Complications of Chronic Otitis

Otolaryngol Clin N Am

39 (2006) 1237–1255

Complications of Chronic OtitisMedia and Cholesteatoma

Jason A. Smith, MD*, Christopher J. Danner, MDDepartment 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 orcontinuous otorrhea. As chronic otomastoiditis and eustachian tube dys-function persist, the tympanic membrane is weakened, which increases thelikelihood 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 theseareas at increased risk of infectious complications. Acute otitis media(AOM) and its complications are more common in young children, whereascomplications secondary to COM with and without cholesteatoma are morecommon in older children and adults. In a large series by Osma and col-leagues [1], 78% of subjects who had complications secondary to COMwere 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 earlydetection and treatment. Furthermore, with the continued development ofmulti–drug-resistant pathogens, these complications may again becomemore prevalent as our current antibiotics become less effective [2].

* Corresponding author.

E-mail address: [email protected] (J.A. Smith).

0030-6665/06/$ - see front matter � 2006 Elsevier Inc. All rights reserved.

doi:10.1016/j.otc.2006.09.001 oto.theclinics.com

mailto:[email protected]

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Extratemporal (extracranial) complications

Subperiosteal abscess

Subperiosteal abscess is the most common extratemporal complicationthat occurs with COM. This abscess occurs over the mastoid cortex whenthe infectious process within the mastoid air cells extends into the subperios-teal space. This extension most commonly occurs as a result of erosion ofthe cortex secondary to acute or coalescent mastoiditis, but can also occuras a result of vascular extension secondary to phlebitis of the mastoid veins[3]. Subperiosteal abscesses are seen more commonly in young children withAOM, but are also found in chronic otitis with and without cholesteatoma.Cholesteatoma can block the aditus ad antrum, preventing communicationof 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 subperiostealabscess or Bezold’s abscess.

DiagnosisOften, 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 certainon clinical evaluation, a contrasted CT scan can demonstrate abscess andpossibly the cortical defect in the mastoid (Fig. 1) [4]. A case can be madefor a contrasted CT scan of the temporal bone in all patients presentingwith these symptoms, to aid in therapeutic planning and to rule out otherpossible complications. Mastoiditis without abscess, lymphadenopathy,superficial abscess, and an infected sebaceous cyst are other possibilitiesthat 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.

1239COMPLICATIONS OF CHRONIC OTITIS MEDIA AND CHOLESTEATOMA

ManagementThe management of a postauricular subperiosteal abscess from otitis me-

dia without cholesteatoma is debatable. Conventional teaching and currenttexts advocate draining the abscess, in conjunction with a cortical mastoid-ectomy [3,4]. In recent years, other, less invasive treatment options haveemerged. Patients have been treated with simple incision and drainage ofthe 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 formaldrainage. In his experience, 14 of the 17 subjects treated in this manner re-solved their abscesses without the need for further intervention, and weredischarged home significantly sooner than those subjects who were managedwith a mastoidectomy. The three subjects who failed needle aspiration wenton to require cortical mastoidectomy [6]. An argument for conservativetreatment 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 ofa cholesteatoma is not as controversial. In this setting, the cholesteatomawarrants surgical intervention, and therefore more conservative alternativesare 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 cholesteatomamatrix 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, ifthe mastoid cortex is violated at its tip, as opposed to its lateral cortex, anabscess will develop in the neck, deep to the sternocleidomastoid. This ab-scess will present as a tender, deep, poorly defined mass in level two ofthe 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 themastoid has extended to the tip. Most of these abscesses result from directextension through the cortex, but transmission through an intact cortex byway 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].

DiagnosisA 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 cervicallymphadenopathy, which is difficult on clinical grounds alone. CT scans

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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.

ManagementThe 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 corticalmastoidectomy to address the mastoiditis [3]. Abscess drainage combinedwith myringotomy and IV antibiotics has not been advocated for Bezold’sabscesses 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 moreunsettling to an otologic surgeon than the presence of an open labyrinthfound 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 accountsfor approximately 90% of these fistulae (Fig. 2). Although the horizontalcanal is usually involved, fistulae have been described in both the superiorcanal and posterior canal, and in the cochlea itself. Cochlear fistulae are as-sociated with a much higher incidence of hearing loss encountered duringsurgical manipulation than are labyrinthine fistulae [10].

