Otolaryngol Clin N Am

39 (2006) 1237–1255

Complications of Chronic Otitis

Media and Cholesteatoma
Jason A. Smith, MD*, Christopher J. Danner, MD
Department of Otolaryngology–Head and Neck Surgery, University of Arkansas for Medical
Sciences, 4301 West Markham Slot #543, Little Rock, AR 72205, USA

Chronic otitis media (COM) is defined as persistent infection or inflam-

mation of the middle ear and mastoid air cells. This condition typically in-
volves a perforation of the tympanic membrane, with intermittent or
continuous otorrhea. As chronic otomastoiditis and eustachian tube dys-
function persist, the tympanic membrane is weakened, which increases the
likelihood of an atelectatic ear or cholesteatoma formation.
The proximity of the middle ear cleft and mastoid air cells to the intra-
temporal and intracranial compartments places structures located in these
areas at increased risk of infectious complications. Acute otitis media
(AOM) and its complications are more common in young children, whereas
complications secondary to COM with and without cholesteatoma are more
common in older children and adults. In a large series by Osma and col-
leagues [1], 78% of subjects who had complications secondary to COM
were found to have cholesteatoma.
The complications of AOM and COM, defined using the same classifica-
tion system, are divided into intracranial and extracranial complications;
extracranial complications are further divided into extratemporal and intra-
temporal complications. The development and appropriate use of antibi-
otics have led to a decrease in these potentially devastating complications.
However, they continue to occur, and clinical vigilance is required for early
detection and treatment. Furthermore, with the continued development of
multi–drug-resistant pathogens, these complications may again become
more prevalent as our current antibiotics become less effective [2].

* Corresponding author.
E-mail address: smithjasona@uams.edu (J.A. Smith).

0030-6665/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.otc.2006.09.001 oto.theclinics.com
1238 SMITH & DANNER

Extratemporal (extracranial) complications

Subperiosteal abscess
Subperiosteal abscess is the most common extratemporal complication
that occurs with COM. This abscess occurs over the mastoid cortex when
the infectious process within the mastoid air cells extends into the subperios-
teal space. This extension most commonly occurs as a result of erosion of
the cortex secondary to acute or coalescent mastoiditis, but can also occur
as a result of vascular extension secondary to phlebitis of the mastoid veins
[3]. Subperiosteal abscesses are seen more commonly in young children with
AOM, but are also found in chronic otitis with and without cholesteatoma.
Cholesteatoma can block the aditus ad antrum, preventing communication
of the infected contents of the mastoid with the middle ear space and the eu-
stachian tube. This obstruction increases the possibility of infectious decom-
pression through the mastoid cortex, presenting clinically as a subperiosteal
abscess or Bezold’s abscess.

Diagnosis
Often, the diagnosis of a subperiosteal abscess is made on clinical
grounds. Commonly, the patient will present with systemic symptoms, in-
cluding fever and malaise, along with local signs, including a protruding au-
ricle that is laterally and inferiorly displaced, and the presence of a fluctuant,
erythematous, tender area behind the ear. When the diagnosis is not certain
on clinical evaluation, a contrasted CT scan can demonstrate abscess and
possibly the cortical defect in the mastoid (Fig. 1) [4]. A case can be made
for a contrasted CT scan of the temporal bone in all patients presenting
with these symptoms, to aid in therapeutic planning and to rule out other
possible complications. Mastoiditis without abscess, lymphadenopathy,
superficial abscess, and an infected sebaceous cyst are other possibilities
that must be excluded.

Fig. 1. An axial CT scan (A) of a 5-month-old child, demonstrating opacification of the left ear
and mastoid with coalescence, and a coronal CT scan (B) of the left temporal bone in the same
patient, demonstrating a subperiosteal abscess.
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1239

Management
The management of a postauricular subperiosteal abscess from otitis me-
dia without cholesteatoma is debatable. Conventional teaching and current
texts advocate draining the abscess, in conjunction with a cortical mastoid-
ectomy [3,4]. In recent years, other, less invasive treatment options have
emerged. Patients have been treated with simple incision and drainage of
the abscess in conjunction with intravenous (IV) antibiotics and a myringot-
omy without sequelae [5]. One investigator advocates the use of IV antibi-
otics, myringotomy, and needle aspiration of the abscess without formal
drainage. In his experience, 14 of the 17 subjects treated in this manner re-
solved their abscesses without the need for further intervention, and were
discharged home significantly sooner than those subjects who were managed
with a mastoidectomy. The three subjects who failed needle aspiration went
on to require cortical mastoidectomy [6]. An argument for conservative
treatment modalities for subperiosteal abscesses from AOM is reasonable,
because the process likely will be self-limited; however, there is not yet a con-
sensus advocating these less aggressive approaches. The approach to a sub-
periosteal abscess resulting from chronic otitis in the presence of
a cholesteatoma is not as controversial. In this setting, the cholesteatoma
warrants surgical intervention, and therefore more conservative alternatives
are not reasonable. The skin incision for the mastoidectomy should be mod-
ified to incorporate the abscess cavity for adequate drainage. Once the ab-
scess is drained, a mastoidectomy is performed and the cholesteatoma
matrix is removed in the standard manner.

