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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


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


12/33

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


17/33

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.


Mastoidectomy (appropriate for disease)



18/33

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)


Treatment of sigmoid sinus thrombophlebitis

Lower intracranial hypertension

Monitor vision carefully

Brain abscess



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




Evaluation of dural integrity; repair of dural defect if present (rare)

Subdural abscess from acute otitis media

Myringotomy


19/33

Neurosurgical consultation for management of subdural abscess

Subdural abscess from subacute or chronic infection




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


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


24/33



Propagation of thrombus to sagittal

sinus and/or internal jugular vein

Pulmonary emboli

Brain abscess


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


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


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


25/33

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


Meningitis

Subdural abscess

Brain herniation with increased intracranial pressure

Seizure

Brain abscess

Meningitis

Subdural abscess

Focal neurologic deficits

Brain abscess

Subdural abscess


28/33

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