neely jg n bailey
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Head & Neck Surgery - Otolaryngology
4th Edition
2006 Lippincott Williams & Wilkins
138
Intratemporal and Intracranial Complications of
Otitis MediaJ. Gail Neely
H. Alexander Arts
Evaluation and DiagnosisDef in i t i on and Classi f icat ionA complication of otitis media is defined as spread of infection beyond the
confines of the pneumatized spaces of the temporal bone and their attendant
mucosa (1). The four intratemporal and six intracranial complications
characteristically considered during discussion of this topic are addressed in
this chapter.Table 138.1lists these complications.
PathophysiologyDetails of the pathophysiology in each of these complications of otitis media are
unknown, and because of their rarity, no systematic studies have been
undertaken in most of these complications. However, these complications stilldo arise even today in the United States and other developed countries at rates
similar to underdeveloped countries (2).
It is important to understand the anatomy in which these infections exist, their
routes of spread, and the characteristic patterns of disease. However, the
primary pathogene sis seems to be a comp lex interaction among the speci fic
organisms involved and the host (3). An important host response leading to
complication is the production of granulation tissue that becomes obstructive to
drainage and aeration and destructive of bone and the consequent development
of an anaerobic environment. Important microbiologic factors seem to pivot
about the synergistic pathogenicity of anaerobic organisms ( 4). Occasionally,the excessively invasive characteristics of Haemophi lu s inf luenzaetype B
become impo rtant .
Precur sors to Compl i cationsEarly clinical signs of an impending complication provide some information
about the pathogenesis (Table 138.2). With the exception of meningitis, most
complications originate from subacute or chronic infection ( Table 138.3).
Therefore, it is important to be alert to the persistence of an acute infection
beyond 2 weeks or the recurrence of symptoms wi thi n a 2 - to 3-week pe riod,
which suggests that the infection is not controlled and is becoming subacute.
Additionally, an acute exacerbation of a chronic infection ma y allow an invasiveacute infection to penetrate previous bony barriers that have been eroded by
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chronic infection and granulations. Fetid discharge concomitant with an acute
exacerbation suggests an uncontrolled deep-seated bone erosive infection and
increased numbers of anaerobic and microaerophilic organisms.
The epidemiology and microbiologic behavior of the organisms found in
complications offer perhaps some insight into the pathogenesis and
pathophysiology of these complications (Table 138.4). For example, infections
with Streptococcus pneumoniae and nontypable H. inf luenzae are the most
common causes of acute suppurative otitis media ( 5). Only about 4% of otitis
media is caused by infection
P.2042
with H. inf lue nzaetype B; however, pediatric patients with otitis media
occurring simultaneously with meningitis or other central nervous system
infections were found to have an unusually high incidence of H. inf luenzae type
B (6).
TABLE 138.1 COMPLICATIONS OTITIS MEDIA
I.
Intratemporal
A. Mastoiditis (most common intratemporal complication from acute otitis
media)
1. Associated with subperiosteal abscess
2. Associated with inferior deep neck abscess (Bezold)
3. Masked mastoiditis
B.
PetrositisC.
Labyrinthitisa
1. Serous or toxic
2.
Suppurative
a. Otogenic
Acute
Chronic
b. Meningogenic
D. Facial paralysis (second most common intratemporal complication from
acute otitis media)
1. Associated with acute infection
2.
Associated with subacute or chronic infection
II.
Intracranial
A. Extradural granulation tissue and/or abscess (most common intracranial
complication from chronic infection)
B. Sigmoid sinus thrombophlebitis
1. Nonoccluding
2.
Occluding
C. Brain abscess1.
Cerebritis
2. Latent period
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3. Abscess
4.
Termination
D. Otitis hydrocephalus (associated with occluding sigmoid sinus
thrombophlebitis)E. Meningitis (most common intracranial complication from acute otitis
media)
1. Associated with acute infection
a. Hematogenous
b. Associated with congenital CSF leaks through otitic
capsule (e.g., severe Mondini), adjacent to otic capsule
(e.g., geniculate ganglion, Hyrtle fissure), or distant to
otiticcapsule (e.g., meningoencephaloceles) (16)
c.
Poststapedectomy or postcraniectomy or posttraumatic
CSF leaks
2.
Associated with subacute or chronic infectiona.
Dural erosion
b. Cholesteatoma labyrinthine fistula
F.
Subdural abscess
CSF, cerebrospinal fluid.aSchuknecht HF. Pathology of the ear, 2nd ed. Philadelphia: Lea & Febiger, 1993.
Uncomplicated chronic otorrhea characteristically cultures Ps eu domonasaeruginosa, Staphylococcus aureus , and a variety of other gram-negative
organisms, such as Proteu s sp., Klebs iella sp., and Escher ichi a col i In contrast,
mastoiditis associated with chronic suppurative otitis media frequently is foul
smelling and in addition contains Ba cteroides fr agi lis (5). Multiple organisms
are found in 57% of chronically draining ears with cholesteatoma, with an
average of three different organisms. However, if these ears are foul smelling,
characteristically 5 to 11 organisms are found, always including both anaerobes
and aerobes. Malodorous discharge is a significant early sign of complication.
Anaerobic organisms are a major cause of foul-smelling discharge. Moraxella
catarrhalis , previously a reasonably uncommon organism in the middle ear, isemerging as a common pathogen for acute suppurative otitis media ( 5).
-Lactamase-producing organisms, such as S. aureus, H. influenzae, B.
catarrhalis , and Bacteroide s 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
(3,4).
TABLE 138.2 EARLY SIGNS OF COMPLICATION
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Impending complicationPersistence of acute infection for 2 weeks
Recurrence of symptoms within 2 weeks
Acute exacerbation of chronic infection, especially if fetidFetid discharge during treatment
Haemophilus influenzaetype B or anaerobes
Early or obvious signs/symptoms of complication (associated complication) Fever associated with a chronic perforation (intracranial complication or extracranial
cellulitis)
Pinna displaced inferolaterally and/or edema of the posterosuperior canal wall skin
(mastoiditis associated with subperiosteal abscess)
Retroorbital pain on side of infected ear (petrositis)
Vertigo and nystagmus in a patient with an infected ear (labyrinthitis)Facial paralysis on the side of an infected ear (facial paralysis)
Headache and/or lethargy (intracranial)
Papilledema (otitic hydrocephalus; brain abscess; meningitis)
Meningismus (meningitis)
Focal neurologic signs and/or seizure (brain abscess)
Catastrophic neurologic signs (subdural abscess; meningitis)
P.2043
Patterns of DiseaseComplications tend to follow fairly predictable patterns; for example, with the
exception of meningitis in infants and young children and some cases of facial
paralys is, which may be associ ated wi th acut e su ppurative ot itis media, mos t
complications tend to be associated with subacute or chronic middle ear
infection (Table 138.3). In subacute or chronic infections, mastoiditis
characteristically is the initial complication. Petrositis is almost never seen
without mastoiditis. Facial paralysis and labyrinthine fistulization most often
result from chronically infected ears with cholesteatoma. The close proximity of
the sigmoid sinus to the large air cells adjacent to its lateral surface, which aremost distant from the eustachian tube, makes it particularly susceptible to bone-
eroding granulations in a subacutely or chronically infected ear. Infection
adjacent to the dura of the sigmoid sinus may incite an intraluminal mural
thrombus (7). If in the presence of infection, the sigmoid sinus becomes
obstructed, intracranial hypertension, known as otitic hydrocephalus, may
result. Retrograde thrombophlebitis may extend intracerebrally, resulting in a
brain abs cess. Subdural abscesses from sup purat ive ear disease are ex tremely
rare; these abscesses are most often found in infants with meningitis. The
meningitis, of course, can result from suppurative ear disease.
