injury and is therefore a possible
target for future therapies in patients with labyrinthitis secondary to meningitis.[31]
Superoxide dismutase
Oxygen free radicals induced by the complement cascade play a critical role in the development of
hearing loss and labyrinthitis ossificans associated with meningitis. Hearing preservation and prevention of
labyrinthitis ossificans with intrathecal superoxide dismutase has been demonstrated in an animal model.[32]
Intra-tympanic corticosteroids
Traditionally corticosteroids have been given orally, but reports suggest that intra-labyrinthine
concentrations can be improved by intra-tympanic injections of the drugs. This mode of therapy is still under
investigation.[33]
Oral corticosteroids
There is some suggestion that oral corticosteroids can prevent hearing loss and labyrinthitis ossificans
in children with pneumococcal meningitis.[34] However, further studies are required to define their role in
preventing hearing loss in these patients.
Patient discussions
Patients should be advised to increase their fluid intake to prevent dehydration. [Labyrinthitis.org.uk]
(http://www.labyrinthitis.org.uk) [NHS Choices: labyrinthitis and vestibular neuritis] (http://
www.nhs.uk/conditions/labyrinthitis) Anti-emetics are often helpful in decreasing the nausea
associated with labyrinthitis. [Better Health Channel: labyrinthitis and vestibular neuritis] (https://
www.betterhealth.vic.gov.au/health/conditionsandtreatments/labyrinthitis-and-vestibular-neuritis)
MANAGEMENT
33
Labyrinthitis Follow up
Monitoring
Monitoring
FOLLOW UP
Viral labyrinthitis may warrant further follow-up if additional episodes of vertigo occur. Patients with
labyrinthitis secondary to meningitis should be followed closely with audiometric and imaging studies
to examine evidence of progressive hearing loss and signs of cochlear obstruction. The presence of
cochlear obstruction on magnetic resonance imaging may warrant expedited cochlear implantation in the
setting of bilateral severe to profound hearing loss.[35] Patients with bacterial meningitis who demonstrate
otic capsule enhancement on gadolinium MRI should have their hearing assessed urgently as they are at
significant risk of developing sensorineural hearing loss.[20]
Complications
Complications Timeframe Likelihood
FOLLOW UP
delayed endolymphatic hydrops short term low
Additional episodes of vertigo often signal the development of delayed endolymphatic hydrops. Typically
occurs months to years after the labyrinthitis episode. Patients experience room-spinning vertigo,
fluctuating hearing, fullness, or tinnitus.
mastoiditis short term low
Occurs rarely. May arise when a bacterial otitis media extends into the mastoid air cells that are contiguous
with the middle ear.
Usually, mastoiditis responds well to parenteral antibiotics. However, some patients may require a
mastoidectomy with tympanoplasty to eradicate all infection and cholesteatoma.
cholesteatoma short term low
If cholesteatoma invades the membranous labyrinth, a labyrinthectomy may be necessary to eradicate the
disease process.[2]
cochlear ossification long term medium
Only occurs in patients with suppurative labyrinthitis after meningitis or otitis media.
Cochlear ossification (labyrinthitis ossificans) has significant implications with respect to the placement of
a cochlear implant if both cochleae are affected.[7] [9] [35] [36] [37]
hearing loss long term medium
Patients with mild to severe hearing loss may benefit from amplification with a hearing aid provided their
speech discrimination is in a serviceable range.
In patients with profound hearing loss a contralateral routing of signals (CROS) hearing aid, Trans-ear
hearing aid, or bone-anchored hearing aid (BAHA) helps with the head-shadow effect.[38]
Deafness only occurs after bilateral labyrinthitis or if the non-affected ear had previous significant hearing
loss.
Bilateral labyrinthitis is more common after bacterial meningitis.
bilateral vestibular hypo-function long term medium
Most commonly associated with bilateral labyrinthitis secondary to bacterial meningitis.
May require the patient to use a cane or walker if other balance risk factors are present.
35
Prognosis
FOLLOW UP
If the patient has no serious neurological sequelae, the prognosis for acute labyrinthitis is generally good.
Patients with other neurological complications from bacterial meningitis such as hydrocephalus or stroke may
require additional therapy such as a ventriculoperitoneal shunt or physiotherapy and occupational therapy.
Patients with cerebral infarcts in critical areas are often left with significant disabilities.
Vestibular compensation
After injury to the inner ear, the brain undergoes a complex set of changes that allow it to adapt to the altered
sensory input and abolish the perception of vertigo. This process is called vestibular compensation. Some
patients may experience problems with incomplete vestibular compensation and so continue to experience
vertigo. This can often be alleviated by a course of vestibular rehabilitation therapy,[29] eliminating the
vestibular suppressants, and increasing daily activities.
Hearing loss
The hearing loss that occurs with suppurative labyrinthitis is typically irreversible. Treatment with
corticosteroids may decrease inflammation and potentially preserve some hearing. Corticosteroids also
decrease the inflammatory response within the cochlea, thus decreasing fibrosis and ossification, which can
make cochlear implantation more challenging in the setting of bilateral suppurative labyrinthitis. Patients with
serous labyrinthitis often recover their hearing. Hearing loss can be permanent in up to 20% of children with
meningitis.
Tinnitus
The type associated with sensorineural hearing loss typically gets less noticeable with time. However,
patients with persistent tinnitus can develop a reactive depression. These patients may benefit from
antidepressant therapy (selective serotonin-reuptake inhibitors), tinnitus re-training, biofeedback, tinnitus
maskers, and amplification with a hearing aid.
Labyrinthitis Guidelines
Diagnostic guidelines
Europe
Hearing loss in adults: assessment and management (ht tps://

