complications of otitis media
Dr. T. Balasubramanian M.S. D.L.O.
of otitis media occur as a result of infection spreading from the
mucosa of the middle ear cleft to the adjacent structures. Usually the
middle ear space is separated from adjacent structures by bone. During
preantibiotic era complications commonly followed acute otitis media.
With the advent of antibiotics it the chronic otitis media which is
causing complications .
the incidence of these complications have drastically reduced after the
advent of potent antibiotics, the morbidity and mortality caused by the
complications are still very high.
complications of otitis media fall under two categories:
Complications within the cranium
Complications within the temporal bone
can be further subclassified into extradural and intradural
Sigmoid sinus thrombosis
Internal carotid artery aneurysm
Subclavian vein thrombosis
Diagramatic representation of intracranial complications of otitis media
Route of spread of
infection from the ear:
Whether acute or chronic,
the infection from the middle ear spreads via:
1. Extension through bone
that has been demineralised during acute infections, or resorbed by
cholesteatoma, or osteitis in chronic disease of the ear.
Demineralisation is brought about by various enzymes that are released
during the acute infections. Cholesteatoma causes bone erosion either
due to pressure necrosis, or halisterisis. Halisterisis is also known
as hyperimic decalcification. As the term itself suggests
decalcification is caused by hyperaemia.
2. Spread through venous
channels: Spreading of infected clot within small veins through the
bone and dura into the dural venous sinuses. If spread via this route
occurs then the infection may find its way into the brain without
involving the bone or dura. Thrombophlebitis from the lateral sinus may
spread to the cerebellum, and from the superior petrosal sinus may
spread to the temproral lobe of the brain.
3. Spread through normal
anatomical pathways: Spread may occur through oval / round windows into
the internal auditory meatus. Spread may also occur through the
cochlear and vestibular aqueducts. Certain areas may have dehiscent
bone as a normal variant i.e. bony covering of the jugular bulb,
dehiscent areas in the tegmen tympani, and dehiscent suture lines of
the temporal bone.
4. Spread may occur through
non anatomical bony defects like those caused due to trauma, (accident,
surgical) or by erosion due to neoplasia.
5. Spread may occur through
surgical defects as caused by fenestration of the oval window during
6. Spread may occur
directly into the brain tissue through the peri arteriolar spaces of
Virchow Robin. This spread does not affect the cortical arterioles
perse, hence abscess occur in the white matter without the involvement
of gray matter of brain.
Diagramatic representation showing the various routes of spread of
infection from the middle ear cavity.
Chronic middle ear disease
cause complications by progressive and relentless erosion of the bone
barriers, exposing the structures at risk to damage - the facial nerve,
labyrinth and the dura. Acute infections cause early complications via
the thrombophlebitis mechanism or extension through already available
Factors that determine the
spread of infection:
I. Patient attributes:
Patient's general condition and immunologic status play an important
role in the spread of infections.
II. Bacterial attributes
like the virulence of the infecting organism is also important. For
example acute infections caused by Strep. pneumoniae type III, and H.
Influenza type B have immense potential to spread.
III. Adequacy / Inadequacy
of treatment of the middle ear condition may also play an important
Is always associated with
involvement of dura mater by the spreading disease, constituting
pachymeningitis. This is commonly preceded by loss of bone, either
through demineralisation in acute infection or erosion by cholesteatoma
in chronic disease. If the cholesteatoma is non infected it may simply
expose the dura without any inflammatory reaction. If cholesteatoma is
infected it is associated with formation of granulation tissue over the
dura. Dura is tough and resists infection. It attempts to wall off the
infection, and collection of pus occur between the dura and the bone.
This is known as extradural abscess and is the commonest of all
A middle cranial fossa
extradural mass may strip the dura from bone on the inner surface of
squamous temporal bone.