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TABLE 138.3 PATTERNS OF DISEASE
Origin of complication
Acute infectionMeningitisinfants and young children
Meningitisadults or children with occult CSF leaks
Facial paralysischildren more commonly
Labyrinthitis
Subdural abscessinfants more commonly
Subacute or chronic infection
Mastoiditis
Petrositis
Facial paralysis
Labyrinthitis
Extradural abscess and granulations
Sigmoid sinus thrombophlebitis
Brain abscess
Otitic hydrocephalic
Meningitis
Subdural abscess
Patterns of associated diseases in usual sequenceMastoiditis or petrositis
Extradural granulation tissue and/or abscess
Sigmoid sinus thrombophlebitisBrain abscess or otitic hydrocephalus
Meningitis
Subdural abscessinfants more commonly
CSF, cerebrospinal fluid.
Diagnosis
High Index of SuspicionThe diagnosis of an impending or manifest intratemporal or intracranialcomplication of otitis media is contingent on a high index of suspicion. 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. If the patient is not improving sufficiently with medical
management, radioimaging followed by any necessary surgical procedure is the
required course of action (8). Key to the differential is the discovery of a host
response or microorganism deviation from the usual
P.2044
onset, progression, and recovery of a noncomplicated infection ( Tables
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138.2and 138.5). The presence of any one of the five conditions listed in Table
138.2suggests the possibility of an impending complication and requires
diligence in attempting rapid resolution of the infection and follow-up of the
patien t to normalcy.
TABLE 138.4 BACTERIOLOGYa,b
Acute suppurative otitis media (in order of prevalence)
1. Streptococcus pneumoniaemost common2.
Haemophilus influenzae(nontypable)
3. Moraxella catarrhalis(emerging common pathogen)
4. Others, far less common
a.
Group A streptococci
b.
Staphylococcus aureus(infrequent)c.
Gram-negative bacilli (infrequent)
Acute mastoiditis (in order of prevalence)
1. Streptococcus pneumoniae
2. Pseudomonas aeruginosa(6)
3. Group A beta-hemolytic Streptococci(e.g., Streptococcus pyogenes)
4. Coagulase-negative Staphylococcusspecies
5.
Others, less commona. S. aureus
b. Proteusspecies
c. Bacteroidesspecies
Chronic otorrhea with or without cholesteatoma (in order of prevalence)
1. Mixed aerobic (also occasionally including S. pneumoniae) and anaerobic
organisms
a.
Foul-smelling ears (especially cholesteatomas) may grow 511organisms; always anaerobes andaerobes
2. Pseudomonas aeruginosa(most common aerobe)
3. S. aureusand Staphylococcus epidermidis
4. Other aerobic organisms, includingProteusspecies,Klebsiellaspecies,
andEscherichia coli
5.
Various anaerobic organisms, includingBacteroides fragilis
Intracranial abscesses (brain and subdural) of otogenic origin (mixed cultures)
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Streptococcussp.
Staphylococcussp.
Proteussp.
Anaerobic organisms (Peptococcus, Peptostreptococcus, B. fragilis)
Bacterial meningitis in childrenS. pneumoniae
H. influenzaetype B
Neisseria meningitidis
aFairbanks DN.Antimicrobial therapy in otolaryngologyhead and neck surgery, 11th
ed. Alexandria, VA: American Academy of OtolaryngologyHead and Neck Surgery
Foundation, 2003.
bPhillips EJ, Simor AE. Bacterial meningitis in children and adults. Changes in
community-acquired disease may affect patient care.Postgrad Med1998;103(3):102
122.
Obvious or Generalized Suggestive SignsWhen faced with a list of 10 possible complications, of which several may
coexist, it is helpful to approach the menu of possibilities using several initial
filters of thought and observation (Table 138.2).
1. The first filter is obvious complications consisting of mastoiditis with
concomitant subperiosteal abscess, labyrinthitis, facial paralysis, and
meningitis. That narrows the list from 10 to 7. Pinna displacement
inferolaterally and edema of the posterior superior canal wall skin are
highly suggestive of mastoiditis; their absence, however, does not rule
out masked mastoiditis. Vertigo and nystagmus in a patient with an
infected ear suggest serous or suppurative labyrinthitis with or without a
labyrinthine fistula from cholesteatoma (chronic labyrinthitis). Facial
paralys is on the side of an inf ected ear strong ly suggests that in fection isthe cause of the paralysis. Meningismus is an obvious sign of meningeal
irritation and is easily detected, except in infants and in the elderly or
debilitated patient.
2. The second filter is retroorbital pain. This filter narrows the list of 7
down to 6. A patient with petrositis has retroorbital pain but usually does
not have abducens paralysis, which is the third of the triad of Gradenigo
syndrome. The absence of retroorbital pain reasonably tends to obviate
the diagnosis of petrositis. However, retroorbital pain is not a symptom
that most patients spontaneously report; it must be specifically elici ted.
P.2045
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Additionally, petrositis can result i n other regions of referred unexplained
head pain.
3. The third filter is symptoms and signs of subdural abscess.
Characteristically, subdural infection creates both a mass effect and an
irritative focus and results in catastrophic rapidly progressive neurologic
signs and symptoms. The fact that subdural abscesses are so rarely
associated with ear infecti ons and, when present, are so catastrophic tends
to reduce the list down to 5.
4. The fourth filter is generalized evidence of increased intracranial
pressur e, or fo cal neu rolog ic lesions. Headache and lethargy are early
signs of intracranial complications. Papilledema is an obvious sign of an
intracranial complication with increased intracranial pressure; however, it
may easily go undetected unless the examiner does a funduscopic
examination. Focal neurologic signs, seizures, or catastrophic neurologicsigns such as coma are obvious signs of intracranial complications. Fever
in association with a chronically draining ear is an early sign of
intracranial complication or extracranial cellulitis.
