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Pathophysiology of OM

Both AOM and COM are bacterial infections involving the middle ear
cleft Risk factors can be complex and interrelated, but are primarily
associated with (a) exposure to pathogens, (b) local anatomy, and (c)
host response.
Exposure to pathogens can be increased or altered by exposure
to day care environments, or crowded or unhygienic living situations.
The specific microbiologic flora is strongly influenced by prior individual
and community antibiotic treatment. Exposure to nasopharyngeal flora
may be enhanced with patent eustachian tubes. In the case of COM,
contamination by pathogens can occur via the external auditory canal
via a tympanic membrane perforation or by direct contamination of
debris within a cholesteatoma. The latter can be enhanced by
exposure to water from swimming or bathing. Different pathogens
have varying degrees of pathogenicity and disease progression. The
bacteriology of OM is summarized in Table 149.2.
The primary anatomic variable affecting the development of OM
is eustachian tube function. Eustachian tube function varies widely in
otherwise normal individuals, but is reduced in patients with cleft
palate, exposure to smoke (smokers and passive exposure), allergic
rhinitis, neoplastic processes involving the cranial base, acromegaly,
and many other conditions. Abnormally patent eustachian tubes result
in reflux of nasopharyngeal contents into the middle ear. Mucosal
disease such as nasal polyposis, ciliary dyskinesia or cystic fibrosis
results in reduced eustachian tube function. If a patient develops
cholesteatoma, the local anatomy has a direct effect on how the
cholesteatoma grows and what bony destruction it causes. The
cholesteatoma and associated inflammation can then, in tum, directly
or indirectly impact eustachian tube function.
Host response factors such as immunodeficiency, immunization
status, ciliary dyskinesia, and history of bottle-feeding also play
importantroles in the development of OM.
Pathophysiology of Complications of OM
Similar factors influence the development of complications of OM, with
the addition of many other variables. It is important to understand the

anatomy in which these infections exist, their routes of spread, and the
characteristic patterns of disease. Infection can spread via direct
extension, via venous structures, or hematogenously. However, the
primary pathogenesis seems to be a complex interaction between the
specific organisms and the host.
An important host response leading to complication is the
production of tissue edema and granulation tissue that subsequently
becomes obstructive to drainage and aeration. This creates an
environment conducive to the growth of anaerobic organisms and the
destruction of bone. Important microbiologic factors seem to pivot
about the synergistic pathogenicity of anaerobic organisms.
The epidemiology and microbiologic behavior of the organisms
found in complications offer some insight into the pathogenesis and
pathophysiology of these complications (Table 149.2). For example.
infections with Streptococcus pneumoniae, nontypeable Haemophilus
influenzae, and Moraxella catarrhalis are the most common causes of
acute suppurative OM. Only about 4% of OM is caused by infection with
H. influenzae type B; however, pediatric patients with OM occurring
simultaneously with meningitis or other central nervous system
infections were found to have an unusually high incidence of H.
injluenzae type B.
Uncomplicated chronic otorrhea characteristically cultures
Pseudomonas aernginosa, Staphylococcus aureus, and a variety of
other Gram-negative organisms, such as Proteus sp., Klebsiella sp.,
and Escherichia coli. In contrast, mastoiditis associated with chronic
suppurative otitis media (CSOM) frequently has a fetid odor and often
cultures positive for Bacteroidesfragilis. Multiple organisms are found
in 57% of chronically draining ears with cholesteatoma, with an
average of three different organisms. However, if these ears have a
fetid discharge, characteristically 5 to 11 organisms are found, always
including both anaerobes and aerobes. Malodorous discharge is a
significant early sign of com- plication. Anaerobic organisms are a
major cause of foul- smelling discharge.
-Lactamase-producing organisms, such as S. aureus, H. influenzae, B.
catarrhalis, and Bacteroides sp., not only survive -Lactam antibiotics
but may also protect other potentially penicillin-susceptible pathogens
from penicillin and other -Lactam antibiotics. Anaerobic organisms
have recently been shown to play major roles in pathogenic synergism
by protecting against host defenses, creating suitable environments for
other organisms, and inactivating antibiotics.