Such an enlarging mass may
cause increasing intracranial tension, causing focal neurological signs
and papilloedema. Sometimes it could erode the skull from inside to the
exterior causing a subperiosteal abscess i.e. the classic Pott's puffy
tumor. Rarely an extradural abscess may develop medial to the arcuate
eminence over the petrous apex. This irritates the Gasserian ganglion
of the trigeminal nerve, and the 6th cranial nerve. This produces the
classic Gradenigo's syndrome (includes facial pain, diplopia and aural
discharge). Posterior fossa extradural abscess is limited by the
attachments of the dura laterally to the sigmoid sinus. Posterior
extension of this abscess around the sigmoid sinus produces the
perisinus abscess. This could also extend to the neck through the
Fig showing extradural abscess
Depends on the site of the
abscess, its size, duration and rate of development. In most patients
the symptoms are vague, and non specific. Sometimes it could be a
incidental finding during mastoid surgery. The common complaint of the
patient being headache accompanied by malaise. If the abscess
communicates with the middle ear the patient may have interim relief
following an episode of aural discharge.
CT scan showing extradural abscess
CT scan is diagnostic.
Surgery must be done as early as possible. Granulation tissue over the
dura should not be disturbed because it could breach the only defence
and the infection could spread to the brain.
abscess (Empyema): When spread of infection breaches the dura it
exposes the subdural space to the perils of the infection. It may
initially be associated with Leptomeningitis, or if the infection is
contained as subdural effusions or subdural abscess. The rate of spread
of the infection determines the clinical presentation. The dura is
highly resistant to infection, the granulation tissue which develops on
the inner side of the dura obliterates the subdural space. Initially
seropurlent effusion develops in the subdural space, and eventually
this becomes frankly purulent. The spread of this effusion is limited
by the granulation tissue which attempts to obliterate the subdural
space. The subdural pus tends to accumulate near the falx cerebri, that
too particularly where it joins the tentorium cerebelli. Healing is
always associated with fibrosis and obliteration of the subdural space
in the area where granulation was present.
The cortical veins in the
adjacent area may become involved by thrombophlebitis, this may be
responsible for some of the clinical features. This may also produce
multiple small abscess in the brain adjacent to the area of subdural
infection. One or numerous multiloculated abscesses over the convex
surface of the cerebral hemispheres may be seen. Commonly Non
haemolytic streptococci have been implicated.
The subdural empyema can be
suspected by the presence of headache and drowsiness. Focal
neurological symptoms like irritative fits and paralysis may follow.
Fits are usually of Jacksonian type, starting locally and spreading to
affect one side of the body this is usually caused by cortical
thrombophlebitis. Paralysis may start with one upper or lower limb and
may gradually become hemiplegia. If dominant lobe is involved aphasia
develops. The site of fits and the pattern of localising signs suggests
the area of empyema. Papilloedema is highly uncommon, and similarly
palsies involving individual cranial nerves are also rare.
Meningism may accompany
headache, despite this feature this can be distinguished from
meningitis by the presence of characteristic neurological localising
signs. In children suspected of meningitis, subdural empyema should be
considered if there is no response to treatment, or if motor seizures
occur. CT scan is diagnostic. While CSF pressure may be elevated, the
sugar contents are normal and the cultures are invariably sterile. In
places where CT scan facilities are unavailable exploratory burr holes
may be made to clinch the diagnosis.
Management: Must be done in
close coordination with neurosurgeon. Massive doses of antibiotics
(systemic) like penicillin and chloramphenicol must be given. The
subdural abscess must be drained and the subdural space irrigated. Ear
disease must be surgically treated only after the subdural empyema has
been cleared or resolved. Acute ear infections may be treated with
myringotomy and chronic infections can be managed with mastoidectomy.
Neurosurgical management includes burr holing the skull thereby
draining the abscess. Antiseizure drugs must be prescribed to supress
sinus thrombosis: Thrombophlebitis can develop in any of the
veins adjacent to the middle ear cavity. Of these the lateral sinus,
which comprise of the sigmoid and transverse sinuses is the largest and
most commonly affected. Initially it is usually preceded by the
development of an extradural perisinus abscess. The mural thrombus
partly fills the sinus. The clot progressively expands and eventually
occlude the lumen. The clot may later become organised, and partly
broken down and may even be softened by suppuration. During this stage
there is a release of infecting organism and infected material into the
circulation causing bacteremia, septicemia and septic embolisation.
Fig showing the various stages of lateral sinus thrombosis
Extension / propagation of
the thrombus upwards may extend to the confluence of the sinuses, and
beyond that to the superior sagittal sinus. Invasion of the superior
and inferior petrosal sinuses may cause the infection to spread to the
cavernous sinus. This spread of venous thrombophlebitis into the brain
substance accounts for the very high association of this complication
with brain abscess. Downward progression of thrombus into and through
the internal jugular vein can reach the subclavian vein.