Bezold’s abscess
A Bezold’s abscess is a cervical abscess that develops from pathology sim-
ilar to the subperiosteal abscess. In the presence of coalescent mastoiditis, if
the mastoid cortex is violated at its tip, as opposed to its lateral cortex, an
abscess will develop in the neck, deep to the sternocleidomastoid. This ab-
scess will present as a tender, deep, poorly defined mass in level two of
the neck. Because the abscess develops from air cells at the tip of the mas-
toid, it is found in older children and adults, where pneumatization of the
mastoid has extended to the tip. Most of these abscesses result from direct
extension through the cortex, but transmission through an intact cortex by
way of mastoid vein phlebitis is known to occur [1]. Although Bezold’s ab-
scess is more commonly a complication of AOM with mastoiditis in chil-
dren, it is a known complication of COM with cholesteatoma [7].

Diagnosis
A contrasted CT scan of the neck and mastoid is recommended to make
the diagnosis of a Bezold’s abscess [8]. The presentation of an enlarged, ten-
der, deep neck mass must be differentiated from inflammatory cervical
lymphadenopathy, which is difficult on clinical grounds alone. CT scans
1240 SMITH & DANNER

of Bezold’s abscesses show a rim-enhancing abscess with surrounding in-

flammation, may demonstrate the bony dehiscence in the tip of the mastoid,
and can help in operative planning.

Management
The commonly recommended conventional approach for management of
a Bezold’s abscess is described as an open incision and drainage of the cer-
vical abscess through a transcervical approach, combined with a cortical
mastoidectomy to address the mastoiditis [3]. Abscess drainage combined
with myringotomy and IV antibiotics has not been advocated for Bezold’s
abscesses in the literature, as it has been for the subperiosteal abscess. How-
ever, time and investigation may prove that this complication can be man-
aged by less aggressive surgical options.

Intratemporal (extracranial) complications

Labyrinthine fistulae
Labyrinthine fistulae continue to be among the most common complica-
tions of chronic otitis with associated cholesteatoma, and have been re-
ported in approximately 7% of cases [9–11]. Few circumstances are more
unsettling to an otologic surgeon than the presence of an open labyrinth
found at the time of cholesteatoma surgery. The risk of significant sensori-
neural hearing loss as a result of surgical manipulation makes the open lab-
yrinth and its management a highly controversial topic.
As a result of its location near the antrum, the horizontal semicircular ca-
nal is the most commonly involved portion of the labyrinth, and accounts
for approximately 90% of these fistulae (Fig. 2). Although the horizontal
canal is usually involved, fistulae have been described in both the superior
canal and posterior canal, and in the cochlea itself. Cochlear fistulae are as-
sociated with a much higher incidence of hearing loss encountered during
surgical manipulation than are labyrinthine fistulae [10].

Fig. 2. Intraoperative picture of a horizontal canal fistula.

 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1241

Erosion of the bone of the otic capsule can occur through two distinct
processes. In the presence of a cholesteatoma, activated mediators from
the matrix, or pressure from the cholesteatoma itself, can lead to osteolysis
and uncovering of the labyrinth. However, labyrinthine fistulae can occur
from resorption of the otic capsule due to inflammatory mediators in the ab-
sence of cholesteatoma, which typically occurs in COM with granulation [4].
One reason for the confusion and controversy in discussing these fistulae
is the lack of an accepted staging system. Multiple staging systems have been
proposed [9,12]. The system introduced by Dornhoffer and Milewski [9] is
the classification used in the authors’ department, and is used in this article
to discuss fistulae and their management (Fig. 3). This system stages fistulae
with respect to the involvement of the underlying labyrinth. Fistulae with
bony erosion and intact endosteum are classified as type I fistulae. If the
endosteum is violated, but the perilymphatic space is preserved, the fistula
is staged as type IIa. When the perilymph is violated by disease or inadver-
tently suctioned, the fistula is labeled as type IIb. Type III fistula indicates
that the membranous labyrinth and endolymph have been disrupted by dis-
ease or surgical intervention [9].