Anatomic variables are tremendously important in the

development of complications. Eustachian tube function plays a critical
role in not only the development of the original infection and its
resolution but also the development of complications. The mucosal
edema resulting from OM itself impairs eustachian tube function and
inhibits resolution of the infection. Highly variable factors, such as the
integrity of bone over the facial nerve or dura, influence access of the
infection and its products to neurovascular structures and the
intracranial space. Numerous venous channels traverse the bone
between the mastoid and middle ear and the dural venous sinuses,
sometimes associated with arachnoid granulations. Inflammation
adjacent to these veins and venules can promote thrombosis. Thrombi
and infection can then propagate to the dural venous sinuses and
subarachnoid space. Cholesteatoma often results in patterns of bone
destruction exposing the dura or facial nerve to the infectious process.
Finally, prior surgery can result in areas of entrapped squamous
epithelium or deficient areas of bone that act as sources of infection
and routes for the infection to spread.
Complications of OM tend to present in predictable patterns (Table
149.3). With the exception of meningitis in children and some cases of
facial paralysis, which are usually associated with AOM, most
complications tend to be associated with COM. Typically, mastoiditis is
the initial complication, with more severe complications developing
secondarily. Petrositis (petrous apicitis), for example, almost never
occurs without preceding mastoiditis. Labyrinthine fistulae virtually
always develop secondary to cholesteatoma. Granulation tissue in air
cells adjacent to the sigmoid sinus can result in erosion of the bone
overlying the sinus, with resultant sigmoid sinus exposure and possible
sigmoid sinus thrombophlebitis. If the sigmoid becomes obstructed
with thrombus, intracranial hypertension, that is, otitic hydrocephalus,
can result. Retrograde thrombophlebitis may extend intracerebrally,
resulting in a brain abscess. Subdural empyema rarely occurs due to
COM, but is a more typical complication of meningitis in infants.
Without a high index: of suspicion, early evidence of an
impending complication will be missed. Early symptoms and signs of
complication are summarized in Table 149.4. Because antibiotic
therapy may have a masking effect on the significant signs and
symptoms of complications, a high level of clinical awareness is

important for early diagnosis. Persistence of acute symptoms for 2

weeks or more or recurrence of symptoms or infection within 2 weeks
is often the first sign of a potential complication. In chronically draining
ears, acute exacerbation of pain or the new development of fetid
drainage should be evaluated. Foul-smelling drainage that fails to
respond to conservative treatment (debridement and topical
antibiotics) portends an impending complication.
Once a complication has begun, signs and symptoms typically
progress rapidly. Fever associated with COM implies some degree of
edema/erythema, edema of the posterior-superior external auditory
canal (EAC) wall, or anterolateral displacement of the pinna indicates
mas- toiditis associated with subperiosteal abscess. Retro-orbital pain
in an infected ear is highly suggestive of petrositis (petrous apicitis).
Vertigo and nystagmus in a patient with OM may indicate serous or
suppurative labyrinthitis, or possibly a labyrinthine fistula. Facial
paralysis ipsilateral to an infected ear may complicate AOM, or COM
with cholesteatoma. Papilledema is an obvious sign of elevated
intracranial pressure, but will go undetected without a fundoscopic
examination. Headache and lethargy usually accompany an
intracranial infectious complication. Meningismus is associated with
meningitis, and focal neurologic signs or seizures are seen in brain
As commonly used clinically, the term mastoiditis is nonspecific and
often misleading. Since the mastoid air cell system is confluent with
the middle ear space, any inflammatory process within the middle ear
will also involve the mastoid. Although it may be pathologically correct
to refer to purulent fluid within the mastoid secondary to OM as
mastoiditis, it is not clinically meaningful or helpful, and does not
represent a complication of OM. An example of this clinically
misleading use of the term mastoiditis is the radiologic diagnosis of
mastoiditis based on the presence of opacification or increased T2
signal intensity alone. This does not imply a complication and does not
require additional therapy beyond that indicated for the primary
middle ear process. True mastoiditis as a complication of OM implies an
invasive or persistent infection involving the mastoid bone and/or

