Clinical
The pathophysiology
of labyrinthitis
Joanne Mildenhall is a Paramedic, Newbury Ambulance Station, South Central Ambulance Service NHS Trust.
Email for correspondance: jo.mildenhall@scas.nhs.uk
T he labyrinth (or inner ear) houses the
delicate membranous structures necessary for
hearing and balance. They are protectively
positioned deep within the temporal bones of the
head, behind the eyes. Within the network of inter-
connecting passages of the labyrinth lies an area
named the vestibule, which contains the sensory
organs; the oval and round windows, the cochlea,
and the three semi-circular canals.
The oval and round windows are openings
located on the wall of the inner ear through which
sound vibrations are conducted to the cochlea.
The cochlea is a small coiled, hollow tube that
contains the specialized Organ of Corti—necessary
for converting sound vibrations into electrical
stimulation. The semi-circular canals have no
auditory function, however, their function is to
provide sensory information on balance and the
position of the head.
All the structures mentioned contain within
them, perilymph (a fluid similar in composition
to cerebrospinal fluid). Furthermore, bathing
the outside of these structures is a fluid called
endolymph, which is comparable to an intracellular
fluid abundant in potassium. Both fluids play
a fundamental role in the resonation of sound
vibrations necessary for the sense of hearing, and
respond to gravitational forces exerted during
body movement to provide sensory information on
balance and position.
Communication between the labyrinthine
structures and the brain/subarachnoid space
occurs via the internal auditory canal, the
cochlea aqueduct and the cochlea nerve, which
subsequently forms the vestibulocochlear nerve
(cranial nerve VIII). This nerve transmits electrical
impulses to the cochlea nuclei in the pons (Kumar
and Clark, 2005).
Labyrinthitis is, according to research, generally
defined as an inflammatory response within the
membranous inner ear structures in response
to infections, an inner ear infection (Swartz and
Longwell, 2005; Boston et al, 2008). The causes
of infection may be attributable to bacterial, viral,
Journal of Paramedic Practice • Vol 2 No 7
Abstract
Labyrinthitis is an inflammatory response within the membranous inner ear
structures in response to infection. It is a generally short-lived minor illness that
has the potential to cause temporary or permanent disablement in terms of
hearing loss. Other symptoms include nausea and vomiting, pain in the affected
ear, vertigo, and fever. Subsequently, it is an illness commonly diagnosed by
health care practitioners working in the community setting. Understanding the
pathophysiological development and the inflammatory and immune response to
such an illness enables the clinician to comprehend the underlying processes of
the presenting signs and symptoms, and to treat accordingly.
Key words
l Ears l Otological disease l Labyrinth l Labyrinthitis l Minor illness
Accepted for publication 4 June 2010
protozoal or fungal insult from localized or systemic
origin. Regardless of specific cause, the symptoms
of labyrinthitis include:
llPain in the affected ear (otalgia)
llVertigo
llHearing loss (which may be unilateral or bilateral,
and mild or profound)
llTinnitus
llDischarge from the ear (otorrhoea)
llFever.
It is an illness commonly seen within general
practice and walk-in centres ( Jayarajan and
Rajenderkumar, 2003; Rouke et al, 2009). Therefore,
it is likely to be encountered by healthcare/
ambulance practitioners working in the community.
Both viral and bacterial causes of labyrinthitis
are relatively common in comparison to fungal
infection. The mechanisms of viral and bacterial
labyrinthitis are distinct, so this article will discuss
them separately.
Bacterial infection
Studies have identified that bacterial aetiology of
labyrinthitis is normally secondary to a previously
acquired infection such as sinusitis or meningitis
(Goebel, 2008). In particular, research studies of
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Clinical
Table 1. Plasma derived mediations of
inflammation
Kinins e.g. bradykinin Causes increased capillary permeability and pain
Complement Causes vasodilation and increased vascular Labyrinthitis may also occur following the
permeability, promotes leukocyte activation,
adhesion and chemotaxis, and activates meningitis from the brain into the labyrinth via the
phagocytosis.
Figure 1. The labyrinth (or inner ear) houses the delicate
membranous structures necessary for hearing and balance.
humans and animals have identified bacterial otitis
media (middle ear infection/ inflammation) as a
significantly influential factor in the development of
labyrinthitis pathophysiology (Goebel, 2008).
Primarily, a build-up of infective discharge
reaches a small chamber that is in direct contact
with the round window (Cureoglu et al, 2005).
This precipitate consists of toxins (Yukiko, 2005),
enzymes and inflammatory chemicals that form
exudate/pus, and will eventually leave the ear as
suppurative otorrhoea. Within this small chamber
is a potential space: the perilymphatic space,
containing the fluid perilymph. Proliferation of the
discharge subsequently extends to the potassium
rich endolymph within the membranous labyrinth.
The interference of the homeostatic environment
of the perilymphatic and endolymphatic fluids
within the labyrinth by bacterial toxins and
inflammatory mediators causes irritation, and also
triggers an inflammatory response. This produces
an inflammatory response within the cochlea
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(Gopen et al, 2006; Keithley et al, 2008), and
has the ability to cause morphological alteration
and dysfunction of sensory cells, resulting in an
irreversible hearing loss (Hughes and Pensak,
2008).
spread of pneumococcai associated with bacterial
internal auditory canal, cochlear aqueduct (which
contains a small amount of dura-mater, creating a
direct link between the perilymphatic space and
the subarachnoid space) or from destruction of the
blood-labyrinthine barrier (similar to the blood-brain
barrier) (Tarlow, 1998; Lee, 2002). Subsequently,
passage of endotoxins and chemical mediators
(Klein et al, 2008) into this delicate area obliterates
cochlea hair cells (stereocilia) within the Organ of
Corti, which are involved in the transmission of
sound vibrations to the vestibulocochlear nerve
(Allen, 2006). In conjunction with spiral ganglion
neuronal cell death situated just prior to the start of
the cochlea nerve, irreversible hearing loss occurs
(Son et al, 2008).
Viral infection
Viral insult, on the other hand, is the most common
pathogenic factor of human labyrinthitis (Swartz
and Longwell, 2005). It is frequently associated as a
complication of influenza, colds, upper respiratory
tract infections or viral otitis media (Vergisen, 2008).
Replication of viruses (protein-coated nucleic
acids) occurs by the hijacking of host cells and
stimulating ribosomal protein synthesis (Marieb,
1998; Underwood, 2004; Mattson-Porth, 2007).
Pathogenically, it is still not known exactly how
the causal relationship between the virus and
labyrinthitis occurs, however, there is evidence
to support congenital transmission in utero
from rubella and cytomegalovirus (Katano et
al, 2007; Cheeran et al, 2009) or transmission as
a characteristic of systemic viral illness such as
influenza, human immunodeficiency virus (Teggi et
al, 2008) or mumps, for example.
In the case of mumps, histopathological
research (Katsuhiko et al, 1988; Guyot, 1999) has
identified haematogenical spread in the form of
a viraemia, producing an infection of the stria
vascularis (external wall of the cochlea duct which
is highly vascularised and secretes endolymph).
This alters the chemical composition and volume
of endolymph, causing irritation as in serous
labyrinthitis. Subsequently, a mild to moderate
unilateral or bilateral hearing loss is experienced
(Merchant et al, 2008). Sudden vertigo also prevails
and is often incapacitating.
Immune/inflammatory response
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 Clinical