Diagnosis
Patients who have significant erosion of the labyrinth classically present
with subjective vertigo and a positive fistula test on examination. Unfortu-
nately, this classic picture is not sensitive in the preoperative identification of
a fistula. Periodic vertigo or significant disequilibrium is found in 62% to
64% of patients who have fistulae preoperatively. The fistula test is positive
in 32% to 50% of patients who are found ultimately to have fistulae during
surgical exploration. Although sensorineural hearing loss is found in most
of these patients (68%), it is not a sensitive indicator of fistula [9,10].
Although the presence of sensorineural hearing loss, vertigo, or a positive
fistula test in a patient who has a cholesteatoma should raise the suspicion
for a fistula, their absence does not guarantee an intact bony labyrinth. It is
for this reason that a prudent surgical approach is to assume the presence of
a fistula in every cholesteatoma case, to prevent unexpected complications.
Although universal imaging of all patients who have cholesteatoma has
not been the standard, review of the literature demonstrates that the use

Fig. 3. A fistula staging system. (Adapted from Dornhoffer JL, Milewski C. Management of the
open labyrinth. Otolaryngol Head Neck Surg 1995;112(3):410–4.)
1242 SMITH & DANNER

of preoperative CT imaging is increasing in this country [10]. Because of the

inability to accurately diagnose fistulae preoperatively on clinical grounds,
the increase in imaging is likely an attempt to increase the detection of an
exposed labyrinth, facial nerve, or dura, to aid in surgical planning
(Fig. 4). Unfortunately, the ability to detect fistulae accurately on preoper-
ative CT has been reported as 57% to 60% [10,13]. In one of these reports,
when subjects had fistulae detected intraoperatively, their preoperative CT
scan was reviewed retrospectively to look for radiologic evidence. Despite
the knowledge of a confirmed fistula, CT evidence could only be found in
60% of these cases [13]. In the labyrinth, where millimeters matter, CT scans
of the temporal bone with 1 mm cuts can miss a thin layer of cortical bone,
which falsely increases the concern for fistula. Also, a small fistula easily can
be missed between cuts on the CT images. Although the debate regarding
the need for preoperative imaging for cholesteatoma cases will continue,
in current reports CT scans are no more sensitive than history and physical
examination in detecting labyrinthine fistulae. The definitive diagnosis for
a fistula is only made intraoperatively, which reaffirms the need to approach
all cholesteatoma cases with caution.

Management
A tympanomastoidectomy is required for the treatment of the cholestea-
toma, but the most appropriate management of the fistula remains an ongo-
ing debate. Some investigators believe that the most appropriate approach
to the fistula is to perform a canal wall down mastoidectomy, remove the
bulk of the cholesteatoma, and leave the fistula covered with the matrix ex-
teriorizing it into the cavity [14,15]. Advocates of this approach argue that
the complete removal of the matrix increases the risk of sensorineural hear-
ing loss, and that by removing the sac itself, the pressure from the cholestea-
toma is relieved and further bony erosion or infectious complications are
unlikely. Other investigators advocate the complete removal of the choles-
teatoma over the fistula, with repair of the bony defect in all circumstances

Fig. 4. A coronal CT scan of a postoperative right ear, revealing a horizontal canal fistula.
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1243

[12,16]. These investigators feel that by removing the matrix in its entirety,
the potential risk of continued bony erosion and infectious complications
such as labyrinthitis can be prevented. Furthermore, they argue the risk
of significant sensorineural hearing loss with complete removal is minimal,
and the long-term risk of sensorineural hearing loss is greater if the matrix
is left intact. Complete removal can be performed in a single setting, or in
a staged manner, with a second-look procedure. A recent review of the liter-
ature found that hearing preservation for patients who underwent complete
removal was equivalent to patients where the matrix was left over the fistula
[10]. It is impossible to know if the extent of disease was similar in these two
groups because an accepted staging system was not used for comparison.
The size, extent, and location of the fistula should be considered when de-
termining whether complete cholesteatoma removal should be attempted.
Multiple studies have demonstrated that larger fistulae have worse hearing
results postoperatively [17,18]. Dornhoffer evaluated hearing results after
single-stage, complete cholesteatoma removal, and compared results, based
on extent of disease [9]. No hearing loss resulted from the removal of type
IIa fistulae where the endosteum was violated but the perilymphatic space
was not disrupted or suctioned significantly. For type IIb and type III fistu-
lae, where the perilymph or endolymph was involved or violated signifi-
cantly, roughly one half of the subjects experienced significant hearing
loss postoperatively (8 of 17). Subjects who had fistulae with significant
labyrinthine involvement (types IIb and III) who received intraoperative
steroids experienced stable or improved hearing 90% of the time (9 of 10);
and the one subject who had hearing loss sustained only moderate high fre-
quency hearing loss. The anatomic location of the fistula also impacts hearing
results significantly. A 35% rate of profound deafness has been reported with
fistulae that involve the promontory, compared with a 3% rate of deafness
with semicircular canal fistulae [10].
The debate over the most appropriate management of labyrinthine fistu-
lae continues, but a review of the literature can help with some recommen-
dations. Small fistulae involving the labyrinth can be removed safely in
a primary setting. The use of corticosteroids at the time of cholesteatoma
removal from fistulae may have a protective effect on hearing. Large fistulae
involving the labyrinth can be treated by carefully removing the cholestea-
toma matrix and covering the defect with bone pâté and fascia (Fig. 5).
However, fistulae involving the cochlea should be approached with more
caution because of the greater risk for iatrogenic sensorineural hearing
loss, and exteriorization of matrix remaining on the fistula may be the best
option.