surrounding structures, distinct from AOM or OM with effusion. With

this in mind, mastoiditis can be subdivided into (a) acute mastoiditis,
(b) coalescent mastoiditis, (c) chronic mastoiditis, and (d) masked
mastoiditis. Clinically, there is often some overlap between these
diagnostic categories.
Acute Mastoiditis
Acute mastoiditis is diagnosed in the presence of postauricular pain,
tenderness, erythema, swelling, and/or auricular protrusion, with or
without evidence of AOM. Acute mastoiditis is most commonly seen in
young children 2 to 6 days following the onset of AOM. Due to partial
treatment with antibiotics, signs and symptoms may be much less
obvious: antibiotic therapy obscuring the presentation but not the
complication. Some authors insist on the presence of AOM for a
diagnosis of acute mastoiditis; however, attic blockage may preclude
otoscopic visualization. Most authors recommend treatment with
parenteral antibiotics, with or without simple mastoidectomy. When
treated with parenteral antibiotics alone, up to one-third of patients will
require mastoidectomy for failure to improve or complications. The
most common complication is subperiosteal abscess. Other
complications of acute mas- toiditis include coalescent mastoiditis,
facial paralysis, meningitis, and Bezold abscess. Antibiotic treatment of
routine AOM has been shown to be associated with a lower incidence o
f acute mastoiditis.
Coalescent Mastoiditis
Coalescent mastoiditis implies breakdown and decalcification of the
bony septa within the mastoid, progressing to bony destruction of the
cortex or other aspects of the mastoid bone. Coalescent mastoiditis is
what is commonly and classically referred to as mastoiditis. This
infection typically affects boys, 4 years or younger, who have
previously well-aerated mastoids and little or no prior history of OM.
Coalescence rarely, if ever, occurs in the setting of COM. Patients
typically present with fever, otalgia, purulent otorrhea, and mastoid
pain, tenderness, erythema, and/or edema. Typically, it occurs in
patients who have had persistent otorrhea or otalgia for 2 weeks or
more following AOM, or when these symptoms recur 10 to 14 days
following AOM. Up to 25% of patients presenting with coalescent
mastoiditis will have a concomitant intracranial complication. S.
pneumoniae is the most common offending organism. Of those with a
simultaneous intra- cranial complication, nearly 30% will culture

positive for anaerobic organisms as well.

Diagnosis. The diagnosis is confirmed by CT imaging, demonstrating
breakdown of bony septa, loss of cortical bone, and opacification of the
air cell system. MR imaging should be obtained if there is any suspicion
of intracranial complication.
Treatment. Treatment of coalescent mastoiditis consists of
myringotomy and intravenous antibiotics, with or without simple
mastoidectomy. If mastoidectomy is not performed, intravenous
antibiotics should be continued for a minimum of 3 to 6 weeks.
Mastoidectomy almost always results in prompt resolution of the
infection and its symptoms, and is the safest and most conservative
Chronic Mastoiditis
As used clinically, chronic mastoiditis is a broad term and implies
chronic inflammation within the mastoid air cell system. It can occur in
typical COM with tympanic membrane perforation, and results in
mucosal disease and/or granulation tissue that causes otorrhea to
persist in spite of antibiotic therapy. Likewise, persistent mastoid
mucosal disease or granulation tissue can be a cause of tympanostomy
tube otorrhea refractory to antibiotics. Mastoidectomy in either of
these settings can be helpful in eradicating otorrhea. Long-term
chronic mastoiditis usually results in sclerosis of the mastoid air cell
commonly seen in CSOM. A key element in the differential diagnosis of
chronic mastoiditis can be skull base osteomyelitis, otherwise known
as malignant otitis externa. Malignant otitis extema is classically seen
in diabetics or renal failure patients. It usually presents with a several
month history of otalgia with or without otorrhea or chronic otitis
extema. Focal osteomyelitis is seen adjacent to granulation tissue in
the external auditory canal. CT imaging demonstrates bone destruction
in the area of osteomyelitis. This topic is discussed more fully
elsewhere in this text.
Masked Mastoiditis
This term is sometimes applied to the rare situation where granulation
or mucosal disease involves some mastoid air cells when there is a
normal tympanic membrane and an otherwise aerated middle ear and
mastoid air cell system. Other areas of infection and inflammation

respond to topical and systemic antibiotics; however, this localized

area does not. Osteitis and bone erosion can occur locally at the site of
the disease. Patients with masked mastoiditis have chronic mild or
moderate postauricular pain and mild postauricular tenderness.
Bezold Abscess
A neck abscess secondary to mastoiditis is called a Bezold abscess.
These are, typically in the upper neck, just deep to the
sternocleidomastoid muscle. They occur by exten- sion of an infection
in the mastoid tip, by osteitis, bone destruction, and direct extension,
or without bone erosion by venous propagation. A neck abscess can
also occur by suppurated lymph nodes related to mastoid pathology,
which is not a true Bezold abscess. Treatment involves surgical
drainage of the neck abscess, appropriate surgical management of the
temporal bone pathology, and paren- teral antibiotics.
Petrositis (Petrous Apicitis)
Petrositis or petrous apicitis is, as the name implies, an infection of the
apex of the petrous portion of the temporal bone and is exceptionally
rare. The petrous apex is contiguous with the middle ear space, and
may be aerated, sclerotic, or consist of diploic bone. Infection occurs in
the petrous apex by direct extension from the middle ear and, like in
the mastoid, can consist of mucosal disease, granulation tissue,
purulence, or coalescence. Petrous apicitis may be associated with any
of the other complications of OM. Due to its location, extension of
infection from the apex may also result in cavernous sinus
Petrous apicitis typically presents with deep, retro-orbital pain in
the setting of COM. The classic triad originally described by Gradenigo
consists of retro-orbital pain, otorrhea, and abducens palsy, although
abducens palsy is rarely seen. Other manifestations can include facial
paralysis, and sensory hearing loss and vertigo due to labyrinthitis.
CT imaging, with or without MR imaging, defines the nature and
location of the disease. Treatment consists of parenteral antibiotics and
surgical drainage. Surgical access to the petrous apex is difficult, and
the route taken depends on the highly variable nature of temporal
bone anatomy. Depending on the specific anatomy, access to the
petrous apex may be obtained via the retro-labyrinthine, infracochlear,
or subarcuate air cell tracts. In some cases, it may be necessary to
perform a canal wall down mastoidectomy or possibly a middle cranial