TABLE 138.5 DIAGNOSIS SUBTLE DISEASE
Masked mastoiditis
Persistent or recurrent pain 2 weeks after specific antibiotic treatment in ear
with nonair-containing mastoid
Radiographic evidence of coalescence
Extradural granulation tissue and/or abscess
Exposure during surgery
Sigmoid sinus thrombophlebitis
MRI intensity signal changes with time and technique in sinus
Exposure during surgery
Brain abscess
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During initial cerebritis
Headache and lethargy for 35 days, spontaneous recovery
MRI evidence of localized cerebral edema
During latent period
Almost impossible to diagnose, even with MRI
During manifest abscess
Focal neurologic deficit and/or seizure
MRI evidence of enhancing hyperintense area surrounding ahypointense center
Otitic hydrocephalus
Headache and lethargy
Severe papilledema
No evidence of meningitis
No evidence of brain abscess on MRI
Documentation of increased intracranial pressure
MRI, magnetic resonance imaging.
Systemati c Appr oach(Tables 138.2,138.3,an d138.5)MastoiditisMastoiditis may present in association with a subperiosteal abscess, commonly
lateral to the mastoid cortex, medial to the concha of the pinna, and rarely into
the neck through the medial tip cells as in Bezold abscess. It may also present
as masked mastoiditis. The advent of antibiotics has made the diagnosis and
definition of mastoiditis more difficult. Classically, the term mastoiditisreferred to acute coalescent mastoiditis with subperiosteal abscess lateral to the
mastoid cortex occurring 2 weeks after onset of acute suppurative otitis media.
The patient would be febrile and, in some cases, toxic; radiographs would
demonstrate extensive bone destruction in t he mastoid region of pneumatization,
characteristically lateral to the sigmoid sinus. Just before extensive
subperiosteal abscess formation, marked edema, erythema, and tenderness over
the mastoid postauricularly and sagging of the posterosuperior canal wall skin
from edema were found. Classically, patients with chronic mastoiditis presented
with fetid purulent chronic discharge, boring pain, and occasional radiographic
evidence of irregular lytic lesions in the temporal bone lateral to the sigmoidsinus surrounded by hyperostotic areas. Today, the signs and symptoms may be
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much less obvious; antibiotics may obscure the presentations but may not
prevent the compl ica tion (9). Persistent or recurrent pain may be the only
symptom or sign of masked mastoiditis. Computed tomography (CT) has
expanded our ability to identify early bone-destructive lesions in the mastoid.
However, meningitis, facial paralysis, brain abscess, otitic hydrocephalus,
sigmoid sinus thrombophlebitis, and extradural abscess all may occur with little
or no CT evidence of bone destruction.
The best diagnostic algorithm is based on the comparison of the expected
clinical course and an appreciation that complications progress medially much
more often than laterally. A person with acute suppurative otitis media should
be expected to respond wi thin 3 to 5 days to appropr iate ant ibioti c th erapy;
within 2 weeks, the purulent-appearing effusion in the middle ear should
convert to a more seromucinous appearance. The ear should clear and aerate
within 1 to 3 months without recurrence of symptoms. There should be no
post erosuperi or canal wall ski n ed ema nor pos tauri cular ede ma or tenderne ss
and certainly no subperiosteal abscess displacing the pinna inferolaterally.If there is no response to antibiotics within the first week, mastoiditis should be
considered possible. If there is postauricular edema, subperiosteal abscess, or
recurrence of paineven mildwithin 2 to 3 weeks after onset of acute
suppurative otitis media, mastoiditis should be considered imminent. Risk
factors for complications also include a more rapidly aggressive course than
expected, younger age, and radiographic evidence of previous significant
infections with resultant hyperostosis (sclerosis).
If these ominous signs appear, myringotomy for culture and sensitivity for
aerobes and anaerobes and high-resolution CT of the temporal bone should be
done. Appropriate antibiotic therapy for 2 to 3 weeks and close periodicexamination, usually on a weekly basis, are necessary until the patient and the
mastoid x-ray films have completely reverted to normal. It is not an unusual
event for the
P.2046
middle ear to clear with myringotomy and antibiotics and for the mastoid to
remain opacified and nonair containing. This condition continues to raise the
specter of masked mastoiditis behind an obstructed aditus ad antrum or
tympanic isthmus. If symptom free, the patient may be followed longer;
however, if symptoms, such as deep boring but subtle pain are present,mastoidectomy may be considered. Magnetic resonance imaging (MRI) with
gadolinium may be useful to detect early extradural abscess formation and
sigmoid sinus thrombophlebitis.
Chronic mastoiditis with osteitis should be suspected when persistent fetid
discharge is found despite local and s ystemic treatment. If the discharge persists
despite treatment after 2 weeks, a diagnosis of chronic mastoiditis with osteitis
should be presumed. High-resolution CT may be helpful to identify subtleties of
osteitic bone destruction, but it is usually disappointing. MRI with gadolinium
may identify early deeper complications; however, in most cases, the diagnosis
is made clinically, and surgical intervention is appropriate at this point.Petrositis
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Petrositis has become exceptionally rare, but still occurs, even in the classic
triad of Gradenigo, that is, retroorbital pain, abducens paralysis, and ipsilateral
acute or chronic otitis media. Petrositis may occur even in a nonpneumatized,
sclerotic, or diploic petrous apex. Diagnosis of petrositis is made in a similar
fashion to that of mastoiditis, with the additional symptom of retroorbital pain
and evidence of petrous apex bone distructions. Abducens paralysis is extremely
rare and is not necessary to make the diagnosis.
LabyrinthitisLabyrinthitis characteristically is viral-induced endolabyrinthitis and is not
potent ially fatal. However, lab yrint hitis seconda ry to mi dd le ea r infect ion can
be fatal if suppurat ive labyrinthi tis and, subsequ en tly, meningi tis occu r.
Therefore, each call from the emergency department to see a patient in whom
severe vertigo and hearing loss occur simultaneously requires the clinician to
determine whether the middle ear is normal. Experimental and human
experience with acute and chronic otitis media reveals serous labyrinthitis and
endolymphatic hydrops are fairly frequent complications of suppurative middleear disease. However, suppurative labyrinthitis is extremely rare and potentially
fatal. These conditions may occur together or separately. Cholesteatomas may
erode the otic capsule, creating perilymph fistulae that may cause mechanical
cochlear effects, serous labyrinthitis, and a preformed pathway for acute
infection to enter the labyrinth; therefore, vertigo in the presence of a
cholesteatoma must be evaluated immediately and very carefully.
Until recently, diagnosis of labyrinthitis was made on clinical grounds. Serous
labyrinthitis, in which toxic or metabolic products of bacteria or the host
inflammatory response enter the inner ear through the round window membrane
or cholesteatoma-induced fistula, results in sensorineural loss and vertigo withnystagmus. However, the degree of loss is not total, and some recovery is
possible. Conversely, sup pur at ive lab yrinthitis from the ent ran ce of bacteria
into the labyrinth through the same route creates similar s ymptoms but profound
losses that never resolve and result in extensive inner ear and spiral ganglia cell
loss. Hegarty et al. (10) have found evidence of labyrinthine disease by
contrast-enhanced MRI; this technique may prove to be helpful in the future to
confirm the presumptive diagnosis of labyrinthitis.