www.nice.org.uk/guidance/ng98)
Published by: National Institute for Health and Care Excellence Last published: 2018
North America
Clinical practice guideline: sudden hearing loss (update) (ht tps://

www.entnet.org/content/clinical-practice-guidelines)
Published by: American Academy of Otolaryngology-Head and Neck Last published: 2019
Surgery
GUIDELINES
ACR Appropriateness Criteria: hearing loss and/or vertigo (ht tp://www.acr.org/
Quality-Safety/Appropriateness-Criteria)
Published by: American College of Radiology Last published: 2018
Treatment guidelines
Europe
Hearing loss in adults: assessment and management (ht tps://

www.nice.org.uk/guidance/ng98)
Published by: National Institute for Health and Care Excellence Last published: 2018
North America
Clinical practice guideline: sudden hearing loss (update) (ht tps://

www.entnet.org/content/clinical-practice-guidelines)
Published by: American Academy of Otolaryngology-Head and Neck Last published: 2019
Surgery
37
Labyrinthitis Online resources
Online resources
1. Labyrinthitis.org.uk (http://www.labyrinthitis.org.uk) (external link)
2. NHS Choices: labyrinthitis and vestibular neuritis (http://www.nhs.uk/conditions/labyrinthitis) (external

link)
3. Better Health Channel: labyrinthitis and vestibular neuritis (https://www.betterhealth.vic.gov.au/health/

conditionsandtreatments/labyrinthitis-and-vestibular-neuritis) (external link)
ONLINE RESOURCES
Labyrinthitis References
Key articles
• Lindeman RC. Acute labyrinthine disorders. Otolaryngol Clin North Am. 1979 May;12(2):375-87.
REFERENCES
Abstract (http://www.ncbi.nlm.nih.gov/pubmed/460880?tool=bestpractice.bmj.com)
• Goldstein NA, Casselbrant ML, Bluestone CD, et al. Intratemporal complications of acute otitis media
in infants and children. Otolaryngol Head Neck Surg. 1998 Nov;119(5):444-54. Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/9807067?tool=bestpractice.bmj.com)
• Davis LE, Johnsson LG. Viral infections of the inner ear: clinical, virologic, and pathologic
studies in humans and animals. Am J Otolaryngol. 1983 Sep-Oct;4(5):347-62. Abstract (http://
• Ryan AF, Harris JP, Keithley EM. Immune-mediated hearing loss: basic mechanisms and options
for therapy. Acta Otolaryngol Suppl. 2002;(548):38-43. Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/12211356?tool=bestpractice.bmj.com)
• Aminpour S, Tinling SP, Brodie HA. Role of tumor necrosis factor-alpha in sensorineural hearing loss
after bacterial meningitis. Otol Neurotol. 2005 Jul;26(4):602-9. Abstract (http://www.ncbi.nlm.nih.gov/
References
1. Lindeman RC. Acute labyrinthine disorders. Otolaryngol Clin North Am. 1979 May;12(2):375-87.
2. Kangsanarak J, Fooanant S, Ruckphaopunt K, et al. Extracranial and intracranial complications of