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


Erosion of the bone of the otic capsule can occur through two distinctprocesses. In the presence of a cholesteatoma, activated mediators fromthe matrix, or pressure from the cholesteatoma itself, can lead to osteolysisand uncovering of the labyrinth. However, labyrinthine fistulae can occurfrom 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 fistulaeis the lack of an accepted staging system. Multiple staging systems have beenproposed [9,12]. The system introduced by Dornhoffer and Milewski [9] isthe classification used in the authors’ department, and is used in this articleto discuss fistulae and their management (Fig. 3). This system stages fistulaewith respect to the involvement of the underlying labyrinth. Fistulae withbony erosion and intact endosteum are classified as type I fistulae. If theendosteum is violated, but the perilymphatic space is preserved, the fistulais 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 indicatesthat the membranous labyrinth and endolymph have been disrupted by dis-ease or surgical intervention [9].

DiagnosisPatients 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 ofa fistula. Periodic vertigo or significant disequilibrium is found in 62% to64% of patients who have fistulae preoperatively. The fistula test is positivein 32% to 50% of patients who are found ultimately to have fistulae duringsurgical exploration. Although sensorineural hearing loss is found in mostof these patients (68%), it is not a sensitive indicator of fistula [9,10].Although the presence of sensorineural hearing loss, vertigo, or a positivefistula test in a patient who has a cholesteatoma should raise the suspicionfor a fistula, their absence does not guarantee an intact bony labyrinth. It isfor this reason that a prudent surgical approach is to assume the presence ofa fistula in every cholesteatoma case, to prevent unexpected complications.

Although universal imaging of all patients who have cholesteatoma hasnot 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.)

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of preoperative CT imaging is increasing in this country [10]. Because of theinability to accurately diagnose fistulae preoperatively on clinical grounds,the increase in imaging is likely an attempt to increase the detection of anexposed 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 CTscan was reviewed retrospectively to look for radiologic evidence. Despitethe knowledge of a confirmed fistula, CT evidence could only be found in60% of these cases [13]. In the labyrinth, where millimeters matter, CT scansof 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 canbe missed between cuts on the CT images. Although the debate regardingthe need for preoperative imaging for cholesteatoma cases will continue,in current reports CT scans are no more sensitive than history and physicalexamination in detecting labyrinthine fistulae. The definitive diagnosis fora fistula is only made intraoperatively, which reaffirms the need to approachall cholesteatoma cases with caution.

ManagementA 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 approachto the fistula is to perform a canal wall down mastoidectomy, remove thebulk of the cholesteatoma, and leave the fistula covered with the matrix ex-teriorizing it into the cavity [14,15]. Advocates of this approach argue thatthe 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 areunlikely. 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.


[12,16]. These investigators feel that by removing the matrix in its entirety,the potential risk of continued bony erosion and infectious complicationssuch as labyrinthitis can be prevented. Furthermore, they argue the riskof significant sensorineural hearing loss with complete removal is minimal,and the long-term risk of sensorineural hearing loss is greater if the matrixis left intact. Complete removal can be performed in a single setting, or ina staged manner, with a second-look procedure. A recent review of the liter-ature found that hearing preservation for patients who underwent completeremoval 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 twogroups 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 hearingresults postoperatively [17,18]. Dornhoffer evaluated hearing results aftersingle-stage, complete cholesteatoma removal, and compared results, basedon extent of disease [9]. No hearing loss resulted from the removal of typeIIa fistulae where the endosteum was violated but the perilymphatic spacewas 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 hearingloss postoperatively (8 of 17). Subjects who had fistulae with significantlabyrinthine involvement (types IIb and III) who received intraoperativesteroids 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 hearingresults significantly. A 35% rate of profound deafness has been reported withfistulae that involve the promontory, compared with a 3% rate of deafnesswith 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 ina primary setting. The use of corticosteroids at the time of cholesteatomaremoval from fistulae may have a protective effect on hearing. Large fistulaeinvolving the labyrinth can be treated by carefully removing the cholestea-toma matrix and covering the defect with bone pate and fascia (Fig. 5).However, fistulae involving the cochlea should be approached with morecaution because of the greater risk for iatrogenic sensorineural hearingloss, and exteriorization of matrix remaining on the fistula may be the bestoption.

Coalescent mastoiditis

Mastoiditis is a spectrum of disease that must be defined appropriately tobe treated adequately. Mastoiditis, defined as mucosal thickening or

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a mastoid effusion, is common in the face of an acute or chronic otitis, and isappreciated routinely on a CT scan performed in this setting. This entity isof little clinical significance. Clinical mastoiditis presenting with postauricu-lar erythema, tenderness, and edema, with an inferiorly and posteriorlydisplaced auricle, is a distinctly different scenario. In this setting, furtherworkup is indicated to determine the most appropriate treatment. Fig. 6demonstrates the difference between coalescent mastoiditis and a mastoideffusion, as seen on CT scan.