The harmful effects are
caused by the release of infective emboli into the circulation, and
also from the haemodynamic disturbances caused to venous drainage from
inside the cranial cavity. The use of antibiotics have greatly reduced
the incidence of lateral sinus thrombosis these days.
Formerly it was commonly
associated with acute otitis media in childhood; now it is commonly
seen in patients with chronic ear disease. In the preantibiotic era the
commonest infecting organism was beta hemolytic streptococci. This
organsim was known to cause extensive destruction of red blood cells
causing anaemia. Now a days the infection is by a mixed flora.
The patients manifest with
severe fever, wasting illness in association with middle ear infection.
The fever is high and swinging in nature, when charted it gives an
appearance of 'Picket fence'. It is always associated with rigors. The
temperature rose rapidly from 39 - 40 degree Centigrade. Headache is a
common phenomenon, associated with neck pain. The patient appear
ematiated and anaemic. When the clot extended down the internal jugular
vein, it will be accompanied by perivenous inflammation, with
tenderness along the course of the vein. This tenderness descended down
the neck along with the clot, and would be accompanied by perivenous
oedema or even suppuration of the jugular lymph nodes. Perivenous
inflammation around jugular foramen can cause paralysis of the lower
three cranial nerves. Raised intracranial pressure produce papilloedema
and visual loss. Hydrocephalus could be an added complication if the
larger or the only lateral sinus is occluded by the thrombus, or if the
clot reaches the superior sagittal sinus. Extension to the cavernous
sinus can occur via the superior petrosal sinus, and may cause chemosis
and proptosis of one eye. If circular sinus is involved it could spread
to the other eye. The propagation of the infected emboli may cause
infiltrates in the lung fields, and may also spread to joints and other
subcutaneous tissues.. These distant effects usually developed very
late in the disease, these could be the presenting features if the
disease is insiduous in onset. Masking by antibiotics could be one of
the causes. Patients always feel ill, and persisting fever is usual.
The patients may have ear ache, in association with mastoid tenderness,
and stiffness along the sternomastoid muscle. The presence of anaemia
is rare now a days. Papilloedema is still a common finding. Other
coexisting intracranial complications must be expected in more than 50
percent of patients.
Extension of infected clot
along the internal jugular vein is always accompanied by tenderness and
oedema along the course of the vein in the neck, and localised oedema
over the thrombosed internal jugular vein may still be seen. One rare
finding is the presence of pitting oedema over the occipital region,
well behind the mastoid process, caused by clotting within a large
mastoid emissary vein, this sign is known as the Griesinger's sign.
Infact there is no single pathognomonic sign for lateral sinus
thrombosis and a high index of suspicion is a must in diagnosing this
A lumbar puncture must be
performed, if papilloedema does not suggest that raised intracranial
pressure may precipitate coning. Examination of CSFis the most
efficient way of identifying meningitis. In uncomplicated lateral sinus
thrombosis the white blood count in the CSF will be low when the cause
is chronic middle ear disease, and somewhat raised in acute otitis
media. The CSF pressure is usually normal. The variations in the level
of CSF proteins and sugar are not useful.
Queckenstedt test: This is
also known as Tobey - Ayer test. This is recommended whenever lumbar
puncture for a possible intracranial infection is performed. The test
involves measurement of the CSF pressure and observing its changes on
compression of one or both internal jugular veins by fingers on the
neck. In normal humans compression of each internal jugular vein in
turn is followed by an increase in CSF pressure, of about 50 - 100mm
above the normal level. When the pressure over the internal jugular
vein is released then there is a fall in the CSF pressure of the same
magnitude. In patients with lateral sinus thrombosis pressure over the
vein draining the occluded sinus cause either no increase, or a low
slow rise in CSF pressure of 10 - 20 mm. Compression of the normal
internal jugular vein produces a rapid pressure rise ranging from 2 - 3
times the normal level. This test is also prone for false negative
results due to the presence of collateral channels draining the venous
sinuses. False positives can occur if a normal lateral sinus is small
or absent that creating an erroneous impression of lateral sinus
Fig showing negative Tobey Ayyer test
Fig showing positive Tobey Ayyer test
CT scanning: is an
essential investigation in these patients. It may show filling defects
within the sinus, and increased density of fresh clots. When contrast
materials like Iothalamate (conray) is used failure of opacification of
the affected lateral sinus may become evident. The presence of septic
thrombosis shows intense inflammatory enhancement of the sinus walls
and of the adjacent dura. This enhancement of the walls, but not of the
contents of the sinus constitutes the empty triangle or 'delta' sign.