suppurative otitis media: report of 102 cases. J Laryngol Otol. 1993 Nov;107(11):999-1004. Abstract
(http://www.ncbi.nlm.nih.gov/pubmed/8288994?tool=bestpractice.bmj.com)
3. Goldstein NA, Casselbrant ML, Bluestone CD, et al. Intratemporal complications of acute otitis media
in infants and children. Otolaryngol Head Neck Surg. 1998 Nov;119(5):444-54. Abstract (http://
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1995 Aug;109(8):719-25. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/7561492?
tool=bestpractice.bmj.com)
5. Davis LE, Johnsson LG. Viral infections of the inner ear: clinical, virologic, and pathologic
studies in humans and animals. Am J Otolaryngol. 1983 Sep-Oct;4(5):347-62. Abstract (http://
6. Merchant SN, Gopen Q. A human temporal bone study of acute bacterial meningogenic labyrinthitis.
Am J Otol. 1996 May;17(3):375-85. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/8817013?
39
7. Isaacson B, Roland PS, Wright CG. Anatomy of the middle-turn cochleostomy. Laryngoscope.
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Laryngol. 1991 Sep;100(9 Pt 1):712-6. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/1952661?
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10. Kenna M. Incidence and prevalence of complications of otitis media. Ann Otol Rhinol Laryngol Suppl.
1990;149:38-9.
11. Nadol JB Jr. Hearing loss as a sequela of meningitis. Laryngoscope. 1978 May;88(5):739-55. Abstract
12. Petri M, Chirilă M, Bolboacă SD, et al. Health-related quality of life and disability in patients with acute
unilateral peripheral vestibular disorders. Braz J Otorhinolaryngol. 2017 Nov-Dec;83(6):611-8. Full text
(https://www.sciencedirect.com/science/article/pii/S1808869416301677?via%3Dihub) Abstract (http://
13. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome:
three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted
imaging. Stroke. 2009 Nov;40(11):3504-10. Full text (https://www.ahajournals.org/doi/full/10.1161/
STROKEAHA.109.551234?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub+
+0pubmed&) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/19762709?tool=bestpractice.bmj.com)
14. Edlow JA. Diagnosing patients with acute-onset persistent dizziness. Ann Emerg Med. 2018
May;71(5):625-31. Full text (https://www.annemergmed.com/article/S0196-0644(17)31795-X/fulltext)
15. Grasland A, Pouchot J, Hachulla E, et al. Typical and atypical Cogan's syndrome: 32 cases
and review of the literature. Rheumatology (Oxford). 2004 Aug;43(8):1007-15. Full text (http://
rheumatology.oxfordjournals.org/cgi/content/full/43/8/1007) Abstract (http://www.ncbi.nlm.nih.gov/
16. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 guidelines for the early management
of patients with acute ischemic stroke: a guideline for healthcare professionals from the
American Heart Association/American Stroke Association. Stroke. 2018 Mar;49(3):e46-110.
Full text (https://www.ahajournals.org/doi/full/10.1161/STR.0000000000000158?
url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed) Abstract (http://
17. Shetty VS, Reis MN, Aulino JM, et al. ACR Appropriateness Criteria head trauma. J Am Coll
Radiol. 2016 Jun;13(6):668-79. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/27262056?
REFERENCES
18. Weinreich HM, Carey JP. Perilymphatic fistulas and superior semi-circular canal dehiscence
syndrome. Adv Otorhinolaryngol. 2019;82:93-100. Abstract (http://www.ncbi.nlm.nih.gov/
19. American College of Radiology. Hearing loss and/or vertigo. 2018 [internet publication]. Full text
(https://acsearch.acr.org/docs/69488/Narrative/)
20. Kopelovich JC, Germiller JA, Laury AM, et al. Early prediction of postmeningitic hearing loss
in children using magnetic resonance imaging. Arch Otolaryngol Head Neck Surg. 2011
May;137(5):441-7. Full text (http://archotol.jamanetwork.com/article.aspx?articleid=716277) Abstract
21. Weinreich HM, Carey JP. Perilymphatic fistulas and superior semi-circular canal dehiscence
syndrome. Adv Otorhinolaryngol. 2019;82:93-100. Abstract (http://www.ncbi.nlm.nih.gov/
22. Fife TD, Colebatch JG, Kerber KA, et al. Practice guideline: cervical and ocular vestibular evoked
myogenic potential testing: report of the Guideline Development, Dissemination, and Implementation
Subcommittee of the American Academy of Neurology. Neurology. 2017 Nov 28;89(22):2288-96.
Full text (https://n.neurology.org/content/89/22/2288.long) Abstract (http://www.ncbi.nlm.nih.gov/
23. Soto E, Vega R. Neuropharmacology of vestibular system disorders. Curr Neuropharmacol. 2010
Mar;8(1):26-40. Full text (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866460/) Abstract (http://
24. European Medicines Agency. European Medicines Agency recommends changes to the use of
metoclopramide. July 2013 [internet publication]. Full text (http://www.ema.europa.eu/ema/index.jsp?
curl=pages/news_and_events/news/2013/07/news_detail_001854.jsp&mid=WC0b01ac058004d5c1)
25. Chandrasekhar SS, Tsai Do BS, Schwartz SR, et al. Clinical practice guideline: sudden hearing
loss (update). Otolaryngol Head Neck Surg. 2019 Aug;161(suppl 1):S1-45. Full text (https://
journals.sagepub.com/doi/full/10.1177/0194599819859885?url_ver=Z39.88-2003&rfr_id=ori
%3Arid%3Acrossref.org&rfr_dat=cr_pub++0pubmed) Abstract (http://www.ncbi.nlm.nih.gov/
26. Hannley MT, Denneny JC 3rd, Holzer SS. Use of ototopical antibiotics in treating 3 common
ear diseases. Otolaryngol Head Neck Surg. 2000 Jun;122(6):934-40. Abstract (http://
27. Ryan AF, Harris JP, Keithley EM. Immune-mediated hearing loss: basic mechanisms and options
for therapy. Acta Otolaryngol Suppl. 2002;(548):38-43. Abstract (http://www.ncbi.nlm.nih.gov/
41
28. Cohen HS, Kimball KT. Decreased ataxia and improved balance after vestibular rehabilitation.
Otolaryngol Head Neck Surg. 2004 Apr;130(4):418-25. Abstract (http://www.ncbi.nlm.nih.gov/
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29. McDonnell MN, Hillier SL. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction.
Cochrane Database Syst Rev. 2015 Jan 13;(1):CD005397. Full text (http://onlinelibrary.wiley.com/
doi/10.1002/14651858.CD005397.pub4/full) Abstract (http://www.ncbi.nlm.nih.gov/
30. Meldrum D, Herdman S, Vance R, et al. Effectiveness of conventional versus virtual reality-based
balance exercises in vestibular rehabilitation for unilateral peripheral vestibular loss: results of a
randomized controlled trial. Arch Phys Med Rehabil. 2015 Jul;96(7):1319-28;e1. Abstract (http://
31. Aminpour S, Tinling SP, Brodie HA. Role of tumor necrosis factor-alpha in sensorineural hearing loss
after bacterial meningitis. Otol Neurotol. 2005 Jul;26(4):602-9. Abstract (http://www.ncbi.nlm.nih.gov/
32. Ge NN, Brodie HA, Tinling SP. Long-term hearing loss in gerbils with bacterial meningitis treated with
superoxide dismutase. Otol Neurotol. 2008 Dec;29(8):1061-7. Abstract (http://www.ncbi.nlm.nih.gov/
33. Battaglia A, Burchette R, Cueva R. Combination therapy (intratympanic dexamethasone + high-