Table 2. Cell derived mediators of inflammation

Histamine A chemical that causes dilation of arterioles and increases the permeability of venules
leading to inflammation and swelling

Arachidonic acid Arachidonic acid is a fatty acid which causes synthesis of prostaglandins via the cyclo-oxygenase pathway, and synthesis of
leukotrienes via the lipoxygenase pathway
Platelet activating Cause platelet aggregation and primes and enhances the functions of neutrophils and factors monocytes, and is a potent
eosinophil attractor. Is also a potent vasodilator of the capillaries at the site of the inflammation
Cytokines Proteins (such as interferon) which cause a variety of effects including activation of T, B and proteins
natural killer cells. Induces fever and stimulates neutrophil production. Induces the inflammatory response
Interleukin 2 A cytokine derived from white blood cells (leukocytes)
Nitrous oxide A messenger molecule that relaxes smooth muscles, reduces platelet aggregation and adhesion, kills microbes via
phagocytic cells
Prostaglandin A fatty acid made in the body that has several functions including causing inflammation in areas of damaged tissue.

Mattson-Porth (2007) and Marieb (1998)

The immunological/inflammatory response is and scala tympani.

initiated subsequent to bacterial or viral pathogenic
invasion of the inner ear; beyond the round and/
or oval windows, and following destruction of the
epithelial membrane of the endolymphatic sac.
This annihilation stimulates the release of chemical
mediators, a collection of substances which are the
precursors of the inflammatory and immune system
response. They are derived from plasma (such as
kinins) (Table 1) or cells (such as lymphocytes)
(Table 2). Cellular mediators, such as histamine, are
located in granule form in mast cells and basophils
and have the effect of capillary vasodilation.
Others such as prostaglandins and cytokines are
synthesized when stimulated, and have similar
effects to histamine (Marieb, 1998).
Following this activation, a cell-mediated response
of phagocytic macrophages and neutrophils are
gathered into the area of the micro-organisms from
the lumen of the endolymphatic sac, perisaccular
tissue and scala tympani of the inner ear. Bi-
products of this phagocytic process include cell
debris and nitrous oxide. While the cell debris
contributes to the development of a suppurative/
purulent, serous or haemorrhagic exudate, little is
currently known about the role of nitrous oxide in
the immune/inflammatory response. However, it
is thought to play a role in destroying pathogens
(Mattson-Porth, 2007) and relaxes the smooth
muscles of the local vasculature. This has the
effect of vasodilation. This effect is undertaken
in conjunction with the release of synthesized
polypeptide cytokines such as histamine from mast
cells, platelets, basophils, leukocytes and helper T
cells from the endolymphatic sac, perisaccular tissue
Cytokines also increase the permeability of
blood vessels and the cell walls of local structures
(Underwood, 2004) by inducing fenestrations
between their cells. This draws fluids and plasma
(white blood cells, complement proteins and
inflammatory mediators) into the extra-cellular
spaces. This occurs due to chemical toxins which
are produced when the wall of the structure/
blood vessels are damaged. Subsequently, an
impairment of the sodium—potassium pump
creates an environment whereby sodium moves
into damaged cells, causing an increased osmotic
pressure; drawing the intracellular fluids out into the
extracellular space (Sanders, 2001). This damage is
also sufficient to activate the immune—inflammatory
cascade. While the presence of exudate gives rise
to localized swelling, morphological changes of the
mutilated cells also give a swollen appearance.
The patient with labyrinthitis is likely to experience
pain (otalgia), which may be attributable to an
increase in pressure within the ear due to the amount
of exudate produced. Furthermore, otoscopic
examination may identify a burst ear-drum (tympanic
membrane), which is a symptom of a middle-ear
infection.
Vasodilation also occurs following activation of
the complement system. Stimulated by the initial
release of macrophages and their phagocytic
action and bacterial proliferation, a collection of
twenty chemotactic protein factors, present within
the blood, act as a cascade reaction via the C3a
pathway to contribute to the destruction of invading
pathogens via cell lysis and phagocytosis (Marieb,
1998).