Facial ParalysisThe major diagnostic challenge in facial paralysis from the suppurative ear
disease is to identify the possibility of a nerve-destructive lesion versusneuropraxia from toxicity or slight compression and edema. Facial paralysis
from acute suppurative otitis media may not be destructive. However, facial
paralys is in the pr esence of a sub acute inf ection , acut e coa lescent mastoi ditis,
masked mastoiditis, petrositis, or chronic suppurative otitis media, with or
without cholesteatoma, may well be destructive, particularly in the tympanic
segment.
The typical topognostic techniques for site-of-lesion identification are useful to
confirm the intratemporal site of lesion. Degree-of-lesion techniques, such as
the nerve excitability test, the maximum nerve excitability test,
electroneurography, and electromyography, are extremely important, althoughimperfect, tools to identify a nerve-destructive lesion. MRI with gadolinium is
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useful in identifying neoplastic and inflammatory lesions of the facial nerve but
as yet cannot determine the degree of lesion. The most useful tool of all is a
detailed careful history of the patients current illness and past medical history
of ear disease with a specific attempt to define the exact pathophysiology that
may be involved with each case. It is probably prudent to err on the side of
assuming a nerve-destructive lesion when in doubt and plan to explore the
nerve.
Cholesteatoma is by far the most common cause of facial paralysis. The lesion
characteristically is most common in the tympanic and upper mastoid segments;
however, the labyrinthine segment also may be involved in deep petrous
cholesteatomas. Degeneration and inflammation are variably present in the
localized area of the facial ner ve and may be partially or more rarely completely
destructive of the facial nerve. Granulation tissue that invades the epineurium is
more dangerous than cholesteatoma matrix; granulation tissue may infiltrate
between ne rv e fibe rs and , if surgi cally pursue d, may result in tra ns ecti on of the
nerve.Extradural Granulation Tissue or AbscessIn our experience and that of others, extradural granulation tissue or abscess can
be, and usually is, compl etel y occult pr eope rative ly ( 2). Even intraoperatively,
huge extradural abscesses may be missed unless painstaking care is
P.2047
taken to observe the dura of the middle fossa and posterior fossa, particularly
over the sigmoid sinus, through thin bone. It is not necessary to remove the
bone co mpl etel y to see whether the dura is normal or abnormal. If the re is any
question or if the dura appears abnormal, it is necessary to remove the bone andinspect the dura directly. In every case of operable disease, extradural
granulation tissue should be expected.
MRI is proving to be superior to CT in demonstrating intracranial suppurative
lesions and may ultimately prove to be able to identify small collections of
extradural granulation tissue and abscess. Larger extradural empyemas
demonstrate a hypointense rim representing displaced dura adjacent to a
hyperintense collection.
Sigmoid Sinus ThrombophlebitisLateral or sigmoid sinus thrombophlebitis may be totally asymptomatic or may
be associ ated wi th the classic intermitten tly spiki ng (pi cket fen ce) fever,gross signs of toxemia, torticollis, and septic embolization. The thrombus can
rarely propagate into the internal jugular vein and jugular bulb, creating a
jugu lar foramen syndr om e or be as sociated wi th retro grade thrombos is of
cerebral veins, leading to brain abscess and/or infarction ( 11). Should the vein
of Labb be thrombosed, speech and language deficits might occur; severe
neurologic consequences, such as coma or death might follow. Prothrombotic
factors, such as elevated levels of lipoprotein apolipoprotein [Lp(a)], antibodies
to beta 2-glycoprotein and to cardiolipin, and heterozygosity for factor V
Leiden mutation, may predispose patients to sigmoid sinus thrombosis during
acute otitis media (12 ). If the sinus is obstructed, it can create serious degrees
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of intracranial hypertension. It is associated with overlying granulation tissue or
cholesteatoma.
MRI with and without gadolinium has proved to be an exceptionally good
diagnostic tool to identify at least major degrees of sigmoid sinus
thrombophlebitis by the presence of increased intraluminal signal on all planes
with all pulse sequences.
Brain AbscessDiagnosing a brain abscess may be difficult or impossible, depending on the
stage of abscess formation and its clinical presentation. It may present with
fever, headache, and seizures but is usually not so obvious. A manifest abscess
may present as a seizure, loss of consciousness, or a focal neurologic deficit.
The abscess may be associated with increased intracranial pressure.
A brain abscess has four clinical stages. A wide range of excellent CT, MRI,
gross, and histologic images may be found through Google, image tab, brain
abscess (http://www.google.com). The first stage is invasion (initial
encephalitis), manifested by low-grade fever, drowsiness, or loss of ability toconcentrate, and headache associated with a general feeling of malaise. These
symptoms are subtle and frequently overlooked and spontaneously resolve after
several days. The second stage, localization (latent or quiescentabscess), is
clinically silent, with no symptoms and possibly lasting for weeks. During the
third stage, enlargement (manifest abscess), an actual abscess forms in the
region of the previous cerebritis and produces focal symptoms of a mass lesion,
seizures, or loss of consciousness. In the fourth stage, termination (rupture of
the abscess), the abscess ruptures into the ventricle or into the subarachnoid
space. This results in a rapidly progressive, frequently fatal, outcome.
CT and MRI with gadolinium easily identify a hypointense center with ahyperintense capsule about a formed abscess. MRI offers additional precision in
identifying extraparenchymal (intraventricular or subarachnoid) spread of the
abscess. Newer sequences such as diffusion-weighted magnetic resonance
imaging (DW-MRI) have proven to be useful in detection and surveillance of an
abscess (13,14).
The real dilemma is in having a high enough index of suspicion to obtain an
MRI to detect the developing abscess in stages I or II or to detect an
asymptomatic manifest abscess in stage III. Again, the most useful tool is a
careful, thoughtful history and physical examination with attention to clinical
indicators that suggest an impending complication, which can easily include abrain abs cess (Table 138.2). If there is any suspicion that a complication may be
occurring, an MRI is advised. Because brain abscesses take several weeks to
manifest, the examiner should remember that if an MRI was ordered initially, a
repeat MRI should be done 2 to 3 weeks later and, occasionally, again 2 to 3
weeks after the second time if the index of suspicion remains high.
Otitic HydrocephalusOtitic hydrocephalus is defined as increased intracranial pressure secondary to
acute or chronic middle ear infection without evidence of meningitis or subdural
or brain abscess. It characteristically presents as headache and lethargy in a
patien t wi th an ear infection. MRI easily ident ifi es si gmoi d sinus thrombo sis
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with total occlusion. Papilledema is most often present; however, papilledema is
not always an adequate predictor of increased intracranial pressure.
MeningitisBacterial meningitis with its three clinical and associated cerebrospinal fluid
(CSF) stages is fairly easy to diagnose because of its presentation of headache,
fever, neck rigidity, and abnormal reflexes such as Kernig (inability to
completely extend the leg) or Brudzinski (active flexion of the hip and knee
when the neck is passively forward flexed) sign.
