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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.
Labyrinthitis
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.
Suppurative
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
deafness.
Intracranial Complications
Meningitis
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
knee).
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
fistula.
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),
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.