fossa approach to access this area.

Labyrinthine Fistula
Labyrinthine fistula consists of the erosive loss of otic capsule bone
with exposure of the interior of the labyrinth. These fistulae occur
almost exclusively secondary to cholesteatoma. The matrix of the
cholesteatoma covers the exposed perilymphatic space; therefore,
there is no leakage of perilymph as seen in perilymphatic fistulae.
Labyrinthine fistulae from cholesteatoma most commonly involve the
horizontal semicircular canal, but can involve any of the canals, the
vestibule, the cochlea, or even the internal auditory canal. In addition
to the bone of the labyrinth, cholesteatoma can erode any bone to
which it comes in contact, commonly including the fallopian canal and
the tegmen tympani. The mechanism of bone erosion due to
cholesteatoma is the subject of considerable investigation and is
discussed in other chapters of this text.
Labyrinthine fistula is frequently asymptomatic and only
discovered on CT imaging or at surgery. Whenever CT demonstrates a
labyrinthine fistula preoperatively, erosion of the fallopian canal or
tegmen tympani should also be considered. If symptoms are present,
they consist of vertigo with Valsalva or straining, motion-or positionprovoked vertigo, Tullio phenomenon (vertigo secondary to auditory
stimuli), vertigo with manipulation of the auricle or EAC, and varying
degrees of hearing loss. Fistulae are usually clearly delineated on CT,
which should always be obtained preoperatively when fistula is a
Proper management of the underlying cholesteatoma is the basis
of treatment of labyrinthine fistula and is dis- cussed elsewhere in this
text. In brief, the matrix of the cholesteatoma can be left over the
fistula when the cholesteatoma is being exteriorized. If the
cholesteatoma is being removed, the matrix must be very carefully
dissected from the fistula and the fistula covered with a soft tissue
graft. Risks of vestibular dysfunction and hearing loss in this setting
are significant. Successful management of labyrinthine fistula usually
improves vestibular symptoms.
Facial Nerve Paralysis
After mastoiditis, facial nerve paralysis is the second most common
complication of AOM. Less commonly, facial paralysis presents as a
complication of COM-virtually always due to cholesteatoma. In either of

these settings, the facial paralysis is secondary to neurapraxia. In AOM,

this is due to inflammation and edema from the adjacent infection. In
COM with cholesteatoma, this is usually due to compression by the
cholesteatoma, with or without local inflammation. Facial paralysis can
also be associated with coalescent mastoiditis, masked mastoiditis,
or petrous apicitis.
AOM typically involves the facial nerve in its tympanic segment.
Although there is no study clearly demonstrating this, it is thought that
most cases of facial paralysis with AOM have dehiscent fallopian canals
in the tympanic segment, which is a common finding in otherwise
normal temporal bones. When facial paralysis occurs due to
cholesteatoma, the site of lesion depends on the anatomy of the
cholesteatoma. Most commonly, the nerve is compressed in the
tympanic segment, due to bone erosion by the cholesteatoma. Other
sites of injury include the geniculate ganglion region (anterior
epitympanic cholesteatoma), the mastoid segment (facial recess/sinus
tympani/ retrofacial cholesteatoma), or the internal auditory canal
(superior perilabyrinthine cholesteatoma). Cholesteatoma may not be
immediately recognized as the cause of cholesteatoma in these more
unusual locations.
Evaluation of facial paralysis associated with OM usually involves
directed imaging. Except perhaps in very straightforward cases of
facial weakness associated with AOM, dedicated temporal bone CT
imaging is very useful and will likely demonstrate the pathology and
site of lesion. MR imaging is helpful if lesions other than cholesteatoma
are considered. Electrophysiologic facial nerve testing is sometimes
useful. Electromyography (EMG), either evoked (electroneuronography)
or spontaneous (standard EMG), can be helpful in predicting prognosis
for recovery in some cases. This topic is fully discussed else where in
this text.
Management of facial paralysis associated with OM consists of
aggressive treatment of the underlying OM. In AOM, myringotomy with
cultures of the aspirate. and parenteral antibiotics are indicated. For
facial paralysis due to COM with cholesteatoma, topical and systemic
antibiotics followed by surgical management of the cholesteatoma are
appropriate. Systemic steroid therapy is probably helpful to reduce
inflammation and edema in the acute phases of facial paralysis for any
type of OM. Surgical decompression of the fallopian canal, proximal
and distal to the site of injury is advocated by some. and may be
helpful in selected cases.