The major diagnostic dilemma is to identify the route of spread to the meninges
and the organism involved with otologic-associated meningitis. Most cases are
in children and occur by hematogenous dissemination of invasive
P.2048
organisms such as H. inf luenzae type B. Pneumococcal m eningitis and otitis
media are usually considered concomitant manifestations of a systemic infection
(15 ). However, in a child with rapid onset of meningitis within hours of anacute suppurative otitis media in which the offending organism is S.
pneumoniaeor nontypable H. inf luen zae and in which the child has a unilateral
or bilateral congenital sensorineural hearing loss and possible vestibular deficit,
a Mondini malformation should be suspected. These malformations allow
abnormal communication from the middle ear to the CSF through the stapes
footplate or round window to the vestibule or cochlea, respectively, and
ultimately the internal auditory meatus. They are easily identified on high-
resolution CT. Adults similarly presenting with rapid onset of meningitis and
acute suppurative otitis media in ears with normal hearing or conductive hearing
loss must be suspected of having a communicating meningoencephalocelethrough the middle fossa or, occasionally, the posterior fossa dura or an occult
CSF leak about the geniculate ganglion or through a patent Hyrtl
(tympanomeningeal) fissure (16 ,17).
Adults or children with meningitis associated with chronic suppurative otitis
media should be suspected of having extension of infecting organisms directly
through the dura. Meningitis has been reported following acute otitis media
following stapedectomy and following cochlear implantation ( 18 ,19).
Additionally, it is possible for bacteria to enter the meninges through the
labyrinth by a cholesteatoma-induced fistula.
Subdural AbscessSubdural abscesses are rare but are much more common with sinusitis than with
otitis media. Because of the mass effect and the close proximity to cerebral
cortex, marked focal irritative neurologic deficits, seizures, and rapid loss of
consciousness may be the presenting symptoms; more subtle presentations can
occur.
CT with intravenous contrast can detect these lesions as hypodense (but more
dense than CSF) extracerebral collections with an enhancing medial border;
however, these may be missed with CT. MRI without contrast may show these
as low intensity on T1-weighted images and high intensity on T2-weighted
images. However, MRI with intravenous gadolinium (GD-DTPA) is more
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sensitive to detect these lesions and tends to demarcate the abscess as a rim of
enhancement (20).
BacteriologyThe final step in diagnosis in all complications is the identification of the
specific organisms involved in both the ear and in the complication ( Table
138.4). It is important to remember that cultures from the discharge from the
external auditory canal, middle ear, and mastoid and the intracranial
complication may differ; therefore, independent and systematic cultures from
these various sites, as t hey become available, are important in guiding antibiotic
therapy.
ManagementManagement of complications of otitis media is the identification of each
organism involved in both the ear and other sites with the complication,
followed by culture-specific antibiotics and surgery for the ear and the
complication (Table 138.6). The primary objectives of treatment are t o eradicate
the infecting organism, to remove destructive a nd obstructing granulation tissue,
and to promote drainage in both the ear and the site of complication. Initial
antibiotics suggested for site of complications are listed in Table 138.6. The
patien t is prompt ly admitted to the ho spita l, and an tibioti cs are adm in istered
parenterally. Mastoidectomy appropriate for the ear disease, as seen in Table
138.6,refers to the three major categories of surgical approaches to and through
the mastoid: intact canal wall technique with facial recess approach to the
middle ear; modified radical mastoidectomy in which at least the eustachian
tube and usually the complete middle ear are separated from the external
environment by a fascia graft; and radical m astoidectomy in which the tympanic
membrane, malleus, incus, and posterior and superior osseous canal wall have
been remov ed and no t recon st ruct ed. The techn ique us ed in a specif ic cas e is
best left to the experienc e and judgment of the su rgeon invo lved and the
particu lar nuances of the case.
It is important to remember that unusual diseases, such as Wegener
granulomatosis, blastomycosis, tuberculosis, neoplasia, fungi, and histiocytosis
X, especially in the immunocompromised patient, can present as bacterial
complications. Therefore, laboratory studies and tissue biopsy are more than
just rou tine in the mana gement of th esepat ients.
M astoidit i sControversy exists as to whether all cases of acute mastoiditis require surgical
intervention. There is evidence that medical treatment alone can result in an
appropriate outcome. However, there is compelling evidence derived from the
study of complications of suppurative ear disease that more serious or fatal
complications can arise from inadequately treated or diagnosed infections,
especially if follow-up is inadequately astute. Therefore, it is advised that
surgically skilled and experienced otologic surgeons be consulted in these cases.
Certainly surgical intervention in cases of chronic mastoiditis is necessa ry.
PetrositisLateral transmastoid, perilabyrinthine approaches to exenterate disease and
drain the petrous apex are usually sufficient to resolve the infection. However,
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if clinical signs and symptoms of persistent infection continue, a middle fossa
approach to the petrous apex may be necessary.
TABLE 138.6 TREATMENT COMPLICATIONS OF OTITIS MEDIA
Initial antibiotics (5,34)Appropriate initial antibiotics, followed by culture-specific antibiotics for the ear and
the complication
Acute (subacute) mastoiditis from acute otitis media
Vancomycin IV plus ceftriaxone (Rocephin) IV
Mastoiditis from chronic otitis media
Ciprofloxacin PO with or without clindamycin
Piperacillin/tazobactam IV (Zosyn)
Meningitis or intracranial complication from acute otitis media (34)
Ceftriaxone
Meningitis or intracranial complication from chronic mastoiditis (34)
Cefotaxime
Surgery and other treatmentAcute or subacute mastoiditis
Large myringotomy
Mastoidectomy, intact canal wall technique with large facial recess approach to
middle ear and removal of middle ear granulations
Chronic mastoiditis
Tympanoplasty and mastoidectomy, intact canal wall technique, with large
facial recess approach to middle ear and removal of middle ear granulations and
cholesteatoma, if present
Tympanoplasty and modified radial mastoidectomy and removal of middle ear
granulations and cholesteatoma, if present
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Petrositis
Lateral, transmastoid, perilabyrinthine approaches to the deep petrous infectedsite
Middle fossa, extradural approaches, with or without lateral approaches, to
otherwise unreachable or recalcitrant deep petrous infected site
Labyrinthitis from acute otitis media
Myringotomy
Labyrinthitis from subacute or chronic infection
Mastoidectomy (appropriate for the ear disease and experience of the surgeon)
Petrosectomy, if necessary
Repair of labyrinthine fistula, if present
Facial paralysis from acute otitis media
Myringotomy
Facial paralysis from subacute or chronic infection
Mastoidectomy (appropriate for the ear disease)
Exploration of facial nerve to thinned fallopian canal bone and/or to nerve
epineurial sheath. DO NOT OPEN NERVE SHEATH, ESPECIALLY
PERINEURIUM.
Petrosectomy, if necessary
Extradural abscess/granulations
Mastoidectomy (appropriate for the ear disease)
Exposure of all diseased dura to normal dura
Removal of pus and excess dural granulations. DO NOT PERFORATE DURA.