dose prednisone taper) for the treatment of idiopathic sudden sensorineural hearing loss. Otol
Neurotol. 2008 Jun;29(4):453-60. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18401285?
34. Hartnick CJ, Kim HH, Chute PM, et al. Preventing labyrinthitis ossificans: the role of steroids.
Arch Otolaryngol Head Neck Surg. 2001 Feb;127(2):180-3. Full text (http://archotol.ama-
assn.org/cgi/content/full/127/2/180) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/11177035?
35. Aschendorff A, Klenzner T, Laszig R. Deafness after bacterial meningitis: an emergency for early
imaging and cochlear implant surgery. Otolaryngol Head Neck Surg. 2005 Dec;133(6):995-6. Abstract
36. El-Kashlan HK, Ashbaugh C, Zwolan T, et al. Cochlear implantation in prelingually deaf children with
ossified cochleae. Otol Neurotol. 2003 Jul;24(4):596-600. Abstract (http://www.ncbi.nlm.nih.gov/
37. Kutz JW, Simon LM, Chennupati SK, et al. Clinical predictors for hearing loss in children with bacterial
meningitis. Arch Otolaryngol Head Neck Surg. 2006 Sep;132(9):941-5. Full text (https://archotol.ama-
assn.org/cgi/content/full/132/9/941) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/16982970?
38. House JW, Kutz JW Jr. Bone-anchored hearing aids: incidence and management of postoperative
complications. Otol Neurotol. 2007 Feb;28(2):213-7. Abstract (http://www.ncbi.nlm.nih.gov/
Labyrinthitis Disclaimer
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Labyrinthitis Disclaimer
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Contributors:
// Authors:
Brandon Isaacson, MD, FACS