It can also exclude accompanying complications like brain abscess and
Angiography: is a
definitive investigation of lateral sinus thrombosis. It helps to
demonstrate the obstruction, its site and the anatomical arrangement of
the veins. There is an impending risk of displacing the infected
with radio opaque dye injected into the carotid artery can show the
venous outflow during the venous phase. This can be clearly visualised
in digital subtraction angiography. This technique involves precise
superimposition of a negative arteriogram on a positive film of bone
structures. This effectively cancels out the skeletal image thus
clearly revealing the vascular pattern.
MRI: Is sufficiently
diagnostic hence angiography can be avoided if MRI could be taken.
Established thrombus shows increased signal intensity in both T1 and T2
weighted images. MRI can also be used to show venous flow. Gadolinum
enhancement may show a delta sign comparable with that seen on CT scans
involves administration of antibiotics, together with exposure of
lateral sinus and incision of the sinus and removal of its contents.
Anticoagulants are not advocated at present. Before exposing the
lateral sinus and clearing its contents it is imperative to clear the
ear of any infections by doing a cortical mastoidectomy. The involved
sinus may feel firm, appear white and opaque thus suggesting occlusion
of the lumen with clot. Dissemination of clot can be prevented by
ligation of the affected internal jugular vein. Now a days the only
indication of internal jugular vein ligation is the presence of
septicemia which is resistant to antibiotics.
It is also known as
Leptomeningitis.(only the piamater and arachnoid are involved). This is
a major and serious complication of middle ear infection. In the pre
antibiotic era the sufferers invariably died. Nowadays, recovery is
usual provided early diagnosis and prompt treatment is initiated.. In
pre antibiotic era meningitis was a common complication of acute middle
ear infections, but now it is a frequent complication of chronic middle
ear disease. Childhood otogenic meningitis is commonly caused by acute
middle ear infections, in adults it is commonly a complication of
chronic middle ear disease. Spread to the meninges may occur via any of
the dehicences in the bony barrier or preformed channels. The rate of
development depends on the virulence of the organism and the resistance
of the host.
can cause meningitis via access to the cerebrospinal spaces through
internal auditory meatus, and through vestibular and cochlear
aqueducts. Rarely rupture of brain abscess into the subarachnoid space
may lead on to meningitis. Meningitis can develop within hours of the
onset of acute otitis media. The organisms usually responsible to acute
infection are H. Influenza type B, and Strep. pneumoniae type III.
Infections from chronic ear diseases nay be caused by gram negative
enteric organisms, proteus, and psuedomonas. Anaerobes and bacteriodes
have also been reported.
The initial inflammatory
response of the pia arachnoid to infection is an outpouring of fluid
into the subarachnoid space, with a rise in CSF pressure. The CSF
becomes permeated with white blood cells and rapidly multiplying
bacteria. These bacteria feed on glucose present in the CSF reducing
its level in CSF a characteristic finding in meningitis. Pus initially
accumulates in the basal cisterns, and more rarely in the vertex. The
free flow of CSF is impeded by the exudate obstructing the ventricular
foramina to cause a non communicating hydrocephalus. Obstruction to CSF
in the subarachnoid spaces may cause communicating hydrocephalus.
Irritation of the upper cervical nerve roots by the exudate cause neck
pain and neck stiffness which are the characteristic features of this
condition. Exudates around the exit foramina of cranial nerves could
cause nerve palsies during the late stage of the disease. Spread of
infection through virchow robin spaces into the brain substance may
lead to the formation of brain abscess.
The most reliable clinical
feature of this condition is the presence of headache and neck
stiffness. At first the headache could be localised to the side of the
affected ear but later it could become generalised and bursting in
nature. There is also associated malaise and pyrexia. Initially neck
stiffness shows resistance only to flexion, but later full rigidity or
retraction may develop. During early stages the patient may have mental
hyperactivity and restlessness. Tendon reflexes becomes exaggerated
during this stage. Photophobia is another constant presenting feature,
and the patient may be prompted to lie curled up away from the light.