Sigmoid sinus thrombophlebitis
Mastoidectomy (appropriate for disease)
Exposure of all diseased dura to normal dura
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Removal of excess extradural granulations
Palpate sinus, extraluminally. Small needle aspiration may be appropriate for
further diagnosis. DO NOT PERFORATE MEDIAL DURAL WALL.
It is not ordinarily necessary to open sinus to remove clot; however, if pus insinus, it may be necessary to evacuate pus, trying not to establish blood flow
If demonstrated emboli from sinus (rare), it may be necessary toevacuate septic
thrombus and anticoagulate (23)
Otitic hydrocephalus
Treatment of sigmoid sinus thrombophlebitis
Lower intracranial hypertension
Monitor vision carefully
Brain abscess
Mastoidectomy (appropriate for disease)
Exposure of all diseased dura to normal dura
Removal of excess dural granulations
Evaluation of dural integrity
Concomitant neurosurgical consultation for management of brain abscess; often
antibiotics only
Meningitis from acute otitis media
Myringotomy
Repair of Mondini malformation (with intralabyrinthine fasciaand cartilage oval
window occlusion to hold fascia) or meningoencephalocele (with intracranial
fascia and cartilage tegmen defect occlusion to hold fascia), if present (rare)
Meningitis from subacute or chronic infection
Mastoidectomy (appropriate for disease)
Exposure of all diseased dura to normal dura
Removal of excess dural granulations
Evaluation of dural integrity; repair of dural defect if present (rare)
Subdural abscess from acute otitis media
Myringotomy
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Neurosurgical consultation for management of subdural abscess
Subdural abscess from subacute or chronic infection
Mastoidectomy (appropriate for disease)
Exposure of all diseased dura to normal dura
Removal of excess dural granulations
Neurosurgical consultation for management of subdural abscess
IV, intravenous; PO, by mouth.
P.2049
Labyr in th i t isThe treatment of labyrinthitis from acute otitis media is focused on clearing the
middle ear infection as rapidly as possible with antibiotics and with
myringotomy. Labyrinthitis from subacute or chronic infection requires
exenteration of middle ear and mastoid disease. Cholesteatoma matrix over
fistulae of the semicircular canals may be removed if extreme care is taken not
to tear the membranous labyrinth. It should be noted that deep fistulae or thoseinto the cochlea may not result in a good outcome and may destroy the ear if the
cholesteatoma matrix is removed. Leaving a small piece of matrix on the fistula
and returning at a later date in a sterile ear, or marsupializing the area, may be a
more appropriate way of managing these difficult cases. However, hearing
P.2050
deterioration still may occur. It is prudent to cover these patients
prophylactically with antibi ot ics in an at tempt to avoid sup pu rative labyrinthi tis
and meningitis.
F acial Paralysi sTreatment of facial paralysis from acute otitis media is directed at clearing the
middle ear infection as rapidly as possible with antibiotics and myringotomy.
Usually more extensive treatment is not necessary, unless the infection persists
or there is evidence of neural degeneration.
In most cases of subacute or chronic infection, particularly with evidence of
neural degeneration, surgical intervention is necessary. Early intervention is
important for a good outcome (21). The purpose of the surgery is to clear the
middle ear and mastoid infection as rapidly as possible and to remove
granulations near the facial nerve. To do this, thinning the fallopian canal bone
to a point where the sheath may be inspected through thin bone is important. Ifthe sheath is involved with cholesteatoma or granulation tissue, careful removal
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of this cholesteatoma matrix or granulation tissue is worthwhile. It should be
emphasized that removing granulation tissue, which can be interspersed among
nerve fibers, can easily cause surgical destruction of the complete cross-section
of the nerve. To avoid this, resection deeper than the plane of the most lateral
surface of the nerve is not recommended. Because the nerve sheath, particularly
the perineurium, is a barrier to infection and because neural tissue, per se, lacks
resistance to infection, it is very important not to incise the sheath of the nerve.
Ex tr adur al Abscess or Granul ation Ti ssueManagement of extradural granulation tissue and abscess begins with discovery.
It depends on a careful inspection of the dura of the tegmen tympani, tegmen
mastoideum, sigmoid sinus, and posterior fossa bone medial to Trautmann
triangle (22 ). The dura may be properly inspected by thinning the bone
carefully; the bone does not need to be removed to identify normal or abnormal
dura. However, it is imperative to extend the mastoidectomy to these limits;
simply sculpturing the bone along the plane of the tegmen and sigmoid sinus is
not satisfactory. If the dura appears normal in these areas, no additional work is
necessary. If the dura is abnormal, the bone should be removed over the
abnormal dura until normal dura is encountered. If an abscess is encountered,
exposure satisfactorily drains the abscess. Excess granulation tissue should be
removed with a blunt instrument, scraping parallel with the plane of the dura.
Care must be taken not to perforate the dura; some granulation tissue will
necessarily be left. No further surgical treatment is necessary.
Sigmoid Sin us Th rombophl ebit i sThe treatment of sigmoid sinus thrombophlebitis, partially obstructive or totally
obstructive, is predominantly to expose diseased dura and remove excess
granulation tissue. If otitic hydrocephalus is present from a totally obstructed,
inflamed sigmoid sinus, the treatment additionally involves lowering
intracranial hypertension and monitoring vision carefully (discussed later in the
section onotitic hydrocephalus). The presence of a septic thrombus, or one that
releases septic or aseptic emboli, is unusual. In these situations, carefully
aspirating or opening the sigmoid sinus and evacuating the septic and friable
thrombus may be appropriate; care must be taken not to violate the medial dural
sinus wall. If bleeding from the proximal sigmoid sinus occurs, it can usuall y be
controlled by extradural compression of the sinus with Surgicel placed between
the bone of the sigmoid sulcus and the most lateral aspect of the dural sinus.
Ligation of the internal jugular vein to avoid further embolization of tissue ormaterial used to control surgical bleeding might be required. Intraluminal
Surgicel can be sparingly used if necessary, but only after ligation of the
internal jugular vein has been performed; however, it may increase sepsis in
severely infected cases. Ligation or hemostatic stapling of the sinus may be
done but usually results in CSF egress from the puncture holes, which is usually
inadvisable in infected cases . The use of heparin may be helpful ( 23).
Br ain AbscessManagement of brain abscess requires surgical intervention in the ear and
treatment of the brain abscess, with neurosurgical consultation. Surgical
treatment of the brain abscess, such as aspiration, may occur simultaneously
with the surgical approach to the ear, or it may precede the ear surgery if the
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intracranial problem is of such severity that it would best be done first.
Increased intracranial pressure may occur. In these cases, it is probably prudent
to lower the intracranial pressure and aspirate the abscess before surgical
approach to the ear. Intravenous antibiotics are the predominant treatment of
brain abs cess and are oc casionall y recommended as the ex cl us ive treatment .
However, shorter hospital stays, better isolat ion of the offending organisms, and
better early and long -term resul ts may be ob tained by ant ibiotics and a surgi cal
approach to the abscess.