Serous or Toxic
Serous labyrinthitis is thought to be due to alteration of the inner ear
tissue fluid environment due to bacterial toxins. Bacterial toxins are
presumed to enter the inner ear via the round or oval window, or via a
labyrinthine fistula. Variable degrees of vertigo and sensory hearing
loss can result. Treatment with appropriate antibiotics and steroids is
probably helpful. Recovery of hearing and vestibular unction is possible
in serous labyrinthitis. Endolymphatic hydrops can be seen
pathologically associated with serous labyrinthitis.
Otogenic suppurative labyrinthitis consists of bacterial invasion of the
inner ear from a suppurative process within the middle ear. This acute
suppurative process results in rapid destruction of inner ear contents,
with associated severe vertigo and sensory hearing loss. In the early
phases, it is not possible to discern serous from suppurative
labyrinthitis-subsequent recovery of hearing and/or vestibular function
indicates that the process was serous in nature. Treatment consists of
parenteral antibiotics (choose drugs with good cerebrospinal fluid
penetration) and timely surgical intervention aimed at preventing
additional extracranial or intracranial complications.
A particular concern with suppurative labyrinthitis is the
development of meningitis. A suppurative process within the labyrinth
can gain access to the subarachnoid space via the fundus of the
cochlea or the cochlear aqueduct. Indeed, otogenic sources are
thought to be a common etiology of bacterial meningitis in childhood.
Conversely, suppurative meningitis may extend into the labyrinth and
result in a secondary suppurative (meningogenic) labyrinthitis. In
either direction, this phenomenon underlies the frequent association
between meningitis and hearing loss. Ossification of the labyrinth
(labyrinthitis ossificans) is frequently seen following suppurative
labyrinthitis, particularly due to S. pneumoniae, and can complicate
cochlear implantation. Early evaluation of hearing following meningitis
and early cochlear implantation when appropriate can result in
substantially better outcomes for patients with post-meningitic
Intracranial Complications

Bacterial meningitis presents with severe generalized headache, fever,
nausea/vomiting, photophobia, and varying levels of altered mental
status (ranging from irritability to unconsciousness). Patients may
develop nuchal rigidity, characterized by pain and limitation of neck
flexion. With progression of disease, papilledema and abnormal
reflexes may develop, including Kernig sign (inability to completely
extend the knee when the leg is flexed at the hip) and Brudzinski sign
(passive neck forward flexion leads to active flexion of the hip and
The clinician evaluating a patient with meningitis should attempt
to identify the route of spread to the meninges and the organism
involved. All patients with meningeal signs should undergo otoscopic
examination to rule out AOM and CSOM. Most cases of otogenic
meningitis in children result from hematogenous dissemination of
invasive organisms during AOM (most commonly S. pneumoniae). Of
note, the introduction of routine vaccination against S.pneumoniae and
H. infiuenzae type B has decreased the rate of meningitis secondary to
these common causative agents-recent reports suggest that brain
abscess may supplant meningitis as the most common intracranial
complication of OM. The presence of otitic meningitis, particularly if
recurrent, should raise suspicion for an abnormal route of
communication from the middle ear and mastoid to the CSF. The rapid
onset of meningitis with AOM in a child with sensorineural hearing loss
may indicate the presence of an inner ear malformation that allows
communication through the oval or round windows to the vestibule,
cochlea, and internal auditory canal. Accordingly, temporal bone
imaging may reveal Mondini malformation, enlarged vestibular
aqueduct, common cavity malformation, or congenital stapes footplate
fixation. Similarly, AOM can lead to rapid onset of meningitis in
patients with CSF leaks associated with tegmen dehiscences
(congenital or iatrogenic), meningoencephaloceles through the middle
or posterior fossae, or through a patent tympanomeningeal fissure.
Bacterial contamination of the CSF may also occur with AOM following
surgical or traumatic dural injury, stapes subluxation, or cochlear
implantation. Patients with meningitis associated with CSOM should be
suspected of having bacterial extension of infecting organ- isms
directly through the dura. Additionally, it is possible for bacteria to
enter the meninges through the labyrinth by a cholesteatoma induced