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Table 3. Glossary of terms

Term Meaning
Bony labyrinth A series of channels running through the bones. Contains the vestibule, cochlea and semi-circular canals
Cochlea A spiral chamber arising from the front of the vestibule. It contains the Organ of Corti
Cochlea aqueduct A cavity within the cochlea that contains endolymph
Endolymph A fluid inside the organs of the labyrinth, which is like intracellular fluid and contains high levels
of potassium and low levels of sodium
Labyrinth The inner ear, which lies deep in the head behind the eyes. It contains all the delicate structures
necessary for receiving information about hearing and balance which is then relayed to the brain
via the cochlear and subsequently the vestibulocochlear nerves
Labyrinthitis An infection of the inner ear, which may be caused by bacteria, viruses and fungus amongst others. It is a
relatively common minor illness which is normally short-lived however, it has the ability to cause temporary
or permanent hearing loss should certain areas of the labyrinth be affected
Membranous labyrinth An area of ducts and membranous sacs contained within the area of the bony labyrinth
Organ of Corti The main receptor organ for auditory vibrations. It is housed within the cochlea. This organ contains millions
of tiny, sensitive hairs called stereocilia which pick up auditory information/ vibrations
Otitis media An infection/ inflammation of the middle ear. Is often resultant of a sore throat or cold. It is very common in
children and is recognized by earache and sometimes hearing loss
Oval window The oval window is a membrane-covered opening that leads from the middle ear to the inner ear
Perilymph A fluid within the bony labyrinth which is like cerebrospinal fluid. Its main role is to enhance the conduction
of noise vibrations
Perilymphatic space The area in which perilymph is contained
Perisaccular tissue Tissue around a group of sensory cells that collect neurosensory information about balance/ head
positioning from the semi-circular canals. This information is then transmitted to the Pons in the brain via
the 8th cranial nerve.
Round window Also known as the cochlea window. It opens into the cochlea of the inner ear from the middle ear. This
window sits below and behind the oval window. The round window membrane can move, which allows
movement of endolymph within the cochlea. This subsequently causes movement of the stereocilia and thus
enables hearing
Scala tympani A cavity within the cochlea. It sits below the cochlear aqueduct and ends at the round window. It forms
part of the bony labyrinth and contains perilymph
Semi-circular canals There are 3 semi-circular canals (anterior, posterior, and lateral) and each are involved in gathering and
feeding information to the brain about movement of the head/ balance.
Spiral ganglion This is the tip of the cochlea nerve which picks up information from the stereocilia within the Organ
of Corti
Stereocilia Small hair-like projections emanating from hair cells within the Organ of Corti. They pick up vibrations/
auditory information which is then passed on to the spiral ganglion prior to the cochlea nerve
Vestibule The centre part of the bony labyrinth, and contained within is perilymphatic fluid. The vestibule is situated
behind the cochlea but in front of the semi-circular canals. Its side wall contains the oval window.

The release of exudate increases the
inflammatory response and initiates the migration
of immune system cells into the area. The
continued activation of cytokines stimulates
a different type of cytokine, interleukin-2 (IL-
2), to travel from the endolymphatic sac to
physiologically alter the endothelial cells of the
spiral modiolar vein of the inner ear (Berrocal and
Ramirez-Camacho, 2002), allowing more immune
system cells to diffuse from the circulation into the