Surgical approaches to the abscess include aspiration, open drainage, and
excision. It is generally thought that aspiration is satisfactory, except in cases in
which air is found within the intracranial abscess; air within the abscess is
indicative of a direct extension from a pneumatized space to the abscess. In
cases of direct extension, CT-guided, percutaneous, transmastoid drainage of the
abscess has been effective. Epilepsy and epileptic foci may occur and seem to
be more frequ ent after excis ion of the abscess; thus, anticonvul sa nt proph ylaxis
may be appropriately considered.
Otit i c Hydr ocephalusTreatment of otitic hydrocephalus requires mastoidectomy appropriate for the
disease, exposure of all diseased dura
P.2051
to normal dura, and removal of excess extradural granulation tissue. A gentle
insertion of a hypodermic syringe or a small opening of the sinus may be
advisable to identify an int raluminal septic thrombus or abscess. This thrombus,
however, is often identifiable from the clinical picture of a high, spiking,
intermittent fever, although a masked abscess is possible. Usually, the thrombusis highly organized and fibrotic. It is not advisable to attempt to do a
thrombectomy, except enough to evaluate an abscess, because of the potential of
releasing emboli and rupturing the sinus intracranially. If intraluminal partial
thrombectomy is necessary, the internal jugular vein must be ligated. Generally,
managing the mastoid is all that is required surgically. Management of otitic
hydrocephalus extends for months beyond the initial surgical approach to the
sinus. It is designed to medically lower intracranial hypertension and monitor
the patients condition carefully for progressive blindness and brain herniation;
a ventricular shunt may be required.
Initial treatment with acetazolamide, prednisone, and repeated lumbar puncturesmay not satisfactorily lower the intracranial hypertension. Furosemide and
mannitol tend to act synergistically, result in more rapid lowering of
intracranial pressure, and remain in effect for a longer period of time than either
agent used alone. The combined use of mannitol and intermittent withdrawal of
CSF fluid also creates some synergism. However, the effect of mannitol may
last for only about 4 hours, and the effect of CSF withdrawal may lower the
pressure fo r onl y about 1 hour. High -dose ba rbiturates have been found to
effectively lower resistant intracranial hypertension ( 24 ). Percutaneous lum-
bope ri ton eal shu nts are effective on a long -term basis for reducing int racrani al
hypertension. Occasionally, all these measures, including lumboperitonealshunting, fail to reverse progressive visual deterioration; in these cases,
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fenestration of the optic nerve sheath has proved to be effective ( 25). In rare
situations, a venous bypass from one lateral sinus to the jugular vein might
prove to be effect ive (26).
Monitoring visual change in these patients includes monitoring not only visual
acuity but visual fields. Occasionally, visual field reduction precedes visual
acuity change.
M eni ngi t i s fr om Acute Oti t i s M ediaIntravenous antibiotics and myringotomy are the mainstays of treatment for
acute bacterial meningitis associated with acute otitis media. However, in
instances in which a Mondini malformation or a spontaneous
meningoencephalocele is diagnosed, repair of the Mondini malformation or
meningoencephalocele is necessary toward the end of the meningitis treatment.
It is probably prudent to extend the treatment a little longer to cover the
periop erati ve peri od .
Despite effective antibiotic treatment, about one third of meningitis survivors
suffer neurologic sequelae such as behavioral disorders, mental retardation, and
deafness, which are thought to be caused by inflammatory mediators such as the
cytokines. Dexamethasone has recently been shown to reduce these
inflammatory sequelae and not to interfere with antibiotic treatment ( 27 ).
M eni ngi t i s fr om Subacuteor Chr onic M astoidi t isIn meningitis from subacute or chronic mastoiditis, a direct extension into the
meninges is more often the case; thus, resistant gram-negative and anaerobic
organisms are encountered. Third-generation cephalosporins, especially
intravenous ceftriaxone (Rocephin) and cefotaxime (Claforan), penetrate the
bloodbrain barrier we ll and are go od ini ti al choi ces (5,28).
Surgically, it is important to exenterate the ear disease carefully, expose all
diseased dura, and remove excess dural granulation tissue. It is also imperative
to carefully inspect the dura that is diseased for perforation and to evacuate any
immediately associated abscesses on either side of the dura. The timing and
planni ng of the se op erations , concomitant ly or sequentiall y, imm ediately or
delayed, necessarily must be done by the otologic surgeon and neurosurgeon.
Small dural repairs, even in the face of infection, can easily be done through the
middle ear and mastoid during initial surgery.
Subdur al AbscessThe management of subdural abscess from acute otitis media consists in
clearing the ear infection as rapidly as possible with intravenous antibiotics and
myringotomy and treating the subdural abscess. Subdural empyemas from
subacute or chronic ear infections require mastoidectomy, appropriate for the
disease, and careful exploration on the dura with removal of excess granulation
tissue. Treatment of subdural abscess usually requires drainage from separate
burr holes or craniotomy and definitely the ins titut ion of lon g-term parent eral
antibiotics.
Complications of TreatmentTable 138.7summarizes possible complications of treatment.
Compl i cations of I nadequate An tibi otics or D r ainage
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Complications arising from treatment are predominantly those of omission,
inadequate treatment, or missed diagnoses. The resulting complications can be
one or more of the 10 complications of suppurative ear disease. It is important
to remember that undertreated complications are more likely to extend medially
into the intracranial cavity than externally.