Coalescent mastoiditis
Mastoiditis is a spectrum of disease that must be defined appropriately to
be treated adequately. Mastoiditis, defined as mucosal thickening or
1244 SMITH & DANNER

Fig. 5. The repair of a labyrinthine fistula after removal of cholesteatoma.

a mastoid effusion, is common in the face of an acute or chronic otitis, and is

appreciated routinely on a CT scan performed in this setting. This entity is
of little clinical significance. Clinical mastoiditis presenting with postauricu-
lar erythema, tenderness, and edema, with an inferiorly and posteriorly
displaced auricle, is a distinctly different scenario. In this setting, further
workup is indicated to determine the most appropriate treatment. Fig. 6
demonstrates the difference between coalescent mastoiditis and a mastoid
effusion, as seen on CT scan.

Diagnosis
In the presence of clinical mastoiditis, a CT scan should be performed to
evaluate for an unappreciated subperiosteal abscess or coalescent mastoid-
itis (see Fig. 1). Coalescent mastoiditis is an acute, infectious process of
the mastoid bone, with characteristic loss of trabecular bone. It is a rare
complication, and is seen usually in young children with AOM. Classically,
coalescent mastoiditis is described as occurring in a well pneumatized mas-
toid with a significant, incompletely treated AOM, whereas chronic otitis
and cholesteatoma occur in a sclerotic temporal bone. However, as many
as 25% of cases of coalescent mastoiditis have been reported to occur in
a sclerotic temporal bone with COM and cholesteatoma [19].

Fig. 6. Coalescent mastoiditis in a sclerotic temporal bone with COM (A), as compared with
a mastoid effusion in a well-aerated temporal bone with AOM (B).
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1245

Management
Coalescent mastoiditis is a serious medical problem that requires aggres-
sive treatment, either surgical or medical. Classically, treatment included IV
antibiotics and mastoidectomy with removal of necrotic, devitalized bone.
In recent years, the use of myringotomy and IV antibiotics has been advo-
cated as an alternative [3,20]. This medical management requires a CT scan
to confirm resolution of the infection and aeration of the mastoid. The pres-
ence of a cholesteatoma is a surgical indication, and therefore coalescent
mastoiditis in this setting is a surgical disease. In this case, a tympanomastoi-
dectomy is performed to remove devitalized bone and the cholesteatoma,
and to re-establish aeration to the mastoid and middle ear.

Petrous apicitis
The petrous apex comprises the anterior, medial portion of the temporal
bone, and has been reported to be pneumatized in 30% of individuals [3].
These air cells, when present, are in continuity with the middle ear and mas-
toid through well-described cell tracts around the labyrinth, allowing for in-
fection involving the mastoid and middle ear cleft to extend into the petrous
apex. Petrous apicitis is a spectrum of disease much like mastoiditis, and can
involve anything from an asymptomatic effusion to coalescence and abscess
formation. Infection of the petrous apex is a dangerous entity because of its
proximity to the middle and posterior cranial fossae and their contents.

Diagnosis
The classic symptomatology associated with petrous apicitis is a triad of
deep retro-orbital pain, aural discharge, and sixth nerve palsy, also known
as Gradenigo’s syndrome. Although these symptoms can be associated
with apicitis, they are by no means pathognomonic of this condition.
Retro-orbital pain and abducens palsy have been reported to occur in
50% and 25% of reported cases, respectively [21]. Petrous apicitis becomes
evident only after failure to control chronic suppurative otomastoiditis with
prolonged medical and surgical management. When apicitis is suspected,
a CT scan should be performed to make the diagnosis and to evaluate sur-
rounding anatomy. A CT scan will also aid in the diagnosis of intracranial
complications that often accompany this condition. Some believe that once
the diagnosis is made with clinical evaluation and CT, an MRI of the brain
or a lumbar puncture should be performed to evaluate for intracranial com-
plications [4].