Lumbar puncture (LP) is performed to confirm the clinical

diagnosis and identify the causative organism. CT or MRI should be
obtained first to identify findings suggestive of increased intracranial
pressure that might predispose to herniation with LP as well as to rule
out intracranial abscess, subdural empyema, or cerebritis. Meningitis
typically leads to elevation of the opening pressure, and the CSF has
high protein, low glucose, and an increased white blood cell content
leading to a cloudy appearance. The CSF should be sent for Gram stain
and culture. As cultures from the CSF and middle ear may differ,
samples should also be taken at the time of myringotomy to assist in
selection of antibiotic therapy. High-resolution CT of the temporal bone
will delineate bony architecture and reveal inner ear malformations,
tegmen defects, and destructive lesions. MRI should be obtained in all
cases to identify additional intracranial complications.
Acute bacterial meningitis associated with AOM is treated with
myringotomy (wide-field or with PE tube placement to maintain
drainage) and intravenous antibiotics. A third-generation cephalosporin
and vancomycin should be instituted empirically while awaiting culture
results that will direct further therapy. Despite effective antibiotic
treatment, about one-third of meningitis survivors suffer neurologic
sequelae such as deafness, behavioral disorders, and cognitive
dysfunction. Dexamethasone, started with or before the first dose of
antibiotics, has been shown to significantly reduce the rates of death
and hearing loss in patients with pneumococcal meningitis, without
interfering with antimicrobial treatment. While most cases do not
require further surgery, inner ear malformations (Mondini) and clear
sources of CSF leak- age (meningoencephalocele) require repair at the
conclusion of meningitis treatment to prevent further infection.
Continuation of antibiotics in the perioperative period is wise in these
When meningitis results from subacute or CSOM, the ear disease
needs to be surgically managed. Direct disease extension into the
meninges has often occurred and it is important to expose the
diseased dura, remove excess dural granulation tissue, and inspect for
dural defects or occult abscesses. The timing of the mastoid operation
is dictated by the patient's neurologic and physiologic condition, and is
generally performed once the patient is deemed stable to undergo
Extradural (Epidural) Granulation Tissueor Abscess

Granulation tissue and abscess may form between the temporal bone
and adjacent dura when acute coalescent infection or chronic otitis
with or without cholesteatoma erode surrounding bone. Pockets of
infection then expand along the face of the posterior or middle fossae.
Epidural granulation tissue and abscesses may present with headache
and fever, but are often clinically silent until large. Contrast-enhanced
CT may reveal erosion of the sigmoid plate or tegmen and, in cases of
larger extradural abscesses, a rim-enhancing lentiform epidural fluid
collection. Enhanced MRI is superior to CT in demonstrating small
intracranial suppurative lesions. An epidural abscess appears as a
crescentic fluid collection that is mildly hyperintense relative to CSF on
T1-weighted images and isointense to CSF on T2-weighted images.
Epidural abscess is often a precursor to other complications that can
be identified with MRI including lateral sinus thrombophlebitis and
brain abscess.
Management of extradural granulation tissue and abscess begins
with intraoperative identification. Extradural abscesses may be missed
unless care is taken to observe the dura of the middle and posterior
fossae through thin bone. The mastoidectomy should be extended to
allow for careful inspection of the dura of the tegmen tympani, tegmen
mastoideum, sigmoid sinus, and posterior fossa bone medial to
Trautmann triangle. Bone overlying abnormal dura should be removed
until normal dura is encountered. Granulation tissue may be carefully
removed with a blunt elevator, scraping parallel to the plane of the
dura. A portion of granulation tissue may be left behind to avoid dural
penetration and CSF contamination. If an abscess is identified,
exposure via removal of the overlying bone suffices for drainage.
Brain Abscess
Otogenic brain abscesses may arise from AOM or COM. Cholesteatoma
has supplanted AOM as the cause of most cases. The infection is
typically polymicrobial with a relatively high proportion of anaerobes.
Venous thrombophlebitis allows bacteria to spread from the mastoid to
the brain parenchyma.
A brain abscess has four clinical stages. The first stage is
invasion (initial cerebritis), during which the destructive brain infection
may present with a low-grade fever, malaise, drowsiness, loss of ability
to concentrate, and headache. These symptoms are subtle and
frequently over-looked and may spontaneously resolve after several
days. The second stage, localization (latent or quiescent abscess),