DiagnosisIn 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 ofthe mastoid bone, with characteristic loss of trabecular bone. It is a rarecomplication, 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 otitisand cholesteatoma occur in a sclerotic temporal bone. However, as manyas 25% of cases of coalescent mastoiditis have been reported to occur ina sclerotic temporal bone with COM and cholesteatoma [19].

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

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).


ManagementCoalescent mastoiditis is a serious medical problem that requires aggres-

sive treatment, either surgical or medical. Classically, treatment included IVantibiotics 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 scanto confirm resolution of the infection and aeration of the mastoid. The pres-ence of a cholesteatoma is a surgical indication, and therefore coalescentmastoiditis 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 temporalbone, 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 petrousapex. Petrous apicitis is a spectrum of disease much like mastoiditis, and caninvolve anything from an asymptomatic effusion to coalescence and abscessformation. Infection of the petrous apex is a dangerous entity because of itsproximity to the middle and posterior cranial fossae and their contents.

DiagnosisThe classic symptomatology associated with petrous apicitis is a triad of

deep retro-orbital pain, aural discharge, and sixth nerve palsy, also knownas Gradenigo’s syndrome. Although these symptoms can be associatedwith apicitis, they are by no means pathognomonic of this condition.Retro-orbital pain and abducens palsy have been reported to occur in50% and 25% of reported cases, respectively [21]. Petrous apicitis becomesevident only after failure to control chronic suppurative otomastoiditis withprolonged 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 intracranialcomplications that often accompany this condition. Some believe that oncethe diagnosis is made with clinical evaluation and CT, an MRI of the brainor a lumbar puncture should be performed to evaluate for intracranial com-plications [4].

ManagementEarly 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 areathat is not easily approached surgically because of its relationship with

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the otic capsule and carotid artery. Because of the difficult surgical approachand the response rate to antibiotics, IV antibiotics are often the first-linetreatment of petrous apicitis. IV antibiotics require a long duration of treat-ment. Serial C-reactive protein levels and erythrocyte sedimentation rateshave 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 presenceof 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 approachesare 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 withoutcholesteatoma, and cholesteatoma. The first usually occurs with a dehiscentfallopian canal within its tympanic segment, allowing direct contact of in-flammatory mediators with the facial nerve itself. COM with or withoutcholesteatoma 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 andis 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].

DiagnosisThe diagnosis of otogenic facial paralysis is made on clinical grounds.

Facial paresis or paralysis in the presence of AOM, COM, or cholesteatomais 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, itcan be useful in therapeutic planning and patient counseling. When choles-teatoma involves the fallopian canal, it may also erode structures such as thelabyrinth or tegmen. Furthermore, the extent of bony erosion of the fallo-pian canal and degree of involvement is better appreciated on CT [23].

ManagementAlthough facial paralysis secondary to AOM usually is treated with ap-

propriate antibiotics and myringotomy, the treatment of paralysis withCOM with or without cholesteatoma requires surgical intervention. Whenfacial paralysis is associated with cholesteatoma, a mastoidectomy is


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 sideof the diseased segment. Once the proximal and distal segments of the fallo-pian canal have been opened, blunt dissection is used to remove the diseasefrom the epineurium. The nerve sheath does not have to be incised unless thecholesteatoma has invaded the nerve itself [4]. Although cholesteatoma caninvolve the facial nerve at any point through its intratemporal course, thetympanic segment and second genu are involved most commonly [24].

Intracranial complications

Meningitis

Meningitis is the most common intracranial complication of acute andCOM; 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 seedingof the meninges and subarachnoid space; spread from the middle ear ormastoid through preformed channels (Hyrtl’s fissures); or through bony ero-sion and direct extension. Of these three possibilities, otogenic meningitismost commonly results from hematogenous seeding [3,4].

DiagnosisThe prompt diagnosis of meningitis relies on the recognition of warning

signs by an astute clinician. Signs that should increase the suspicion of anintracranial complication include persistent or intermittent fever; nauseaand vomiting; irritability; lethargy; or persistent headache. Ominous signsvirtually diagnostic of an intracranial process include visual changes; newonset seizures; nuchal rigidity; ataxia; or decreased mental status [3]. Ifany of these suspicious or ominous signs occur, immediate treatment andfurther workup are critical. Broad-spectrum antibiotics, such as third-gener-ation cephalosporins, should be administered while diagnostic tests areordered 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 ofa significant mass effect on imaging, a lumbar puncture should be performedto confirm the diagnosis and to allow for culture and sensitivity.