TABLE 138.7 COMPLICATIONS TREATMENT
Inadequate treatment or failure to treat
aggressivelyMastoiditis
Subperiosteal abscess
Osteitis/osteomyelitis of skull
Petrositis
Facial paralysis
All intracranial complications
Petrositis
Osteitis/osteomyelitis of skull
Carotid rupture
Facial paralysis
All intracranial complications
Labyrinthitis
Progressive sensorineural hearing
loss
Delayed endolymphatic hydrops
Benign paroxysmal positional
vertigo
Suppurative labyrinthitis
Meningitis Facial paralysis
Facial paralysis
Permanent destruction of facialnerve
Labyrinthine fistula
Extradural granulation and/or abscess
Complications of surgical
exenteration and drainageDuring myringotomy
Canal skin laceration
Excessive laceration of
tympanic membranes
Fracture of ossicles
Laceration of jugular bulb
Laceration of internal carotid
artery
Oval or round window
traumatic fistula
Facial nerve laceration
Meningitis
During mastoidectomy
Wound infection
Dural perforation
Cerebrospinal otorrhea or
rhinorrhea
Brain herniation
Laceration of sigmoid sinus
Facial nerve contusion or
laceration
Ossicular disruption
Sensorineural hearing loss Labyrinthine fistula
Excessive blood loss
During petrosectomy
Same as mastoidectomy, with
increased risk
Laceration of internal carotid
artery
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All intracranial complications
Sigmoid sinus thrombophlebitis
Propagation of thrombus to sagittal
sinus and/or internal jugular vein
Pulmonary emboli
Brain abscess
Otitic hydrocephalus
Brain abscess
Meningitis
Ventriculitis
Brain herniation
Diffuse cerebritis/multiple
abscesses
Seizure disorder
Focal neurologic deficits
Death
Otic hydrocephalus
Blindness
Brain herniation
Death
Meningitis
Brain abscess
Subdural abscess Retardation
Deafness
Multiple neurologic deficits
Death
Subdural abscess
Seizures
Coma
Temporal lobe infarction
During facial nerve exploration
Same as mastoidectomy, with
increased risk
Total destruction of facial
nerve
During management of labyrinthine
fistula by cholesteatoma
Deterioration of inner ear if
matrix remains
Sudden loss of inner earfunction during matrix removal
Meningitis
During labyrinthectomy
Certain loss of hearing and
unilateral balance function
Same as mastoidectomy, with
increased risk, especially facial
nerve injury
During lumbar puncture
Brain herniation
Spinal headache
Lower extremity neural deficit
Meningitis
During removal of dural granulation
tissue
Cerebrospinal otorrhea
Meningitis
During sigmoid sinus exploration
Hemorrhage externally
Hemorrhage into posterior
fossa
Cardiac or pulmonary emboli
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Local neurologic deficits
Meningitis
Death
Air emboli
During aspiration of brain abscess
Meningitis
Ventriculitis
Cerebritis
Intracerebral hemorrhage
During subdural drainage
Meningitis
Cerebral contusion or
infarction
P.2052
P.2053
Compl i cations of Sur ger y
The second group of complications of treatment are those secondary to surgicalexenteration and drainage procedures ( Table 138.7). All the complications that
may arise from middle ear and mastoid surgery may certainly occur in addition
when treating these complications. However, because of the extensive nature of
the disease, which includes excessive granulation tissue and unusual patterns of
bone ero sion, the surgical ris ks are increas ed bo th to t he struct ures wit hi n the
temporal bone and to those within the cranium. A few of these complications
deserve special mention.
Excessive Blood LossExcessive blood loss, particularly in children, can be an unexpected
complication from mastoidectomy. The granulation tissue can be extremelyvascular in acute or subacute mastoiditis, and 250 to 300 mL of blood can be
lost rapidly during the course of mastoidectomy. This blood loss continues until
all the granulation tissue is removed. If the anatomy, or the skill of the operator,
hinders rapid mastoidectomy and if excessive blood loss is still occurring, it is
probabl y most pr ud en t to stop the op eration at tha t point and return at a later
date after the antibiotics have had a longer period during which to wor k.
Brain HerniationBrain herniation deserves special mention, both as a potential complication of
disease or as a complication of diagnostic or therapeutic intervention. It is well
known that lumbar puncture in the presence of elevated intracranial pressure,particu larl y with evide nc e of a mass lesi on, can result in res pirat or y arrest,
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cervical cord compression, transtentorial herniation with cerebral and brainstem
compression, and infarction. Papilledema is not always an adequate predictor of
dangerous intracranial hypertension or a possible complication from lumbar
punc tu re. Seve ral imp ortan t landmarks see n on CT or MRI that help identify
patien ts at risk for bra in herni ation are lateral shi ft of midline st ructures, loss of
suprachiasmatic and basilar cisterns, obliteration of the fourth ventricle, and
obliteration of the superior cerebellar and quadrigeminal plate cisterns with
sparing of the ambient cistern. Immediate neurosurgical attendance during any
necessary lumbar puncture in these cases is prudent.
Brain herniation is diagnosed by MRI or CT, demonstrating such things as
herniation of the cerebellar tonsils into the foramen magnum, herniation of the
temporal lobe, uncus herniation filling the homolateral perimesencephalic
cistern, and the disappearance of the perimesencephalic cistern. Auditory
brains tem responses and parti cularl y somatosen sor y evo ked potentials ha ve also
been foun d to be sens itive to increased int ra cranial pr essur e; seve re brain inj ury
may occur if intracranial pressure exceeds 30 mm Hg, which requiresdecompression within 1.5 hours (29 ). Some of the effective measures to reduce
intracranial hypertension are discussed under the section on management
ofotitic hydrocephalusearlier in this chapter.
Pulmonary EmboliPulmonary emboli, a very rare potential complication of sigmoid sinus
thrombophlebitis, may manifest suddenly and catastrophically with
cardiovascular and respiratory collapse; on the other hand, onset may be subtle.
Ventilation-perfusion scanning using radioisotope-labeled gases has become the
standard of early diagnosis. Pulmonary angiography is reserved for
confirmation. Anticoagulation is appropriate. Thrombolysis is not usuallyrecommended (30).
Air EmbolismAir embolism is possible during manipulation of the sigmoid sinus. Air
embolism during surgery can result in coma and seizures, a variety of
decerebrate conditions, cortical blindness, and cardiovascular and pulmonary
collapse with significant lung injury. Air embolism creates sudden right heart
failure, which may intraoperatively respond to occluding the venous bleeding,
turning the patient onto the left side, placing the table in Trendelenburg,
aspirating air from the central venous catheter, flooding the wound with saline,
giving 100% oxygen and stopping nitrous oxide administration, possiblyadministering dobutamine or ephedrine, and providing supportive measures for
hypotension and arrhythmias (31 ). The mainstay of longer treatment is
hyperbaric oxygen administered as rapidly as possible.
EmergenciesTable 138.8summarizes emergencies that can arise in suppurative ear disease.
Def in i t ionAll the complications of suppurative ear disease represent emergencies.
However, a few emergencies require special mention. In these conditions,
immediate assessment or treatment is required to avoid or minimize significant
morbidity or mortality. These may be considered true emergencies.
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Emergent Pr esentati on of D i sease
Vertigo and Nystagmus with Ear InfectionThe patient presenting with acute vertigo, nystagmus, and associated decrease in
hearing must be evaluated immediately for the presence or absence of middle
ear or mastoid infection. If such infection is present or if a cholesteatoma is
present , there is an immediate po ten ti al fo r sup pu rative lab yrinthi tis fol lo wed
by meni ngi tis withi n mi nutes to hours. It is not po ssib le to in itially sepa rate
serous
P.2054
labyrinthitis from suppurative labyrinthitis, and it is not possible to presuppose
with confidence that suppurative labyrinthitis will not occur. Affected patients
should be immediately admitted to the hospital and placed on appropriate
antibiotic therapy and local care to the ear as previously mentioned. As the
condition resolves, the patient may be allowed to leave the hospital on
continued therapy, if necessary.
TABLE 138.8 EMERGENCIES SUPPURATIVE EAR
DISEASE
Vertigo and nystagmus with ear infection
Labyrinthitis
Facial paralysis with ear infectionHeadache and lethargy/coma
Brain abscess
Otitic hydrocephalus
Meningitis
Subdural abscess
Brain herniation with increased intracranial pressure
Seizure
Brain abscess
Meningitis
Subdural abscess
Focal neurologic deficits
Brain abscess
Subdural abscess
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Meningismus