when the tissue becomes necrotic and edematous, may be clinically

silent and last for weeks. During the third stage, enlargement
(manifest abscess), an actual abscess forms in the region of the
previous cerebritis. Patients may present with high fever, headache,
focal neurologic symptoms, or loss of consciousness. Abscesses of the
temporal lobe may present with seizures, visual field deficits, and
hemiparesis. Cerebellar abscesses may present with vertigo,
nystagmus, ataxia, and dysmetria. In the fourth stage, termination
(rupture of the abscess), the abscess capsule ruptures into the
ventricle or into the subarachnoid space. This results in a rapidly
progressive, frequently fatal, outcome.
Diagnosing a brain abscess at an early stage may be difficult and
calls for a high level of clinical suspicion when confronted with signs of
a possible impending complication (Table 149.4). CT and MRI with
gadolinium will identify a hypointense centerwith a hyperintense
capsule about a formed abscess. MRI offers additional precision in
identifying extraparenchymal (intraventricular or subarachnoid)
spread. Diffusion-weighted MR imaging may be used for abscess
surveillance and to distinguish abscesses from ring- enhancing
malignancies. Since brain abscesses can take several weeks to
manifest, even ifan initial MRI is negative, repeat scanning should be
considered in 2 to 3 week intervals if the index of suspicion remains
Management of a brain abscess requires immediate broadspectrum parenteral antimicrobial therapy and neurosurgical
consultation. If surgical treatment of the brain abscess is
recommended it takes priority over management of the otologic
disease. A surgical approach to treat the ear disease can be
undertaken once neurologic stability has been achieved with
antibiotics, aspiration, open drainage, or abscess excision.
Subdural Empyema
Subdural empyema is a purulent infection that has formed between
the dura and the pia-arachnoid membranes. The subdural space may
be seeded via venous channels or infection in adjacent bone or brain. It
is the rarest complication of OM. Because of the mass effect and the
dose proximity to the cerebral cortex, symptoms progress rapidly and
patients present with severe headache, marked focal neurologic
deficits, seizures, and loss of conscious- ness. Meningeal signs are

CT with intravenous contrast may miss early subdural abscesses but

can detect larger lesions as hypodense extracerebral collections with
an enhancing medial border. Contrast-enhanced MRI is more sensitive
and may readily demarcate the enhancing rim and extension of
infection. Lumbar puncture may precipitate herniation in this setting
and should be avoided if the lesion is detected by imaging first.
Subdural empyema is a neurosurgical emergency. Treatment of
subdural abscess requires emergent drainage and the institution of
parenteral antibiotics. Treatment of the associated ear disease is
accomplished after neurologic stabilization.
Sigmoid Sinus Thrombophlebitis
Sinus thrombophlebitis may develop when overlying coalescent
infection, granulation tissue, or cholesteatoma incites sinus wall
inflammation. The sigmoid sinus is most susceptible because of its
prominent location adjacent to the mastoid air cells. Retrograde
thrombosis of cerebral veins (Labbe) and sinuses (transverse, sagittal,
petrosal, and cavernous) may result in dangerous degrees of
intracranial hypertension, brain abscess, infarct, and death. The
thrombus may propagate to the internal jugular vein and jugular bulb,
generating septic emboli and/or a jugular foramen syndrome. While
AOM remains a common inciting factor in children, COM with
cholesteatoma is an increasingly frequent cause in adults and older
pediatric populations. Prothrombotic factors, including elevated levels
of lipoprotein apolipoprotein, antibodies to beta 2-glycoprotein and
cardiolipin, and heterozygosity for factor V Leiden mutation, may
predispose patients to sigmoid sinus thrombophlebitis during AOM.
Modem antibiotic therapy has decreased the incidence of
sigmoid sinus thrombosis and altered the typical clinical presentation.
In regions and circumstances in which AOM and COM go untreated,
sigmoid sinus thrombosis may present with the rapid onset of
prominent otologic symptoms (otorrhea, otalgia, postauricular
pain/erythema), severe headache, torticollis, and the classic highspiking picket fence" fever of sepsis with leukocytosis. When there is
greater access to care, patients often have a history of AOM or COM
that was treated with antibiotics in preceding weeks and may have
only mild symptoms. Headache and unilateral neck pain are still
common, but fevers may be low grade and leukocytosis may be
absent. The symptom duration is longer (often more than 2 weeks) and
neurologic symptoms are more prevalent, including diplopia from CN VI