ManagementThe presence of symptoms suspicious for otogenic intracranial complica-

tions warrants the use of broad-spectrum IV antibiotic therapy while the

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workup is being performed. If meningitis is confirmed by imaging and lum-bar puncture, IV antibiotics should be continued. In the presence of COMwith or without cholesteatoma, gram-negative and anaerobe coverage isnecessary. In addition to IV antibiotics, the use of systemic corticosteroidsis beneficial because they have been shown to decrease auditory and neuro-logic sequelae [29]. Corticosteroids should be administered as early in thecourse as possible to maximize their efficacy. The role of mastoidectomyin this diagnosis is not completely clear. Indications for mastoidectomy in-clude the presence of cholesteatoma; coalescent mastoiditis; bony erosionwith direct extension of disease; or persistence of symptoms despite maximalmedical therapy [3]. Although debated, a trial of IV antibiotics, steroids, andmyringotomy is a reasonable treatment option for meningitis secondary toAOM or COM without cholesteatoma [3].

Brain abscess

Brain abscess is the second most common intracranial complication ofotitis media after meningitis, but it is perhaps the most lethal. In contrastto meningitis, which is caused more frequently by AOM, brain abscesses al-most exclusively result from COM [30]. The temporal lobe and cerebellumare affected most often. These abscesses develop as a result of hematogenousextension secondary to thrombophlebitis in virtually all cases, but tegmenerosion with epidural abscess can lead to temporal lobe abscess. Culturesof these abscesses are often sterile, and, when positive, usually reveal mixedflora; however Proteus is cultured more frequently than any other pathogen[30]. The clinical progression seen in these patients occurs in three namedstages. The first stage is described as the encephalitic stage, and includesthe flu-like symptoms of fever, rigors, nausea, vomiting, headache, and men-tal status changes or seizures. This stage is followed by the quiescent, orlatent, 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 stageis attributable to rupture or expansion of the abscess cavity [3].

DiagnosisAs with meningitis, the presence of any symptoms that might indicate in-

tracranial involvement requires prompt action. In the presence of thesesymptoms, 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 scangives valuable information about bony erosion of the mastoid, and can helpin determining the cause of the abscess and the most appropriate treatmentoptions. The imaging itself is diagnostic of a significant parenchymalabscess, and a thorough evaluation of the imaging is required to rule out


concomitant intracranial complications, or evidence of increased intracra-nial pressure.

ManagementImmediate initiation of broad-spectrum antibiotics that cover gram pos-

itives, gram negatives, and anaerobes is necessary because of the severity ofthis infection and its polymicrobial nature. As in otitic meningitis, these an-tibiotics should be initiated while further workup is being performed. Oncethe diagnosis of a brain abscess is made, surgical intervention is required.Drainage of the abscess requires neurosurgical intervention, but the patientmust be stabilized from a neurologic standpoint. IV steroids are often givento decrease brain edema, and anticonvulsants are given to prophylax againstseizures. 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 theabscess, but provides a culture, enabling antibiotic therapy to be tailored.Drainage of the brain abscess is paramount, and should be performedwithin 24 hours of presentation, if the patient is stable [3].

However, the most appropriate way to treat the otologic component issomewhat controversial. In the setting of AOM, myringotomy with evacu-ation of the purulent effusion is sufficient. In the presence of COM withor without cholesteatoma, a mastoidectomy is required to eradicate thesource 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 fromthe abscess and neurosurgical drainage. Current recommendations, how-ever, are to perform a mastoidectomy at the time of abscess drainage to

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.

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remove the infectious focus, assuming the patient is stable enough to toler-ate this additional surgery. However, specific parameters dictating stagedversus 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 CTscans with contrast followed to assure resolution of the abscess [3].

Lateral sinus thrombosis

Sigmoid sinus or lateral sinus thrombosis is a well-known complication ofotitis media that compromises 17% to 19% of intracranial complications[26,31]. The proximity of the middle ear and mastoid air cells to the duralvenous 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 erosionsecondary to COM and cholesteatoma, with direct extension of the infec-tious process to the perisinus space, or from the seeding of the space fromthrombophlebitis of mastoid emissary veins. Once the sinuses have becomeinvolved, and an intramural thrombus develops, any number of seriouscomplications can result. Otitic hydrocephalus is known to complicate a sig-nificant number of these cases. The infected clot can propagate proximallyto involve the confluence of sinuses (torcular herophili) and sagittal sinus,causing life-threatening hydrocephalus, or propagate distally to involvethe internal jugular vein [3]. Involvement of the internal jugular vein in-creases the risk of septic pulmonary emboli.