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affected area. It also acts chemotactically to draw
these cells into the perilymph. Interestingly, studies
have recently identified that IL-2 is only detected
in perilymph if stimulating pathogenic conditions
are present (Hughes and Pensak, 2008; Luxon et al,
2003). Therefore, this seems to be a physiological
indicator of the presence of labyrinth infection.
However, realistically, this information appears
to be of no clinical benefit at the current time, as
perilymph is not a fluid which is accessible for
laboratory testing due to its anatomical location,
deep within the temporal bones of the head.
Temperature
Pyrogenic (heat/fever producing) cytokines such
as interleukin-1 (IL-1) and tumour necrosing
factor alpha (TNF α) are distributed within the
systemic circulation and act directly upon the
thermoregulatory centre in the hypothalamus. This
acts upon arachidonic acid, and converts it into
prostaglandin (PG) E2 via the cyclo-oxygenase
pathway (Underwood, 2004; Guyton and Hall,
2006). This chemical not only induces inflammation
and exacerbates the effects of histamine and other
inflammatory mediators, but also displaces the
body’s thermostat to a higher temperature; having
the systemic effect of initiating heat producing
physiological mechanisms such as mild tachycardia
and tachypnoea, and activation of hepatic processes
(Marieb, 1998).
Similarly, heat conserving behaviours such as
shivering and vasoconstriction are also experienced,
giving rise to the feeling of being hot yet cold.
Confirmation of a recorded temperature above 38˚C
in association with these symptoms is characteristic
of a fever (NHS Direct, 2010). Fever is indicative to
the clinician that an infection is present. Once the
pathogen has been removed, and cytokine expression
subsides to normal, then the fever will resolve and
the hypothalamus will reset to the normal parameters
of body temperature (35.5–37.5˚C) (Sund-Lavander,
Forsberg and Wahren, 2002).
A thorough systematic history-taking will usually
determine the nature and location of the infection.
Although in some cases, investigations such as
urine analysis or CRP (C-Reactive Protein) blood
testing, as part of a full blood count, may be
necessary. This however, should not normally be
required in the case of a labyrinthine infection.
A rise in body temperature was often thought
of as a physiological method of ‘cooking’ the
pathogen to destroy it, but what has been
known for some time is that microbes optimally
proliferate and grow when internal conditions
are approximately 36.2˚C. At significantly higher
temperatures, the pathogen is simply unable to
grow (Mains et al, 2008). It has been established
Journal of Paramedic Practice • Vol 2 No 7
Clinical
that a small rise in temperature enhances immune
function, as there is a positive correlation in white
blood cell activity, T cell activation and interferon
production (Kluger, 1986). Subsequently, the
immune system cells remove the invading particles
from the body.
In conjunction with a mild fever being
established in labyrinthitis, the immune and
inflammatory response continues to be active. The
cellular response is incredibly complex and is not
yet fully understood in terms of any aetiology, let
alone in the detailed physiology of the inner ear.
Immunoglobulins
Also activated by the proliferation of cytokines is
an adaptive humoral immune antigen–antibody
response. Composite protein parts of the invading
microorganism are triggers for such an immune
response in which antibodies are produced in
the body by activated B cells as a defence. These
defenders are also referred to as immunoglobulins
and are resident within the blood as the gamma-
globulin protein portion (Mattson-Porth, 2007).
In terms of inner ear defence, once an invading
pathogen has been established by primary
mechanisms, immunoglobulins are stimulated
to cross the blood—labyrinthine barrier (similar
to the blood—brain barrier) into the inner ear.
Similarly, immunoglobulin’s are thought to enter the
perilymph and endolymph via the perilymphatic
blood vessels (Luxon et al, 2003). However, many
researchers believe that certain immunoglobulin’s
reside permanently within the inner ear fluids in a
concentrated form, as in cerebrospinal fluid (Hughes
and Pensak, 2008).
Fundamentally, it is known that immunoglobulin’s
IgA, IgG, and IgM play a key role in the humoral
immune response to inner ear infection. IgG, for
example, is a widely available antibody within the
plasma, and is the main fighter in this immune
response. Certainly, IgG2 has been shown to be
particularly effective against bacteria such as
S. pneumoniae and H. influenzae—both of which
are capable of causing otitis media, which can lead
to labyrinthitis. IgA, on the other hand, is limited
within the plasma but is abundant within other
body fluids. It is thought to be in significant volume
in labyrinthine fluids and plays a role in preventing
microorganisms in attaching to epithelium.
IgM is an important antibody because it activates
and works collaboratively with the complement
system. It does this by binding to the infected cell,
which expresses viral proteins on its membranous
surface (Rhoades and Pflanzer, 2002). This
binding of antibodies to the surface antigen
morphologically alters its structure, enabling
chemo-attraction of the primary component of
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Clinical