Vomiting projectile in nature is another important feature. As the
condition worsens the symptoms also become progressively severe. When
neck stiffness is marked the patient may manifest poitive kernigs sign.
The stiffness may become more severe enough to cause opisthotonus.
Brudzinski's sign is involuntary lifting of the legs in meningeal
irritation when lifting a patient's head. Kernig's sign is resistance
and pain when knee is extended with hips fully flexed. Patients may
also show opisthotonus; spasm of the whole body that leads to legs and
head being bent back and body bowed forward.
Is made by the examination
of CSF. Any patient with suspected menigitis must undergo lumbar
puncture. The CSF analysis show increased white cells and reduced
glucose levels from 1.7-3 mmol/l to 0.. Chloride content may fall from
120 mmol/l to 80mmol/l. Bacteria may also be isolated from the CSF.
Recently polymerase chain reaction have been used to detect bacterial
DNA from CSF.
The mainstay in the medical
management is large doses of systemic antibiotics. Penicillin is the
drug of choice. Streptomycin may also be used as an adjunct.
Chloramphenicol may also be used. Ceftrioxine a third generation
cephalosporin is widely used these days in the treatment of meningitis.
This has a broad spectrum activity. Metronidazole is also used because
of its usefulness in treating anaerobes.
After the patient recovers
from the acute problem, effort must be made to remove the middle ear
pathology which was the cause for this problem. In chronic middle ear
infections modified radical mastoidectomy is the procedure of choice,
in acute middle ear infections cortical mastoidectomy is the preferred
Otogenic brain abscess
always develop in the temporal lobe or the cerebellum of the same side
of the infected ear. Temporal lobe abscess is twice as common as
cerebellar abscess. In children nearly 25% of brain abscesses are
otogenic in nature, whereas in adults who are more prone to chronic ear
infections the percentage rises to 50%. The routes of spread of
infection has already been discussed above, the commonest being the
direct extension through the eroded tegment plate. Although dura is
highly resistant to infection, local pachymeningitis may be followed by
thrombophlebitis penetrating the cerebral cortex, sometimes the
infection could extent via the Virchow - Robin spaces in to the
cerebral white matter. Cerebellar abscess is usually preceded by
thrombosis of lateral sinus. Abscess in the cerebellum may involve the
lateral lobe of the cerebellum, and it may be adherent to the lateral
sinus or to a patch of dura underneath the Trautmann's triangle.
Fig showing evolution of brain abscess
Stages of formation of
Stage of cerebral oedema:
This is infact the first stage of brain abscess formation. It starts
with an area of cerebral oedema and encephalitis. This oedema increases
in size with spreading encephalitis.
Walling off of infection by
formation of capsule: Brain attempts to wall off the infected area with
the formation of fibrous capsule. This formation of fibrous tissue is
dependent on microglial and blood vessel mesodermal response to the
inflammatory process. This stage is highly variable. Normally it takes
2 to 3 weeks for this process to be completed.
Infected brain within the capsule undergoes liquefactive necrosis with
eventual formation of pus. Accumulation of pus cause enlargement of the
Stage of rupture:
Enlargement of the abscess eventually leads to rupture of the capsule
containing the abscess and this material finds its way into the
cerebrospinal fluid as shown in the above diagram.
Cerebellar abscess which
occupy the posterior fossa cause raised intra cranial tension earlier
than those above the tentorium. This rapidly raising intra cranial
pressure cause coning or impaction of the flocculus or brain stem into
the foramen magnum. Coning produces impending death. If the walling off
process (development of capsule) is slow, softening of brain around the
developing abscess may allow spread of infection into relatively
avascular white matter, leading to the formation of seconday abscesses
separate from the original or connected to the original by a common
stalk. This is how multilocular abscesses are formed. Eventually the
abscess may rupture into the ventricular system or subarachnoid space,
causing meningitis and death.
The mortality rate of brain
abscess is around 40%, early diagnosis after the advent of CT scan has
improved the prognosis of this disease considerably..