Management
Early in the twentieth century, before the widespread use of antibiotics,
surgical intervention for petrous apex abscesses and petrous apicitis was rel-
atively common. However, as the use of antibiotics has increased, the prev-
alence of apicitis has decreased significantly. The petrous apex is an area
that is not easily approached surgically because of its relationship with
1246 SMITH & DANNER

the otic capsule and carotid artery. Because of the difficult surgical approach
and the response rate to antibiotics, IV antibiotics are often the first-line
treatment of petrous apicitis. IV antibiotics require a long duration of treat-
ment. Serial C-reactive protein levels and erythrocyte sedimentation rates
have been used to monitor for response of bony infections to medical man-
agement elsewhere in the body [22], and are a reasonable option for follow-
ing a patient who has petrous apicitis to assess for response. In the presence
of abscess, necrotic bone, or persistent infection despite medical therapy,
surgical drainage is required. Air cell tracts extend to the apex below, above,
and anterior to the labyrinth. In a hearing ear, these three air cell tracts al-
low several possibilities for surgical approach including: infracochlear,
infralabyrinthine, retrolabyrinthine, subarcuate, and even middle fossa [4].
In a nonhearing ear, the translabyrinthine or transcochlear approaches
are reasonable and give wide exposure to the affected area. One disadvan-
tage of these two approaches is that they could potentially expose the cere-
brospinal fluid (CSF) to the infectious process.

Facial paralysis
Otogenic causes of facial nerve paralysis include AOM, COM without
cholesteatoma, and cholesteatoma. The first usually occurs with a dehiscent
fallopian canal within its tympanic segment, allowing direct contact of in-
flammatory mediators with the facial nerve itself. COM with or without
cholesteatoma can result in facial paralysis through involvement of a dehis-
cent nerve, or through bony erosion. Facial paralysis secondary to AOM of-
ten presents in children with incomplete paresis that comes on abruptly and
is usually short-lived with appropriate treatment. On the other hand, paral-
ysis secondary to COM or cholesteatoma often presents with slowly pro-
gressive facial paralysis and has a worse prognosis [3].

Diagnosis
The diagnosis of otogenic facial paralysis is made on clinical grounds.
Facial paresis or paralysis in the presence of AOM, COM, or cholesteatoma
is not a difficult diagnosis to make by examination alone. The role of diag-
nostic CT imaging is questionable. Although a CT scan is not required, it
can be useful in therapeutic planning and patient counseling. When choles-
teatoma involves the fallopian canal, it may also erode structures such as the
labyrinth or tegmen. Furthermore, the extent of bony erosion of the fallo-
pian canal and degree of involvement is better appreciated on CT [23].

Management
Although facial paralysis secondary to AOM usually is treated with ap-
propriate antibiotics and myringotomy, the treatment of paralysis with
COM with or without cholesteatoma requires surgical intervention. When
facial paralysis is associated with cholesteatoma, a mastoidectomy is
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1247

performed to remove the cholesteatoma or granulation tissue that is contact-

ing the facial nerve. The nerve is approached on both sides of the involve-
ment, and a diamond burr is used to expose the epineurium on either side
of the diseased segment. Once the proximal and distal segments of the fallo-
pian canal have been opened, blunt dissection is used to remove the disease
from the epineurium. The nerve sheath does not have to be incised unless the
cholesteatoma has invaded the nerve itself [4]. Although cholesteatoma can
involve the facial nerve at any point through its intratemporal course, the
tympanic segment and second genu are involved most commonly [24].

Intracranial complications
Meningitis
Meningitis is the most common intracranial complication of acute and
COM; conversely, AOM is the most common secondary cause of meningitis
[25,26]. In a recent series of COM complications, meningitis occurred in ap-
proximately 0.1% of subjects [1,4]. Although this remains a significant com-
plication, the mortality rate from otitic meningitis has declined significantly,
from 35% in the preantibiotic era to 5% in the postantibiotic era [27]. Men-
ingitis can arise from three distinct otogenic routes: hematogenous seeding
of the meninges and subarachnoid space; spread from the middle ear or
mastoid through preformed channels (Hyrtl’s fissures); or through bony ero-
sion and direct extension. Of these three possibilities, otogenic meningitis
most commonly results from hematogenous seeding [3,4].

Diagnosis
The prompt diagnosis of meningitis relies on the recognition of warning
signs by an astute clinician. Signs that should increase the suspicion of an
intracranial complication include persistent or intermittent fever; nausea
and vomiting; irritability; lethargy; or persistent headache. Ominous signs
virtually diagnostic of an intracranial process include visual changes; new
onset seizures; nuchal rigidity; ataxia; or decreased mental status [3]. If
any of these suspicious or ominous signs occur, immediate treatment and
further workup are critical. Broad-spectrum antibiotics, such as third-gener-
ation cephalosporins, should be administered while diagnostic tests are
ordered and arranged. A contrasted CT scan or MRI will show character-
istic meningeal enhancement and rule out additional intracranial complica-
tions known to occur in up to 50% of these cases [28]. In the absence of
a significant mass effect on imaging, a lumbar puncture should be performed
to confirm the diagnosis and to allow for culture and sensitivity.