the complement cascade to the base of the ‘Y’
shaped antibody in a region known as the fragment
crystallisable region.
Activation of the classical complement system
(C3b pathway) stimulates cell lysis via phagocytic
opsonization of the microbe (Marieb, 1998; Ravetch
and Bolland, 2001).
Viral management
Essentially, antibodies also provide an immune
response to free viruses by binding to them,
effaciously prohibiting their adherence to, and
invasion of a host cell. Critically, viruses such
as rhinoviruses, influenza and adenoviruses are
pathogens that can initiate labyrinthitis. In order
for these acellular organisms to replicate, they
must assemble within a host cell. This replicative
process primarily occurs with ‘attachment’
whereby the proteinous, viral-encoded genome
coat of the virus specifically binds to receptors
on the membranous surface of the host cell. This
specificity determines which host cells the virus
will favour, they will only ‘choose’ cells in which
they are capable of replicating.
Attachment to the host membrane receptor
results in a pathophysiological alteration of normal
cell function by inducing the construction of a
‘lipoprotein envelope’ to provide the virus with
morphological distinction from other pathogens,
and which allows for the fusion of viral and cellular
membranes (Mattson-Porth, 2007: 31).
Antibodies, however, provide an acute humoral
neutralization response to prevent the virus from
attaching to the host cell. This requires a highly
specific interaction (induced fit) between the
antigen and antibody. Antibody recognition of
specific antigenic epitopes (small, unique chemical
units within the virus) allows complementary
convergence at the fragment antigen-binding site of
the antibody; which are situated at the tips of its ‘Y’
shaped structure (Mattson-Porth, 2007).
Finally, immunoglobulin’s also contribute to viral
defence by stimulating a cell-mediated response.
Primarily, this is by infiltration of macrophages
to the infected area, but also involves specialized
cells such as natural killer, cytotoxic CD8+ T,
CD4+ T cells and interferon. Natural killer cells,
for example, provide a rapid non-specific cellular
immune response prior to the activation of
cytotoxic CD8+ T cells. They adhere to the infected
cell membrane upon primary exposure, and cause
apoptosis cell death by cytotoxic lysis of the
membrane (Sherwood, 2005).
If the virus is able to overcome this initial assault
by the host immune system, it enters the host cell
following membrane fusion or through receptor
mediated endocytosis. Subsequently, a period of
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‘uncoating’ occurs whereby degradation of the
protein coat by enzymes results in the release of
the viral genomic nucleic acid (ribonucleic acid
(RNA) or deoxyribonucleic acid (DNA)). Synthesis
of viral proteins and the genome are required for
replication. Transcription from viral messenger
RNA occurs within the host cell cytoplasm, giving
an expression of genes required to reproduce the
virus. This is translated into a protein ‘list’ upon
which replication occurs via ribosomal protein
synthesis.
It is at this transcription and translation stage that
small protein cytokines, interferons, are activated
by the host immune system to interfere with viral
replication (Marieb, 1998; Mattson-Porth, 2007).
Interferon alpha (IFN α) and interferon beta
(IFN β) are produced by a variety of cells, and
diffuse to nearby uninfected cells binding with
receptors on its cell membrane. Here, they stimulate
synthesis of an enzyme; protein kinase R (PKR),
which is significant in the inhibition of ribosomal
protein synthesis, thereby interfering with viral
replication (Sherwood, 2005).
Interferon gamma (IFN γ) provides the initial
adaptive immune by activating the localization of
macrophages and natural killer cells.
Interestingly, the pharmacological intra-nasal
use of interferons for viral upper respiratory
tract infections is currently being used in Eastern
Europe and Russia (Kreider et al, 1998; Ison et
al, 2004). While many researchers are sceptical
of their use (as the exact actions of interferon
upon otorhinolaryngological structures are not yet
understood), a contemporary study being jointly
undertaken in the UK and USA is examining
pharmaceutical interferon use for otitis illnesses
(Garrett-Nichols et al, 2008). It must be noted
that a pharmaceutical company is supporting this
work and therefore this may be influential in any
outcomes.
However, studies now identify that some viruses
have evolved to inhibit interferon production and
function (Katze et al, 2002), with implications for
successful immuno-ability to combat previously short-
lived infections. While further scientific exploration of
these pathogens and counteractive pharmaceuticals
is required, perhaps the focus should widen to
take account of the influential holistic factors in the
proliferation and transference of pathogens; namely
the environmental and social determinants of health
(Vergison, 2008) which have so recently been
fundamental in the spread of viral influenza A (Swine
Flu) (World Health Organisation, 2009). Additionally,
personal factors that impinge on the effectiveness
of the immune system and inflammatory response,
such as dietary factors and levels of stress, require
consideration to promote health.
Vol 2 No 7 • Journal of Paramedic Practice