Professor
Department of Otolaryngology-Head & Neck Surgery, University of Texas Southwestern Medical Center,
Dallas, TX
DISCLOSURES: BI is an author of a reference cited in this topic.
// Peer Reviewers:
Marc Bennet t, MD
Associate Professor
The Otology Group of Vanderbilt, Nashville, TN
DISCLOSURES: MB declares that he has no competing interests.
Joni K. Doherty, MD, PhD

Assistant Professor
Neurotology Otolaryngology-Head & Neck Surgery, USC Keck School of Medicine, San Diego, CA
DISCLOSURES: JKD declares that she has no competing interests.
Iain Swan, MD, FRCS

Senior Lecturer in Otolaryngology
Honorary Consultant Otolaryngologist, Glasgow Royal Infirmary, Glasgow, UK
DISCLOSURES: IS declares that he has no competing interests.

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Labyrinthitis

Straight to the point of care

Last updated: Jul 30, 2020

Typical presentation includes vertigo, imbalance, and hearing loss.

Diagnosis is supported by history, physical examination, and audiometry.

• Caused by inflammation of the labyrinth only

• Follows direct bacterial invasion of the inner ear

Important questions that are critical in establishing the diagnosis include:

• Describe your dizziness (e.g., room spinning, imbalance, floating, lightheaded)

• there is a central pattern of nystagmus

• there is skew deviation

• there is a negative head impulse test (in patients with nystagmus)

• the patient is unable to sit or walk unaided.

History and exam

nausea and vomiting (common)

hearing loss (common)

Other diagnostic factors

vertigo-related quick head or body movements (common)

influenza-like symptoms (common)

chronic suppurative otitis media

acute otitis media

inner ear malformations

Other tests to consider

Condition Differentiating signs / Differentiating tests

Benign parox ysmal • Similar presentation to • Normal audiogram.

Meniere's disease • Fluctuating hearing loss, • Complete audiological

Vestibular schwannoma • Small acoustic tumours • MRI with gadolinium contrast

Posterior fossa • Ataxia, negative Romberg's • Audiogram reveals

Condition Differentiating signs / Differentiating tests

Inner ear malformations • Progressive hearing loss. • MRI or CT scan of head

Multiple sclerosis • Symptoms are often • MRI head reveals

Labyrinthine haemorrhage • Similar presentation to • MRI T1-weighted images

Symptomatic control of vertigo, nausea, and vomiting

• Commonly used treatments include antihistamines with anticholinergic properties (e.g.,

• The acute vertigo symptoms typically resolve over 72 hours.

Persistent vestibular symptoms

Treatment algorithm overview

1st vestibular suppressant/anti-emetic#

bacterial: secondary to otitis media

1st treatment of underlying condition

plus vestibular suppressant/anti-emetic

bacterial: secondary to meningitis

1st treatment of underlying condition

plus vestibular suppressant/anti-emetic

1st treatment of underlying condition

plus vestibular suppressant/anti-emetic

1st treatment of underlying condition

plus vestibular suppressant/anti-emetic

1st treatment of underlying condition

plus vestibular suppressant/anti-emetic

1st vestibular rehabilitation

1st vestibular suppressant/anti-emetic#

» promethazine: children ≥2 years of age:

» cyclizine: children 6-11 years of age: 25

» dimenhydrinate: children 2-5 years of age:

» prochlorperazine: children 2-12 years of

» metoclopramide: adults: 5-10 mg orally/

» ondansetron: children and adults: consult

» Commonly used treatments include

» The acute vertigo symptoms typically resolve

» It is important to consider fluid and electrolyte

» prednisolone: children: 1 mg/kg/day orally;

» For patients with sudden sensorineural hearing

» Treatment course: 10 to 14 days with a 5-day