palsy and symptoms of intracranial hypertension (headache, nausea,

neck stiffness, photophobia, dizziness/ataxia). Nevertheless, the
otoscopic examination is usually abnormal, revealing AOM, effusion,
retraction, or signs of COM. Recent series demonstrate that
bacteriology may diverge from beta-hemolytic Streptococcus and S.
pneumoniae to include mixed infections with Pseudomonas,
Enterococcus, Proreus, and anaerobes.
After a careful otologic examination, the diagnosis is confirmed
with imaging studies. Head and temporal bone CT, with contrast will
reveal associated pathology in the mastoid and perisinus
enhancement. The enhancement of the triangular sinus wall around
non-enhancing intraluminal thrombus produces the pathognomonic,
delta sign in up to one-third of cases. MRI with MRV/MRA is more
sensitive in detecting sigmoid sinus thrombosis and delineates the
extent of the thrombus and the integrity of collateral circulation while
also identifying other intracranial complications.
The treatment of lateral sinus thrombophlebitis entails prompt
initiation of broad-spectrum antibiotics combined with surgery. A wide
myringotomy is performed or a pressure equalization tube is placed.
Mastoidectomy is performed to expose the inflamed sinus wall and
diseased dura and to remove excess granulation tissue. Subperiosteal
and epidural abscesses can be treated concomitantly. The opinions of
experienced surgeons differ over the extent of additional surgery that
is necessary, ranging from none to sinus resection. The bone over the
sinus and surrounding dura may be removed and the sinus may be
care- fully aspirated to detect free blood flow. Venotomy may be
performed for the evacuation of infected thrombus or intraluminal
abscess. Some have advocated Fogarty catheter thrombectomy be
used with caution to reestablish flow, after gaining control of the
internal jugular vein in the neck. The authors consider this unwise due
to the potential of releasing emboli and rupturing the sinus
intracranially. Ligation of the internal jugular may be considered in the
presence of septic emboli. Recanalization has been observed in
patients receiving a range of treatments, from nonsurgical medical
management, mastoidectomy; and venotomy with or without
thrombectomy. Currently, there is no dear evidence that a given
treatment approach is superior to another in its ability to reduce
recovery time and increase the likelihood of recanalization.
The use of anticoagulation to prevent thrombus propagation is also a

matter of debate. It is unlikely to be of benefit when the thrombus is

isolated to the sigmoid sinus, but it should be considered in patients
with imaging evidence of thrombus progression or extension to
additional sinuses, neurologic changes, embolic events, or persistent
fevers despite surgical intervention. The risk of bleeding can be
significant particularly in the pediatric population. Thrombolytics are
not recommended as they may dislodge septic emboli in infected
vessel walls.
Otitic Hydrocephalus
Otitic hydrocephalus is defined as increased intracranial pressure
without ventricular dilatation, meningitis, or intracranial abscess in
patients with acute or chronic middle ear infection. Increased
intracranial pressure may manifest with headache, nausea and
vomiting, papilledema, and diplopia from ipsilateral abducens nerve
(cranial nerve VI) palsy.
The etiology of otitic hydrocephalus is hypothesized to be
diminished CSF resorption by arachnoid granulations secondary to
thrombosis in a dominant lateral dural venous sinus. Modern imaging
has demonstrated that sagittal sinus thrombosis is not a necessary
precursor, but inadequate cross-communication at the torcula with
occlusion of the dominant outflow tract may impairvenous drainage
sufficiently to raise intracranial pressure.
MRI with MRV readily identifies lateral sinus thrombosis with total
occlusion. If lumbar puncture is deemed safe based on central imaging,
opening pressure will be elevated, but CSF studies will reveal normal
biochemistry and cytology. Patients should undergo neuroopthalmologic examination.
Treatment of otitic hydrocephalus requires mastoidectomy
appropriate for the disease, exposure of all diseased dura to normal
dura, and removal of excess extradural granulation tissue.
Management of sigmoid sinus thrombophlebitis is discussed above.
The treatment additionally involves medically lowering intracranial
hypertension and careful monitoring for reductions in visual fields and
acetazolamide, mannitol, furosemide, and/or repeat lumbar puncture.
As resolution of symptoms is observed in patients even in the setting
of persistent lateral sinus thrombosis, recovery from otitic
hydrocephalus is purported to be secondary to development of
compensatory collateral venous drainage. Thus, management often

extends for months beyond the initial surgical approach to the sinus
and ventriculoperitoneal shunts may be necessary to reduce intracranial hypertension on a long-term basis. Failure of these measures to
reverse progressive visual deterioration necessitates fenestration of
the optic nerve sheath.