Management
The presence of symptoms suspicious for otogenic intracranial complica-
tions warrants the use of broad-spectrum IV antibiotic therapy while the
1248 SMITH & DANNER

workup is being performed. If meningitis is confirmed by imaging and lum-

bar puncture, IV antibiotics should be continued. In the presence of COM
with or without cholesteatoma, gram-negative and anaerobe coverage is
necessary. In addition to IV antibiotics, the use of systemic corticosteroids
is beneficial because they have been shown to decrease auditory and neuro-
logic sequelae [29]. Corticosteroids should be administered as early in the
course as possible to maximize their efficacy. The role of mastoidectomy
in this diagnosis is not completely clear. Indications for mastoidectomy in-
clude the presence of cholesteatoma; coalescent mastoiditis; bony erosion
with direct extension of disease; or persistence of symptoms despite maximal
medical therapy [3]. Although debated, a trial of IV antibiotics, steroids, and
myringotomy is a reasonable treatment option for meningitis secondary to
AOM or COM without cholesteatoma [3].

Brain abscess
Brain abscess is the second most common intracranial complication of
otitis media after meningitis, but it is perhaps the most lethal. In contrast
to meningitis, which is caused more frequently by AOM, brain abscesses al-
most exclusively result from COM [30]. The temporal lobe and cerebellum
are affected most often. These abscesses develop as a result of hematogenous
extension secondary to thrombophlebitis in virtually all cases, but tegmen
erosion with epidural abscess can lead to temporal lobe abscess. Cultures
of these abscesses are often sterile, and, when positive, usually reveal mixed
flora; however Proteus is cultured more frequently than any other pathogen
[30]. The clinical progression seen in these patients occurs in three named
stages. The first stage is described as the encephalitic stage, and includes
the flu-like symptoms of fever, rigors, nausea, vomiting, headache, and men-
tal status changes or seizures. This stage is followed by the quiescent, or
latent, stage, in which acute symptoms abate, but general fatigue and list-
lessness persist. The third and final stage marks the return of acute symp-
toms, including severe headaches, vomiting, fevers, mental status changes,
hemodynamic changes, and increased intracranial pressure. This third stage
is attributable to rupture or expansion of the abscess cavity [3].

Diagnosis
As with meningitis, the presence of any symptoms that might indicate in-
tracranial involvement requires prompt action. In the presence of these
symptoms, a contrasted CT scan or MRI should be ordered while IV anti-
microbial therapy is initiated. For brain abscesses, MRI is superior (Fig. 7).
Although the MRI gives better detail regarding the abscess itself, a CT scan
gives valuable information about bony erosion of the mastoid, and can help
in determining the cause of the abscess and the most appropriate treatment
options. The imaging itself is diagnostic of a significant parenchymal
abscess, and a thorough evaluation of the imaging is required to rule out
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1249

Fig. 7. An axial T1-weighted MRI (A) and a coronal T2-weighted MRI (B) demonstrating
a large right cerebellar brain abscess with resulting hydrocephalus.

concomitant intracranial complications, or evidence of increased intracra-

nial pressure.

Management
Immediate initiation of broad-spectrum antibiotics that cover gram pos-
itives, gram negatives, and anaerobes is necessary because of the severity of
this infection and its polymicrobial nature. As in otitic meningitis, these an-
tibiotics should be initiated while further workup is being performed. Once
the diagnosis of a brain abscess is made, surgical intervention is required.
Drainage of the abscess requires neurosurgical intervention, but the patient
must be stabilized from a neurologic standpoint. IV steroids are often given
to decrease brain edema, and anticonvulsants are given to prophylax against
seizures. When the patient is stable, neurosurgical drainage is performed,
either through an open craniotomy with drainage or excision, or by stereo-
tactic aspiration through a burr hole. This procedure not only drains the
abscess, but provides a culture, enabling antibiotic therapy to be tailored.
Drainage of the brain abscess is paramount, and should be performed
within 24 hours of presentation, if the patient is stable [3].
However, the most appropriate way to treat the otologic component is
somewhat controversial. In the setting of AOM, myringotomy with evacu-
ation of the purulent effusion is sufficient. In the presence of COM with
or without cholesteatoma, a mastoidectomy is required to eradicate the
source of infection. The most appropriate time to perform the mastoidec-
tomy is controversial. It has been conventional teaching that a mastoidec-
tomy is performed in a delayed manner after the patient recovers from
the abscess and neurosurgical drainage. Current recommendations, how-
ever, are to perform a mastoidectomy at the time of abscess drainage to
1250 SMITH & DANNER

remove the infectious focus, assuming the patient is stable enough to toler-
ate this additional surgery. However, specific parameters dictating staged
versus simultaneous surgery have not yet been reported or established.
One recent report has advocated primary mastoidectomy with needle aspi-
ration of the abscess through the dura exposed in the mastoidectomy cavity
[30]. Regardless of the type of surgical intervention, when it has been com-
pleted, IV antibiotics should be continued for several weeks and serial CT
scans with contrast followed to assure resolution of the abscess [3].