DiagnosisThe 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 highdegree of suspicion is required because the spiking fevers may be blunted byconcurrent antibiotic use.With the presence of high spiking fevers, or concernfor increased intracranial pressure, a contrasted CT scan should be performedto 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 andmagnetic resonance venogram (MRV) are warranted, because they can beused serially to evaluate for clot propagation or resolution.

ManagementDural 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


required. The sigmoid sinus is exposed and the surrounding epidural abscessor granulation is removed. The best way to manage the sinus itself is a pointof contention in the otology literature. Classically, most texts recommenda 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 openedand at least a portion of the infected clot is evacuated. However, recent re-ports have challenged this dictum, and demonstrated that if the surroundinggranulation 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, myringotomyand IV antibiotics resolved the infection, and the sinus was shown to recan-nulate in three subjects without mastoidectomy [33]. Ligation of the internaljugular 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, atwhich point a repeat MRI and MRV should be performed to rule out thedevelopment of a secondary intracranial complication such as brain abscess,or propagation of the thrombus into the superior sagittal sinus. [2] Systemicanticoagulation is not necessary unless the clot is shown to involve the sag-ittal sinus, or signs of increased intracranial pressure persist despite medicalmanagement.

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

Fig. 8. A contrasted axial CT scan demonstrating right sigmoid sinus thrombosis with an

‘‘empty delta’’ sign.

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cholesteatoma or from coalescent mastoiditis. The signs and symptoms donot differ significantly from those found in COM. Occasionally, dural irrita-tion can result in increased otalgia or headaches that serve as a concerningsign in the background of COM. Because this complication can be subtle inpresentation, it is often found incidentally at the time of cholesteatoma sur-gery or CT scan for other purposes.

DiagnosisUnlike 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 presenceof increased otalgia or headache should raise the suspicion for an intracra-nial complication, and warrants imaging. A contrasted CT scan or MRI issufficient to diagnose this abscess. Even with a careful evaluation, this diag-nosis is often made at the time of surgery.

ManagementWhen an epidural abscess is appreciated intraoperatively or on CT scan,

surgical drainage is necessary. A mastoidectomy is performed to treat theunderlying pathology, paying careful attention to thin the bony tegmenand bone overlying the posterior fossa dura as much as possible, so epiduralpus 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 ofthe 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 conditioncan be found in the absence of otitis, and patients do not have dilated ven-tricles indicative of true hydrocephalus. Symonds [34], who coined the termotitic hydrocephalus, felt that this condition developed from infection of thelateral (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 thearachnoid villi, resulting in increased intracranial pressure. This infectiousthrombophlebitis 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 usuallyin the presence of otitic hydrocephalus, cases have been reported withoutthrombosis of the dural sinuses [36].


DiagnosisThe 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 pressureand include diffuse headaches, nausea, vomiting, visual changes, and leth-argy. The presence of these symptoms requires a thorough examinationand imaging. A dilated fundoscopic examination should be conducted toevaluate 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 sinusthrombosis with obstruction. Increased intracranial pressure with clinicalsymptoms and papilledema in the absence of ventricular dilation or menin-gitis is enough to make this diagnosis. MRV will confirm the presence andextent of dural sinus thrombosis, but is not required to make a diagnosis ofotitic hydrocephalus.

ManagementThe 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 (withor without cholesteatoma) in the presence of dural sinus thrombosis, a mas-toidectomy should be performed to remove the infectious process and thecholesteatoma, and to address the dural venous sinus. In the absence ofa 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. Systemicanticoagulation is not required unless an MRV shows sinus thrombophlebi-tis involves the sagittal sinus. In these cases, the risk of neurologic sequelaeand 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. Ifprolonged drainage is required because of recalcitrant papilledema, a shuntmay be required [4,35].

Summary

The incidence of extracranial and intracranial complications of COM andcholesteatoma has decreased since the proliferation of antibiotics early inthe twentieth century. However, these complications continue to occur,and can be lethal if they are not identified and treated properly. Therapyfor the complications associated with COM, unlike those of AOM, usuallyincludes surgical intervention, in addition to medical therapy. As medical(antibiotic) therapy continues to improve, and new imaging techniques areintroduced, 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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Complications of Chronic Otitis