Conclusion
As it remains, the current UK best practice in
treating labyrinthitis pharmacologically is by over-
the-counter medications such as paracetamol for
fever and pain management, and allowing the
body to undertake its natural course in managing
the illness (NHS Choices, 2010). However, if
symptoms are severe, vestibular suppressants
may be prescribed for dizziness; antiemetics
given for nausea/ sickness; steroids for reducing
inflammation, and if the cause is thought to be
bacterial, antibiotics may be required.
To conclude, labyrinthitis is generally a short-
lived minor illness that has the potential to cause
temporary or permanent disablement in terms of
hearing loss. Understanding the pathophysiological
development and the inflammatory and immune
response to such an illness enables the clinician
to comprehend the underlying processes of the
presenting signs and symptoms, and to treat
accordingly.
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Journal of Paramedic Practice • Vol 2 No 7
Clinical
Key points
llLabyrinthitis is an inflammation of the inner ear in
response to infection. This illness has the potential to
cause temporary or permanent hearing loss, with other
symptoms including earache and fever.
llAetiology of labyrinthitis are attributable to bacterial,
viral and fungal insult. However, fungal infections are
less common than the other two.
llRegardless of cause, the complex inflammatory and
immune response is activated to locally defend the
inner ear structures, and systemically defend the body
against infection.
llTreatments include over-the-counter medications such
as paracetemol for fever and pain management, and
allowing the body to take its natural course in managing
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