Lateral sinus thrombosis

Sigmoid sinus or lateral sinus thrombosis is a well-known complication of
otitis media that compromises 17% to 19% of intracranial complications
[26,31]. The proximity of the middle ear and mastoid air cells to the dural
venous sinuses predisposes them to thrombosis and thrombophlebitis sec-
ondary to infection and inflammation in the middle ear and mastoid. In-
volvement of the sigmoid or lateral sinus can result from bony erosion
secondary to COM and cholesteatoma, with direct extension of the infec-
tious process to the perisinus space, or from the seeding of the space from
thrombophlebitis of mastoid emissary veins. Once the sinuses have become
involved, and an intramural thrombus develops, any number of serious
complications can result. Otitic hydrocephalus is known to complicate a sig-
nificant number of these cases. The infected clot can propagate proximally
to involve the confluence of sinuses (torcular herophili) and sagittal sinus,
causing life-threatening hydrocephalus, or propagate distally to involve
the internal jugular vein [3]. Involvement of the internal jugular vein in-
creases the risk of septic pulmonary emboli.

Diagnosis
The classic presentation of sigmoid or lateral sinus thrombosis is the pres-
ence of high spiking fevers in a ‘‘picket fence’’ pattern, often seen with head-
aches and general malaise [2]. Like many of these complications, a high
degree of suspicion is required because the spiking fevers may be blunted by
concurrent antibiotic use. With the presence of high spiking fevers, or concern
for increased intracranial pressure, a contrasted CT scan should be performed
to screen for thrombophlebitis. The sinus wall will enhance brightly with con-
trast and produce the characteristic delta sign associated with sinus thrombo-
sis (Fig. 8). With the presence of significant sinus thrombosis, an MRI and
magnetic resonance venogram (MRV) are warranted, because they can be
used serially to evaluate for clot propagation or resolution.

Management
Dural venous thrombosis in the presence of chronic otomastoiditis with
or without cholesteatoma is a surgical disease. At a minimum, a mastoidec-
tomy with removal of chronic infection, granulation, and cholesteatoma is
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1251

Fig. 8. A contrasted axial CT scan demonstrating right sigmoid sinus thrombosis with an
‘‘empty delta’’ sign.

required. The sigmoid sinus is exposed and the surrounding epidural abscess
or granulation is removed. The best way to manage the sinus itself is a point
of contention in the otology literature. Classically, most texts recommend
a diagnostic needle aspiration of the affected sinus, once it is exposed surgi-
cally. If the aspiration reveals normal blood return, then the sinus is left in-
tact; but if the aspiration is negative or reveals frank pus, the sinus is opened
and at least a portion of the infected clot is evacuated. However, recent re-
ports have challenged this dictum, and demonstrated that if the surrounding
granulation tissue and inflammation are removed through a mastoidectomy,
the sinus will recannalize without clot evacuation [32]. One report demon-
strated that with sinus thrombosis in the presence of AOM, myringotomy
and IV antibiotics resolved the infection, and the sinus was shown to recan-
nulate in three subjects without mastoidectomy [33]. Ligation of the internal
jugular vein is not necessary unless there is evidence of continued septic em-
bolization after surgical intervention and IV antibiotics. After surgical inter-
vention, the patient should remain on IV antibiotics for at least 2 weeks, at
which point a repeat MRI and MRV should be performed to rule out the
development of a secondary intracranial complication such as brain abscess,
or propagation of the thrombus into the superior sagittal sinus. [2] Systemic
anticoagulation is not necessary unless the clot is shown to involve the sag-
ittal sinus, or signs of increased intracranial pressure persist despite medical
management.

Epidural abscess
The presence of an epidural abscess can often be insidious in develop-
ment. These abscesses develop as a result of bony destruction from
1252 SMITH & DANNER

cholesteatoma or from coalescent mastoiditis. The signs and symptoms do

not differ significantly from those found in COM. Occasionally, dural irrita-
tion can result in increased otalgia or headaches that serve as a concerning
sign in the background of COM. Because this complication can be subtle in
presentation, it is often found incidentally at the time of cholesteatoma sur-
gery or CT scan for other purposes.