The bacteriological flora
is usually a mixture of aerobes and obligate anaerobes. Anaerobic
streptococci are the commonest organisms involved. Pyogenic
staphylococci is common in children. Gram negative organims like
proteus, E coli and Pseudomonas have also been isolated.
The earliest stage where
the brain tissue is invaded (stage of encephalitis) is marked by the
presence of headache, fever, malaise and vomiting. Drowsiness
eventually follow. These early features may be masked by the
complications such as meningitis or lateral sinus thrombosis. If this
stage progresses rapidly to generalised encephalitis before it could be
contained by the formation of the capsule, drowsiness may progress to
stupor and coma followed by death.. Usually the period of local
encephalitis is followed by a latent period during which the pus
becomes contained within the developing fibrous capsule. During this
latent phase the patient may be asymptomatic.
During the next state
(stage of expansion) the enlarging abscess first cause clinical
features due to the alteration of CSF dynamics, and site specific
features may also be seen due to focal neurological impairement. The
pulse rate slows with rising intracranial pressure, the temperature may
fall to subnormal levels. Drowsiness may alternate with periods of
irritability. Papilloedema is also found due to elevated CSF pressure.
Clinical features also vary
according to the site of involvement. Hence the differences that are
seen between the cerebral and cerebellar abscess.
A cerebral abscess in the
dominant hemisphere often cause nominal aphasia, where in the patient
has difficulty in naming the objects which are in day to day use. He
clearly knows the function of these objects. Visual field defects arise
from the involvement of optic radiations. Commonly there is quadrantic
homonymous hemianopia, affecting the upper part of the temporal visual
fields, more rarely it may also involve the lower quadrants. The visual
field loss are on the side opposite to that of the lesion. This can be
assessed by confrontation method. Upward development affects facial
movements on the opposite side, and then progressively paralysis of the
upper and lower limbs. If the expansion occur in inward direction then
paralysis first affects the leg, then arm and finally the face.
The focal features
associated with cerebellar abscess is weakness and muscle
incoordination on the same side of the lesion. Ataxia causes the
patient to fall towards the side of the lesion. Patient may also
manifest intention tremors which may become manifest by the finger nose
test. This test is performed by asking the patient to touch the tip of
the nose with the index finger first with the eyes open and then with
the eyes closed. The patient may often overshoot the mark when
attempted with the eyes closed in case of cerebellar abscess. The
patient may also have spontaneous nystagmus. Dysdiadokinesis is also
positive in these patients.
CT scan and MRI scans are
the present modes of investigation. Scan is ideally performed using
contrast media. These scans not only reveal the position and size of
the abscess, the presence of localised encephalitis can be
distinguished from that of an encapsulated abscess. Associated
conditions such as subdural abscess, and lateral sinus thrombosis can
also be seen.
Is frought with danger
because of the risk of coning. Lumbar puncture must be performed in
these patients only in a neurosurgical unit where immediate
intervention is possible if coning occurs.
Treatment: involves use of
large doses of antibiotics. Ideally the abscess should be controlled
neurosurgically and with antibiotics. After the patient recovers
mastoidectomy is performed to remove the focus of infection. Abscess
can be drained by placement of burr holes, and excision of the necrotic
tissue along with the capsule.
Is one of the common
complication of middle ear infection. It is a syndrome of raised
intracranial pressure during or following middle ear infection. This
condition is also known as Pseudotumor cerebri.
The aetiology is unknown.
The relationship of this condition with that of lateral sinus
thrombosis has been documented. The inference is that obstruction of
the lateral sinus affects cerebral venous outflow, or the extension of
the thrombus into the superior sagittal sinus impedes CSF resorption by
The leading symptoms are
3. blurred vision
6. diplopia (rarely)
The onset may occur many
weeks after acute otitis media, or many years after the start of the
chronic middle ear disease. Clincial examination may show papilloedema.
Lateral rectus palsy on one or both sides are also commonly seen. This
occur due to the stretching of the 6th nerve due to increased
intracranial pressure. CT scan is diagnostic.
Revolves around the
management of the elevated intra cranial tension. It includes use of
steroids, diuretics and hyperosmolar dehydrating agents. Repeated
lumbar punctures may also be used to reduce the tension. Surgical
clearance of the infection of the middle ear should also follow.
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