Diagnosis
Unlike other intracranial complications, there are no sensitive or specific
symptoms suggestive of this disease process. A high degree of clinical suspi-
cion is required to diagnose an epidural abscess preoperatively. The presence
of increased otalgia or headache should raise the suspicion for an intracra-
nial complication, and warrants imaging. A contrasted CT scan or MRI is
sufficient to diagnose this abscess. Even with a careful evaluation, this diag-
nosis is often made at the time of surgery.

Management
When an epidural abscess is appreciated intraoperatively or on CT scan,
surgical drainage is necessary. A mastoidectomy is performed to treat the
underlying pathology, paying careful attention to thin the bony tegmen
and bone overlying the posterior fossa dura as much as possible, so epidural
pus or granulation can be appreciated. The bone overlying the dura is re-
moved to evacuate the pus and granulation until normal dura is encountered
[4]. Postoperative antibiotics are continued at least until the symptoms of
the abscess and otitis have resolved.

Otitic hydrocephalus
Otitic hydrocephalus is described as signs and symptoms indicative of in-
creased intracranial pressure with normal CSF studies on lumbar puncture,
which can present as a complication of AOM, COM, or otologic surgery.
‘‘Otitic hydrocephalus’’ is somewhat of a misnomer, and its pathophysiol-
ogy is not understood completely. It is a misnomer because this condition
can be found in the absence of otitis, and patients do not have dilated ven-
tricles indicative of true hydrocephalus. Symonds [34], who coined the term
otitic hydrocephalus, felt that this condition developed from infection of the
lateral (transverse) sinus, with extension of thrombophlebitis into the con-
fluence of sinuses to involve the superior sagittal sinus. Inflammation or in-
fection of the superior sagittal sinus prevents CSF absorption through the
arachnoid villi, resulting in increased intracranial pressure. This infectious
thrombophlebitis usually occurs as a result of otologic infection, but multi-
ple cases have been described in the absence of otitis or otologic surgery
[34,35]. Furthermore, although lateral sinus thrombosis is found usually
in the presence of otitic hydrocephalus, cases have been reported without
thrombosis of the dural sinuses [36].
 COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA 1253

Diagnosis
The diagnosis of otitic hydrocephalus is one of exclusion, and requires
a high degree of suspicion to recognize the suggestive symptoms. The symp-
toms found in these patients are a result of increased intracranial pressure
and include diffuse headaches, nausea, vomiting, visual changes, and leth-
argy. The presence of these symptoms requires a thorough examination
and imaging. A dilated fundoscopic examination should be conducted to
evaluate for papilledema as evidence of increased intracranial pressure.
An MRI and MRV should be performed to evaluate for ventricular enlarge-
ment, or coexisting intracranial complications, such as significant sinus
thrombosis with obstruction. Increased intracranial pressure with clinical
symptoms and papilledema in the absence of ventricular dilation or menin-
gitis is enough to make this diagnosis. MRV will confirm the presence and
extent of dural sinus thrombosis, but is not required to make a diagnosis of
otitic hydrocephalus.

Management
The goal in the treatment of otitic hydrocephalus is to treat any underly-
ing infectious otitis, decrease intracranial pressure, and prevent the poten-
tially devastating complication of optic nerve atrophy. With COM (with
or without cholesteatoma) in the presence of dural sinus thrombosis, a mas-
toidectomy should be performed to remove the infectious process and the
cholesteatoma, and to address the dural venous sinus. In the absence of
a surgical indication such as cholesteatoma or tumor, the treatment is med-
ical in nature, and should include acetazolamide, fluid restriction, and cor-
ticosteroids to decrease intracranial pressure and cerebral edema. Systemic
anticoagulation is not required unless an MRV shows sinus thrombophlebi-
tis involves the sagittal sinus. In these cases, the risk of neurologic sequelae
and death are significant enough to warrant anticoagulation [35]. If aggres-
sive medical management does not normalize the intracranial pressure, lum-
bar drainage of CSF can be performed serially or by a lumbar drain. If
prolonged drainage is required because of recalcitrant papilledema, a shunt
may be required [4,35].

Summary
The incidence of extracranial and intracranial complications of COM and
cholesteatoma has decreased since the proliferation of antibiotics early in
the twentieth century. However, these complications continue to occur,
and can be lethal if they are not identified and treated properly. Therapy
for the complications associated with COM, unlike those of AOM, usually
includes surgical intervention, in addition to medical therapy. As medical
(antibiotic) therapy continues to improve, and new imaging techniques are
introduced, less invasive treatment modalities may be shown to be as effec-
tive as the classic, time-tested, surgical options.
1254 SMITH & DANNER

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